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  • 1
    Online Resource
    Online Resource
    Joints Fatigue Damage Prediction for a Steel Truss Suspension Bridge Considering Corrosion Environment
    Springer Science and Business Media LLC ; 2022
    In:  Arabian Journal for Science and Engineering Vol. 47, No. 4 ( 2022-04), p. 4879-4892
    Details
    In: Arabian Journal for Science and Engineering, Springer Science and Business Media LLC, Vol. 47, No. 4 ( 2022-04), p. 4879-4892
    Type of Medium: Online Resource
    ISSN: 2193-567X , 2191-4281
    URL: Article
    DOI: 10.1007/s13369-021-06318-8
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2022
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    SSG: 11
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  • 2
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    Inhibition of HtrA2 alleviated dextran sulfate sodium (DSS)-induced colitis by preventing necroptosis of intestinal epithelial cells
    Springer Science and Business Media LLC ; 2019
    In:  Cell Death & Disease Vol. 10, No. 5 ( 2019-04-24)
    Details
    In: Cell Death & Disease, Springer Science and Business Media LLC, Vol. 10, No. 5 ( 2019-04-24)
    Abstract: Necroptosis of intestinal epithelial cells has been indicated to play an important role in the pathogenesis of inflammatory bowel disease (IBD). The identification of dysregulated proteins that can regulate necroptosis in dextran sulfate sodium (DSS)-induced colitis is the key to the rational design of therapeutic strategies for colitis. Through tandem mass tag (TMT)-based quantitative proteomics, HtrA2 was found to be downregulated in the colon of DSS-treated mice. UCF-101, a specific serine protease inhibitor of HtrA2, significantly alleviated DSS-induced colitis as indicated by prevention of body weight loss and decreased mortality. UCF-101 decreased DSS-induced colonic inflammation, prevented intestinal barrier function loss and inhibited necroptosis of intestinal epithelial cells. In vitro, UCF-101 or silencing of HtrA2 decreased necroptosis of HT-29 and L929 cells. UCF-101 decreased phosphorylation of RIPK1 and subsequent phosphorylation of RIPK3 and MLKL during necroptosis. Upon necroptotic stimulation, HtrA2 translocated from mitochondria to cytosol. HtrA2 directly interacted with RIPK1 and promoted its degradation during a specific time phase of necroptosis. Our findings highlight the importance of HtrA2 in regulating colitis by modulation of necroptosis and suggest HtrA2 as an attractive target for anti-colitis treatment.
    Type of Medium: Online Resource
    ISSN: 2041-4889
    URL: Article
    DOI: 10.1038/s41419-019-1580-7
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2019
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  • 3
    Online Resource
    Online Resource
    A pan-RAF inhibitor LY3009120 inhibits necroptosis by preventing phosphorylation of RIPK1 and alleviates dextran sulfate sodium-induced colitis
    Portland Press Ltd. ; 2019
    In:  Clinical Science Vol. 133, No. 8 ( 2019-04-30), p. 919-932
    Details
    In: Clinical Science, Portland Press Ltd., Vol. 133, No. 8 ( 2019-04-30), p. 919-932
    Abstract: A dramatic increase in the incidence of inflammatory bowel disease (IBD) has been observed in the past two decades, mainly in developed countries and also in developing regions. Necroptosis has been found to play an important role in the pathogenesis of IBD, suggesting its inhibitors are promising in clinic. However, clinical drugs targeting necroptosis are seriously lacking. Through screening a clinical compound library that contains 611 inhibitors, a pan-RAF inhibitor LY3009120 was found to be promising as a necroptosis inhibitor. LY3009120 inhibited necroptosis in vitro, and its inhibition against necroptosis was independent of its well-known activity to inhibit RAF. Surprisingly, LY3009120 prevented phosphorylation of receptor interacting serine/threonine kinase 1 (RIPK1) and subsequently phosphorylation of receptor interacting serine/threonine kinase 3 (RIPK3) and mixed lineage kinase domain like pseudokinase (MLKL) which happened during necroptosis. In vivo, LY3009120 significantly alleviated dextran sulfate sodium (DSS)-induced colitis as indicated by prevention of body weight loss, colon shortening, and decreased mortality. Furthermore, LY3009120 inhibited necroptosis of intestinal epithelial cells (IECs) and prevented intestinal barrier function loss. Consistently, LY3009120 decreased DSS-induced colonic inflammation, as indicated by decreased infiltration of macrophages and neutrophils, and decreased colonic TNF-α, IL-6, and IL-1β level in DSS treated mice. These results indicate that an anti-cancer pan-RAF inhibitor LY3009120 is a necroptosis inhibitor and may serve as a potential therapeutic drug for colitis.
    Type of Medium: Online Resource
    ISSN: 0143-5221 , 1470-8736
    URL: Article
    DOI: 10.1042/CS20181081
    Language: English
    Publisher: Portland Press Ltd.
    Publication Date: 2019
    detail.hit.zdb_id: 206835-7
    detail.hit.zdb_id: 1484392-4
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  • 4
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    Online Resource
    Phosphorescent Cationic Iridium(III) Complexes with 1,3,4-Oxadiazole Cyclometalating Ligands: Solvent-Dependent Excited-State Dynamics
    AIP Publishing ; 2017
    In:  Chinese Journal of Chemical Physics Vol. 30, No. 3 ( 2017-06-27), p. 259-267
    Details
    In: Chinese Journal of Chemical Physics, AIP Publishing, Vol. 30, No. 3 ( 2017-06-27), p. 259-267
    Abstract: To elucidate the nature of low-lying triplet states and the effect of ligand modifications on the excited-state properties of functional cationic iridium complexes, the solvent-dependent excited-state dynamics of two phosphorescent cationic iridium(III) complexes, namely [Ir(dph-oxd)2(bpy)]PF6 (1) and [Ir(dph-oxd)2(pzpy)] PF6 (2), were investigated by femtosecond and nanosecond transient absorption spectroscopy. Upon photoexcitation to the metal-to-ligand charge-transfer (MLCT) states, the excited-state dynamics shows a rapid process (τ=0.7−3 ps) for the formation of solvent stabilized 3MLCT states, which significantly depends on the solvent polarity for both 1 and 2. Sequentially, a relatively slow process assigned to the vibrational cooling/geometrical relaxation and a long-lived phosphorescent emissive state is identified. Due to the different excited-state electronic structures regulated by ancillary ligands, the solvation-induced stabilization of the 3MLCT state in 1 is faster than that in 2. The present results provide a better sight of excited-state relaxation dynamics of ligand-related iridium(III) complexes and solvation effects on triplet manifolds.
    Type of Medium: Online Resource
    ISSN: 1674-0068 , 2327-2244
    URL: Article
    DOI: 10.1063/1674-0068/30/cjcp1703058
    Language: English
    Publisher: AIP Publishing
    Publication Date: 2017
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    detail.hit.zdb_id: 2381472-X
    SSG: 6,25
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  • 5
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    Fibrinogen/AKT/Microfilament Axis Promotes Colitis by Enhancing Vascular Permeability
    Elsevier BV ; 2021
    In:  Cellular and Molecular Gastroenterology and Hepatology Vol. 11, No. 3 ( 2021), p. 683-696
    Details
    In: Cellular and Molecular Gastroenterology and Hepatology, Elsevier BV, Vol. 11, No. 3 ( 2021), p. 683-696
    Type of Medium: Online Resource
    ISSN: 2352-345X
    URL: Article
    DOI: 10.1016/j.jcmgh.2020.10.007
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2021
    detail.hit.zdb_id: 2819778-1
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  • 6
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    The mechanism study of mixed Ar/O2 plasma-cleaning treatment on niobium surface for work function improvement
    Elsevier BV ; 2019
    In:  Applied Surface Science Vol. 475 ( 2019-05), p. 143-150
    Details
    In: Applied Surface Science, Elsevier BV, Vol. 475 ( 2019-05), p. 143-150
    Type of Medium: Online Resource
    ISSN: 0169-4332
    URL: Article
    DOI: 10.1016/j.apsusc.2018.12.156
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2019
    detail.hit.zdb_id: 52886-9
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  • 7
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    TSSK4 upregulation in alveolar epithelial type-II cells facilitates pulmonary fibrosis through HSP90-AKT signaling restriction and AT-II apoptosis
    Springer Science and Business Media LLC ; 2021
    In:  Cell Death & Disease Vol. 12, No. 10 ( 2021-10-13)
    Details
    In: Cell Death & Disease, Springer Science and Business Media LLC, Vol. 12, No. 10 ( 2021-10-13)
    Abstract: Alveolar epithelial injury is one of the important pathological changes in idiopathic pulmonary interstitial fibrosis (IPF), but the regulatory mechanism remains unclear. Here, we reported that alveolar epithelial type-II cells (AT II) play important roles in pathological process of pulmonary fibrosis. Through iTRAQ (isobaric tagging for relative and absolute quantification) quantitative proteomics, TSSK4 was identified to be upregulated in bleomycin-induced fibrotic mice model, which was further confirmed in clinical IPF patients’ tissue specimens. TSSK4 is a germ-related protein, but its expression in other tissues and the association with other diseases are not reported. Immunofluorescence staining showed that TSSK4 selectively expressed in AT-II cells, which are essential for inflammation-induced AT-II loss during fibrosis. Luciferase assay and other molecular biological experiments proved that TSSK4 expression is regulated by TNF-α-mediated NF-κB signaling. The TSSK4 kinase activity is found to be closely related to the function of HSP90-AKT pathway that TSSK4 can phosphorylate its substrate HSP90β on serine 255, to inhibit the ATPase activity of HSP90β and reduce its molecular chaperone function on AKT. Under this condition, kinase activity of AKT is diminished to interfere its survival function, subsequently facilitating AT-II cellular apoptosis through the mitochondrial death machinery. Our findings highlight the importance of TSSK4 in regulating pulmonary fibrosis by facilitating AT-II loss through HSP90-AKT signaling, all of which suggest TSSK4 and the regulating mechanism as attractive targets for the clinical intervention of pulmonary injury and fibrosis.
    Type of Medium: Online Resource
    ISSN: 2041-4889
    URL: Article
    DOI: 10.1038/s41419-021-04232-3
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2021
    detail.hit.zdb_id: 2541626-1
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  • 8
    Online Resource
    Online Resource
    Biomechanical Properties and Cellular Responses in Pulmonary Fibrosis
    MDPI AG ; 2024
    In:  Bioengineering Vol. 11, No. 8 ( 2024-07-24), p. 747-
    Details
    In: Bioengineering, MDPI AG, Vol. 11, No. 8 ( 2024-07-24), p. 747-
    Abstract: Pulmonary fibrosis is a fatal lung disease affecting approximately 5 million people worldwide, with a 5-year survival rate of less than 50%. Currently, the only available treatments are palliative care and lung transplantation, as there is no curative drug for this condition. The disease involves the excessive synthesis of the extracellular matrix (ECM) due to alveolar epithelial cell damage, leading to scarring and stiffening of the lung tissue and ultimately causing respiratory failure. Although multiple factors contribute to the disease, the exact causes remain unclear. The mechanical properties of lung tissue, including elasticity, viscoelasticity, and surface tension, are not only affected by fibrosis but also contribute to its progression. This paper reviews the alteration in these mechanical properties as pulmonary fibrosis progresses and how cells in the lung, including alveolar epithelial cells, fibroblasts, and macrophages, respond to these changes, contributing to disease exacerbation. Furthermore, it highlights the importance of developing advanced in vitro models, based on hydrogels and 3D bioprinting, which can accurately replicate the mechanical and structural properties of fibrotic lungs and are conducive to studying the effects of mechanical stimuli on cellular responses. This review aims to summarize the current understanding of the interaction between the progression of pulmonary fibrosis and the alterations in mechanical properties, which could aid in the development of novel therapeutic strategies for the disease.
    Type of Medium: Online Resource
    ISSN: 2306-5354
    URL: Article
    DOI: 10.3390/bioengineering11080747
    Language: English
    Publisher: MDPI AG
    Publication Date: 2024
    detail.hit.zdb_id: 2746191-9
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  • 9
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    Online Resource
    ATM participates in fine particulate matter‐induced airway inflammation through regulating DNA damage and DNA damage response
    Wiley ; 2023
    In:  Environmental Toxicology Vol. 38, No. 11 ( 2023-11), p. 2668-2678
    Details
    In: Environmental Toxicology, Wiley, Vol. 38, No. 11 ( 2023-11), p. 2668-2678
    Abstract: The relationship between fine particulate matter (PM2.5) and chronic airway inflammatory diseases, such as chronic obstructive pulmonary disease and asthma, have garnered public attention, while the detailed mechanisms of PM2.5‐induced airway inflammation remain unclear. This study reveals that PM2.5 induces airway inflammation both in vivo and in vitro, and, moreover, identifies DNA damage and DNA damage repair (DDR) as results of this exposure. Ataxia telangiectasia‐mutated heterozygous (ATM +/− ) and wild‐type C57BL/6 (WT) mice were exposed to PM2.5. The results show that, following exposure to PM2.5, the number of neutrophils in broncho alveolar lavage fluid and the mRNA expression of CXCL‐1 in lung tissues of the ATM +/− mice were lower than those of the WT mice. The mRNA expression of FANCD2 and FANCI were also down‐regulated. Human bronchial epithelial (HBE) cells were transfected with ATM‐siRNA to induce down‐regulation of ATM gene expression and were subsequently stimulated with PM2.5. The results show that the mRNA expression of TNF‐α decreased in the ATM‐siRNA‐transfected cells. The mRNA expression of CXCL‐1 and CXCL‐2 in peritoneal macrophages, derived from ATM‐null mice in which experiments showed that the protein expression of FANCD2 and FANCI decreased, were also decreased after PM2.5 exposure in ATM‐siRNA‐transfected HBE cells. In conclusion, PM2.5‐induced airway inflammation is alleviated in ATM +/− mice compared with WT mice. ATM promotes PM2.5‐induced airway inflammation, which may be attributed to the regulation of DNA damage and DDR.
    Type of Medium: Online Resource
    ISSN: 1520-4081 , 1522-7278
    URL: Issue
    URL: Article
    DOI: 10.1002/tox.v38.11
    DOI: 10.1002/tox.23901
    Language: English
    Publisher: Wiley
    Publication Date: 2023
    detail.hit.zdb_id: 2027534-1
    detail.hit.zdb_id: 1463449-1
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  • 10
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    Bioinformatics analysis identifies potential autophagy key genes and immune infiltration in preeclampsia
    Wiley ; 2024
    In:  Journal of Obstetrics and Gynaecology Research Vol. 50, No. 4 ( 2024-04), p. 618-632
    Details
    In: Journal of Obstetrics and Gynaecology Research, Wiley, Vol. 50, No. 4 ( 2024-04), p. 618-632
    Abstract: Preeclampsia (PE) is a disease that seriously threatens maternal and fetal health. Appropriate autophagy can shield the placenta from oxidative stress, but its role in PE is unclear. Objective To identify potential autophagy‐related genes in PE. Methods Microarray datasets from the Gene Expression Omnibus database, compassing the test dataset GSE10588, along with validation datasets GSE4707 and GSE60438 GPL10558, were utilized. Differentially expressed genes (DEGs) were identified using the limma R package, intersected with autophagy‐related genes. Hub genes were obtained using the Cytoscape software and analyzed via gene set enrichment analysis (GSEA). The diagnostic capability of hub genes was evaluated using receiver operating characteristic (ROC) curve analysis. Analysis of immune cell infiltration was conducted using single‐sample gene set enrichment analysis (ssGSEA) and CIBERSORT methods. Placental tissues were collected from 10 normal pregnant women and 10 preeclamptic pregnant women, and the expression of hub genes was validated through immunohistochemistry and western blot analysis. Results Analysis of the microarray data identified 2224 DEGs, among which 26 were autophagy‐related DEGs identified through intersection with autophagy genes. Ten hub genes were identified. Immune cell infiltration analysis suggested the potential involvement of T regulatory cells (Tregs), natural killer cells, neutrophils, and T follicular helper cells in the pathogenesis of PE. ROC curve analysis indicated promising diagnostic capabilities for EGFR and TP53. Additionally, levels of EGFR and TP53 were significantly higher in placental tissue from PE pregnancies compared to normal pregnancies. Conclusion EGFR and TP53 may play a role in PE by influencing autophagy.
    Type of Medium: Online Resource
    ISSN: 1341-8076 , 1447-0756
    URL: Issue
    URL: Article
    DOI: 10.1111/jog.v50.4
    DOI: 10.1111/jog.15902
    Language: English
    Publisher: Wiley
    Publication Date: 2024
    detail.hit.zdb_id: 1327307-3
    detail.hit.zdb_id: 2079101-X
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