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  • Frontiers Media SA  (5)
  • Chen, Xiaofeng  (5)
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  • Frontiers Media SA  (5)
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  • 1
    Online Resource
    Online Resource
    Table_1.docx
    Frontiers Media SA ; 2022
    In:  Frontiers in Oncology Vol. 12 ( 2022-5-11)
    Details
    In: Frontiers in Oncology, Frontiers Media SA, Vol. 12 ( 2022-5-11)
    Abstract: The natural product pectolinarigenin exerts anti-inflammatory activity and anti-tumor effects, and exhibits different biological functions, particularly in autophagy and cell cycle regulation. However, the antineoplastic effect of pectolinarigenin on glioblastoma (GBM) remains unclear. In the present study, we found that pectolinarigenin inhibits glioblastoma proliferation, increases autophagic flux, and induces cell cycle arrest by inhibiting ribonucleotide reductase subunit M2 (RRM2), which can be reversed by RRM2 overexpression plasmid. Additionally, pectolinarigenin promoted RRM2 protein degradation via autolysosome-dependent pathway by increasing autophagic flow. RRM2 knockdown promoted the degradation of CDK1 protein through autolysosome-dependent pathway by increasing autophagic flow, thereby inhibiting the proliferation of glioblastoma by inducing G2/M phase cell cycle arrest. Clinical data analysis revealed that RRM2 expression in glioma patients was inversely correlated with the overall survival. Collectively, pectolinarigenin promoted the degradation of CDK1 protein dependent on autolysosomal pathway through increasing autophagic flux by inhibiting RRM2, thereby inhibiting the proliferation of glioblastoma cells by inducing G2/M phase cell cycle arrest, and RRM2 may be a potential therapeutic target and a prognosis and predictive biomarker in GBM patients.
    Type of Medium: Online Resource
    ISSN: 2234-943X
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    DOI: 10.3389/fonc.2022.887294
    DOI: 10.3389/fonc.2022.887294.s001
    DOI: 10.3389/fonc.2022.887294.s002
    DOI: 10.3389/fonc.2022.887294.s003
    DOI: 10.3389/fonc.2022.887294.s004
    DOI: 10.3389/fonc.2022.887294.s005
    DOI: 10.3389/fonc.2022.887294.s006
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2022
    detail.hit.zdb_id: 2649216-7
    Location Call Number Limitation Availability
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    Online Resource
  • 2
    Online Resource
    Online Resource
    Renoprotective Effect of the Recombinant Anti-IL-6R Fusion Proteins by Inhibiting JAK2/STAT3 Signaling Pathway in Diabetic Nephropathy
    Frontiers Media SA ; 2021
    In:  Frontiers in Pharmacology Vol. 12 ( 2021-5-13)
    Details
    In: Frontiers in Pharmacology, Frontiers Media SA, Vol. 12 ( 2021-5-13)
    Abstract: Diabetic nephropathy the main reason for end stage renal disease is a common microvascular complication in patients with type 1 and type 2 diabetes. The interleukin-6 (IL-6), acting as a pleiotropic cytokine, play key roles in main autoimmune disorders. The recombinant anti-IL-6R fusion proteins (VHH-0031) constructed and obtained in our lab is a dual target-directed single domain-based fusion protein against the interleukin-6 receptor. This study aims to explore the renoprotective effect of VHH-0031 in diabetic nephropathy. VHH-0031 treatment alleviated renal inflammation, morphologic injury and renal insufficiency in both Goto-Kakizaki rats and STZ-induced Sprague Dawley rats. These renoprotective effects of VHH-0031 are associated with alleviating inflammation and suppression of the JAK2/STAT3 signaling pathway. The mesangial cells treated with VHH-0031 exhibited anti-proliferation, anti-inflammation and inactivation of JAK2/STAT3 pathway under high glucose condition. In conclusion, this study demonstrates that VHH-0031 exhibited a potent protective effect in kidney of diabetic rats and its mechanism may be concerned with the inhibition of the IL-6R/JAK2/STAT3 pathway of glomerular mesangial cells.
    Type of Medium: Online Resource
    ISSN: 1663-9812
    URL: Article
    DOI: 10.3389/fphar.2021.681424
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2021
    detail.hit.zdb_id: 2587355-6
    SSG: 15,3
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    Online Resource
  • 3
    Online Resource
    Online Resource
    Table_4.xlsx
    Frontiers Media SA ; 2022
    In:  Frontiers in Immunology Vol. 13 ( 2022-7-6)
    Details
    In: Frontiers in Immunology, Frontiers Media SA, Vol. 13 ( 2022-7-6)
    Abstract: Lung adenocarcinoma featured as mixed ground-glass opacity (mGGO) doubled its volume half of the time in comparison with that featured as pure ground-glass opacity (pGGO). The mechanisms underlying the heterogeneous appearance of mGGO remain elusive. In this study, we macro-dissected the solid (S) components and ground-glass (GG) components of mGGO and performed single-cell sequencing analyses of six paired components from three mGGO patients. A total of 19,391 single-cell profiles were taken into analysis, and the data of each patient were analyzed independently to obtain a common alteration. Cancer cells and macrophages were the dominant cell types in the S and GG components, respectively. Cancer cells in the S components, which showed relatively malignant phenotypes, were likely to originate from both the GG and S components and monitor the surrounding tumor microenvironment (TME) through an intricate cell interaction network. SPP1 hi macrophages were enriched in the S components and showed increased activity of chemoattraction, while macrophages in the GG components displayed an active antimicrobial process with a higher stress-induced state. In addition, the CD47–SIRPA axis was demonstrated to be critical in the maintenance of the GG components. Taken together, our study unraveled the alterations of cell components and transcriptomic features between different components in mGGOs.
    Type of Medium: Online Resource
    ISSN: 1664-3224
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    URL: Article
    DOI: 10.3389/fimmu.2022.903513
    DOI: 10.3389/fimmu.2022.903513.s001
    DOI: 10.3389/fimmu.2022.903513.s002
    DOI: 10.3389/fimmu.2022.903513.s003
    DOI: 10.3389/fimmu.2022.903513.s004
    DOI: 10.3389/fimmu.2022.903513.s005
    DOI: 10.3389/fimmu.2022.903513.s006
    DOI: 10.3389/fimmu.2022.903513.s007
    DOI: 10.3389/fimmu.2022.903513.s008
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2022
    detail.hit.zdb_id: 2606827-8
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    Online Resource
  • 4
    Online Resource
    Online Resource
    DataSheet1.docx
    Frontiers Media SA ; 2021
    In:  Frontiers in Materials Vol. 8 ( 2021-11-10)
    Details
    In: Frontiers in Materials, Frontiers Media SA, Vol. 8 ( 2021-11-10)
    Abstract: The repair of bone defects in load-bearing positions still faces great challenges. Tantalum (Ta) has attempted to repair bone defects based on the excellent mechanical properties. However, the osseointegration of Ta needs to be improved due to the lack of osteoinduction. Herein, tantalum–gelatin–methacryloyl–bioactive glass (Ta–GelMA–BG) scaffolds were successfully fabricated by loading BG in 3D-printed Ta scaffolds through a chemical crosslinking method. The results showed that the composite scaffolds have the ability to promote cell adhesion and proliferation. The incorporation of BG resulted in a significant increase in apatite-forming and osteogenesis differentiation abilities. In vivo results indicated that the Ta–GelMA–BG scaffolds significantly enhanced the osteointegration at the early stage after implantation. Overall, the Ta–GelMA–BG scaffolds are a promising platform for the load bearing bone regeneration field.
    Type of Medium: Online Resource
    ISSN: 2296-8016
    URL: Article
    URL: Article
    DOI: 10.3389/fmats.2021.701268
    DOI: 10.3389/fmats.2021.701268.s001
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2021
    detail.hit.zdb_id: 2759394-0
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  • 5
    Online Resource
    Online Resource
    Video_1.MP4
    Frontiers Media SA ; 2022
    In:  Frontiers in Surgery Vol. 8 ( 2022-1-18)
    Details
    In: Frontiers in Surgery, Frontiers Media SA, Vol. 8 ( 2022-1-18)
    Abstract: Surgical resection is currently the mainstay of treatment for tracheobronchial mucoepidermoid carcinoma (TMEC). The parenchymal sparing secondary carinal resection and reconstruction for TMEC under the uniportal thoracoscopic approach has seldomly been reported in the literature. Here, we report a case of a 42-year-old male patient complaining of the incidental finding of a 1.5 × 1.2 cm neoplasm at the opening of the right bronchus intermedius and a 5.1 × 3.1 cm patchy lesion located at the left upper lobe by chest CT scans in February 2021. This patient successively underwent fiberoptic bronchoscopic biopsy of the bronchial neoplasm and CT-guided biopsy of the left upper lobe lesion. Pathological examination confirmed the diagnosis of the endobronchial mass in the right bronchus intermedius as low-grade mucoepidermoid carcinoma and left upper lobe lesion as tuberculosis. This patient successfully underwent uniportal thoracoscopic parenchymal sparing tumor resection, reconstruction of the secondary carina and lymphadenectomy at our center. Intraoperative frozen section showed no residual cancer at any bronchial stumps. Postoperative pathology indicated that no metastases were seen in any of the resected lymph nodes. The patient recovered well after surgery. He received a 9-month course of anti-tuberculosis treatment postoperatively. He did not complain of any special discomfort and there was no local recurrence at the 9-month postoperative follow-up. Although technical demanding, this case highlights that uniportal video-assisted thoracoscopic parenchymal sparing secondary carinal resection and reconstruction for TMEC is safe and feasible with the preservation of lung function and excellent outcomes.
    Type of Medium: Online Resource
    ISSN: 2296-875X
    URL: Article
    URL: Article
    DOI: 10.3389/fsurg.2021.823281
    DOI: 10.3389/fsurg.2021.823281.s001
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2022
    detail.hit.zdb_id: 2773823-1
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