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  • Wiley  (3)
  • Liu, Jingqi  (3)
  • 1
    Online Resource
    Online Resource
    The role of hepatitis B core‐related antigen in predicting hepatitis B virus recurrence after liver transplantation
    Wiley ; 2019
    In:  Alimentary Pharmacology & Therapeutics Vol. 50, No. 9 ( 2019-11), p. 1025-1036
    Details
    In: Alimentary Pharmacology & Therapeutics, Wiley, Vol. 50, No. 9 ( 2019-11), p. 1025-1036
    Abstract: Hepatitis B core‐related antigen (HBcrAg) is a viral marker for the development of cirrhosis and hepatocellular carcinoma (HCC) in patients with chronic hepatitis B (CHB). However, the relationship between HBcrAg and HBV recurrence after liver transplantation (LT) is unclear. Aim To investigate the correlation of serum HBcrAg level with HBV recurrence post‐LT to evaluate the prognostic role of the pre‐LT HBcrAg level. Methods This retrospective cohort study enrolled 357 CHB patients who received LT for a median of 36.6 months. Univariate and multivariate analyses and time‐dependent receiver operating characteristic (ROC) curves for markers associated with HBV recurrence were analysed. Results 48 patients (13.4%) had HBV recurrence after LT. HBcrAg, detectable HBV DNA, HCC and HCC recurrence were associated with HBV recurrence. In a multivariate analysis, HBcrAg level was independently associated with HBV recurrence, and the relationship between HBcrAg level and incident HBV recurrence was significant and graded (HR: 3.17 per unit; 95% CI: 1.97‐5.11; P for trend  〈  .001). Additionally, HBcrAg level was superior to HBV DNA level in predicting HBV recurrence by time‐dependent ROC analysis. Patients with an HBcrAg ≥ 5.0 log U/mL had a significantly higher 5‐year cumulative recurrence rate than those with an HBcrAg  〈  5.0 log U/mL (37.6% vs 6%, P   〈  .001); the adjusted hazard ratio was 5.27 (95% CI 2.47‐11.25, P   〈  .001). Conclusion An elevated serum HBcrAg level was independently associated with the risk of HBV recurrence in patients with CHB after LT.
    Type of Medium: Online Resource
    ISSN: 0269-2813 , 1365-2036
    URL: Issue
    URL: Article
    DOI: 10.1111/apt.v50.9
    DOI: 10.1111/apt.15429
    Language: English
    Publisher: Wiley
    Publication Date: 2019
    detail.hit.zdb_id: 2003094-0
    SSG: 15,3
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  • 2
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    Online Resource
    Molecular mechanism underlying the difference in proliferation between placenta‐derived and umbilical cord‐derived mesenchymal stem cells
    Wiley ; 2020
    In:  Journal of Cellular Physiology Vol. 235, No. 10 ( 2020-10), p. 6779-6793
    Details
    In: Journal of Cellular Physiology, Wiley, Vol. 235, No. 10 ( 2020-10), p. 6779-6793
    Abstract: The placenta and umbilical cord are pre‐eminent candidate sources of mesenchymal stem cells (MSCs). However, placenta‐derived MSCs (P‐MSCs) showed greater proliferation capacity than umbilical cord‐derived MSCs (UC‐MSCs) in our study. We investigated the drivers of this proliferation difference and elucidated the mechanisms of proliferation regulation. Proteomic profiling and Gene Ontology (GO) functional enrichment were conducted to identify candidate proteins that may influence proliferation. Using lentiviral or small interfering RNA infection, we established overexpression and knockdown models and observed changes in cell proliferation to examine whether a relationship exists between the candidate proteins and proliferation capacity. Real‐time quantitative polymerase chain reaction, western blot analysis, and immunofluorescence assays were conducted to elucidate the mechanisms underlying proliferation. Six candidate proteins were selected based on the results of proteomic profiling and GO functional enrichment. Through further validation, yes‐associated protein 1 (YAP1) and β‐catenin were confirmed to affect MSCs proliferation rates. YAP1 and β‐catenin showed increased nuclear colocalization during cell expansion. YAP1 overexpression significantly enhanced proliferation capacity and upregulated the expression of both β‐catenin and the transcriptional targets of Wnt signaling, CCND1, and c‐MYC, whereas silencing β‐catenin attenuated this influence. We found that YAP1 directly interacts with β‐catenin in the nucleus to form a transcriptional YAP/β‐catenin/TCF4 complex. Our study revealed that YAP1 and β‐catenin caused the different proliferation capacities of P‐MSCs and UC‐MSCs. Mechanism analysis showed that YAP1 stabilized the nuclear β‐catenin protein, and also triggered the Wnt/β‐catenin pathway, promoting proliferation.
    Type of Medium: Online Resource
    ISSN: 0021-9541 , 1097-4652
    URL: Issue
    URL: Article
    DOI: 10.1002/jcp.v235.10
    DOI: 10.1002/jcp.29572
    Language: English
    Publisher: Wiley
    Publication Date: 2020
    detail.hit.zdb_id: 1478143-8
    SSG: 12
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  • 3
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    Online Resource
    Immunosuppressive effect of mesenchymal stem cells on lung and gut CD8 + T cells in lipopolysaccharide‐induced acute lung injury in mice
    Wiley ; 2021
    In:  Cell Proliferation Vol. 54, No. 5 ( 2021-05)
    Details
    In: Cell Proliferation, Wiley, Vol. 54, No. 5 ( 2021-05)
    Abstract: Acute lung injury (ALI) not only affects pulmonary function but also leads to intestinal dysfunction, which in turn contributes to ALI. Mesenchymal stem cell (MSC) transplantation can be a potential strategy in the treatment of ALI. However, the mechanisms of synergistic regulatory effects by MSCs on the lung and intestine in ALI need more in‐depth study. Materials and methods We evaluated the therapeutic effects of MSCs on the murine model of lipopolysaccharide (LPS)‐induced ALI through survival rate, histopathology and bronchoalveolar lavage fluid. Metagenomic sequencing was performed to assess the gut microbiota. The levels of pulmonary and intestinal inflammation and immune response were assessed by analysing cytokine expression and flow cytometry. Results Mesenchymal stem cells significantly improved the survival rate of mice with ALI, alleviated histopathological lung damage, improved intestinal barrier integrity, and reduced the levels of inflammatory cytokines in the lung and gut. Furthermore, MSCs inhibited the inflammatory response by decreasing the infiltration of CD8 + T cells in both small‐intestinal lymphocytes and Peyer's patches. The gut bacterial community diversity was significantly altered by MSC transplantation. Furthermore, depletion of intestinal bacterial communities with antibiotics resulted in more severe lung and gut damages and mortality, while MSCs significantly alleviated lung injury due to their immunosuppressive effect. Conclusions The present research indicates that MSCs attenuate lung and gut injury partly via regulation of the immune response in the lungs and intestines and gut microbiota, providing new insights into the mechanisms underlying the therapeutic effects of MSC treatment for LPS‐induced ALI.
    Type of Medium: Online Resource
    ISSN: 0960-7722 , 1365-2184
    URL: Issue
    URL: Article
    DOI: 10.1111/cpr.v54.5
    DOI: 10.1111/cpr.13028
    Language: English
    Publisher: Wiley
    Publication Date: 2021
    detail.hit.zdb_id: 2019986-7
    SSG: 12
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