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  • 1
    Online Resource
    Online Resource
    A new criteria for acute on preexisting kidney dysfunction in critically ill patients
    Informa UK Limited ; 2023
    In:  Renal Failure Vol. 45, No. 1 ( 2023-12-31)
    Details
    In: Renal Failure, Informa UK Limited, Vol. 45, No. 1 ( 2023-12-31)
    Type of Medium: Online Resource
    ISSN: 0886-022X , 1525-6049
    URL: Article
    DOI: 10.1080/0886022X.2023.2173498
    Language: English
    Publisher: Informa UK Limited
    Publication Date: 2023
    detail.hit.zdb_id: 2015459-8
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  • 2
    Online Resource
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    Comprehensive analysis of alternative polyadenylation regulators concerning CD276 and immune infiltration in bladder cancer
    Springer Science and Business Media LLC ; 2022
    In:  BMC Cancer Vol. 22, No. 1 ( 2022-09-29)
    Details
    In: BMC Cancer, Springer Science and Business Media LLC, Vol. 22, No. 1 ( 2022-09-29)
    Abstract: Alternative polyadenylation (APA) is emerging as a crucial regulatory mechanism in bladder cancer (BC), while it remains elusive whether APA influences the tumor immune microenvironment (TIME) in BC. We identified two distinct subtypes of BC by APA-related regulatory genes expression profiles. The two subtypes have different pathological grades, prognostic outcomes, tumor immune infiltration characteristics, and pathway enrichment. Subsequently, CPSF3 was identified as a potential immune infiltration-related gene in BC. Highly expressed CPSF3 was positively correlated with unfavorable prognosis and high CD276 expression in BC. Moreover, we verified the expression of CPSF3 in BC tissues and cell lines by qRT-PCR. In conclusion, the study indicates that APA regulatory factors play an important role in immune infiltration of BC, and that CPSF3 was a potentially prognostic marker and immunotherapy target for BC.
    Type of Medium: Online Resource
    ISSN: 1471-2407
    URL: Article
    DOI: 10.1186/s12885-022-10103-7
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2022
    detail.hit.zdb_id: 2041352-X
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  • 3
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    Administration of protopine prevents mitophagy and acute lung injury in sepsis
    Frontiers Media SA ; 2023
    In:  Frontiers in Pharmacology Vol. 14 ( 2023-6-8)
    Details
    In: Frontiers in Pharmacology, Frontiers Media SA, Vol. 14 ( 2023-6-8)
    Abstract: Introduction: Sepsis is a severe life-threatening infection that induces a series of dysregulated physiologic responses and results in organ dysfunction. Acute lung injury (ALI), the primary cause of respiratory failure brought on by sepsis, does not have a specific therapy. Protopine (PTP) is an alkaloid with antiinflammatory and antioxidant properties. However, the function of PTP in septic ALI has not yet been documented. This work sought to investigate how PTP affected septic ALI and the mechanisms involved in septic lung damage, including inflammation, oxidative stress, apoptosis, and mitophagy. Methods: Here, we established a mouse model induced by cecal ligation and puncture (CLP) and a BEAS-2B cell model exposed to lipopolysaccharide (LPS). Results: PTP treatment significantly reduced mortality in CLP mice. PTP mitigated lung damage and reduced apoptosis. Western blot analysis showed that PTP dramatically reduced the expression of the apoptosis-associated protein (Cleaved Caspase-3, Cyto C) and increased Bcl-2/Bax. In addition, PTP decreased the production of inflammatory cytokines (IL-6, IL-1β, TNF-α), increased glutathione (GSH) levels and superoxide dismutase (SOD) activity, and decreased malondialdehyde (MDA) levels. Meanwhile, PTP significantly reduced the expression of mitophagy-related proteins (PINK1, Parkin, LC-II), and downregulated mitophagy by transmission electron microscopy. Additionally, the cells were consistent with animal experiments. Discussion: PTP intervention reduced inflammatory responses, oxidative stress, and apoptosis, restored mitochondrial membrane potential, and downregulated mitophagy. The research shows that PTP prevents excessivemitophagy and ALI in sepsis, suggesting that PTP has a potential role in the therapy of sepsis.
    Type of Medium: Online Resource
    ISSN: 1663-9812
    URL: Article
    DOI: 10.3389/fphar.2023.1104185
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2023
    detail.hit.zdb_id: 2587355-6
    SSG: 15,3
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  • 4
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    Stanniocalcin‐1 attenuates collagen‐induced arthritis through inhibiting STAT3 phosphorylation and Th17 response
    Wiley ; 2023
    In:  Scandinavian Journal of Immunology Vol. 97, No. 2 ( 2023-02)
    Details
    In: Scandinavian Journal of Immunology, Wiley, Vol. 97, No. 2 ( 2023-02)
    Abstract: Rheumatoid arthritis (RA) is an autoimmune disease, associated with chronic inflammation and the imbalance of Th17/Treg. Stanniocalcin‐1 (STC‐1), a glycoprotein, was found to have anti‐inflammatory, anti‐oxidative stress and anti‐apoptosis properties. The present study aimed to investigate the immunomodulatory effect of STC‐1 and its potential value in the treatment of RA. Here, a mouse model of collagen‐induced arthritis (CIA) was established. Then body weight, joint erythema and swelling were measured in CIA mice with or without STC‐1 treatment. Haematoxylin and eosin (H and E) staining was performed to determine histopathological change. Moreover, the percentage of Th17 and Treg cells in the spleen and inguinal lymph nodes (ILNs) and the culture supernatant in polarizing conditions were examined by flow cytometry. Cytokines in serum were detected by ELISA. As a result, the arthritis score, histologic inflammation and cartilage destruction were decreased in CIA mice treated with STC‐1. STC‐1 increased the level of transforming growth factor‐β and inhibited the expression of interleukin‐17. In CIA mice, the percentage of CD4 + IL‐17A + cells in the spleen and ILNs were decreased after STC‐1 treatment, while the level of CD4 + Foxp3 + cells did not change significantly. In vitro, STC‐1 inhibited Th17 cell differentiation and STAT3 phosphorylation in CD4 + T cells under Th17 cell‐polarizing conditions. Collectively, the results demonstrated that STC‐1 alleviated RA by inhibiting Th17 cell differentiation through regulating STAT3 phosphorylation. STC‐1 may be a potential drug for the treatment of RA.
    Type of Medium: Online Resource
    ISSN: 0300-9475 , 1365-3083
    URL: Issue
    URL: Article
    DOI: 10.1111/sji.v97.2
    DOI: 10.1111/sji.13226
    RVK:
    XA 10000
    Language: English
    Publisher: Wiley
    Publication Date: 2023
    detail.hit.zdb_id: 2020954-X
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  • 5
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    Ginkgolic acid promotes inflammation and macrophage apoptosis via SUMOylation and NF-κB pathways in sepsis
    Frontiers Media SA ; 2023
    In:  Frontiers in Medicine Vol. 9 ( 2023-1-19)
    Details
    In: Frontiers in Medicine, Frontiers Media SA, Vol. 9 ( 2023-1-19)
    Abstract: Excessive inflammation and increased apoptosis of macrophages contribute to organ damage and poor prognosis of sepsis. Ginkgolic acid (GA) is a natural constituent extracted from the leaves of Ginkgo biloba , that can regulate inflammation and apoptosis. The present study aims to investigate the potential effect of GA in treating sepsis and its possible mechanisms. Materials and methods Here, a classic septic mice model and a lipopolysaccharide (LPS)-induced RAW 264.7 inflammation model were established. Cytokines in serum and culture supernatant were detected by ELISA, and the mRNA levels of them were examined by PCR. Hematoxylin and eosin (H & amp;E) staining was performed to determine histopathological changes in liver, lung and kidney. Bacterial burden in the blood, peritoneal lavage fluids (PLFs) and organs were observed on Luria-Bertani agar medium. Flow cytometry and western blotting was used to detect apoptosis and the expression level of apoptosis related molecules, respectively. Moreover, the levels of SUMOylation were detected by western blotting. The activity of NF-κB p65 was assessed by immunofluorescence staining and western blotting. Results The result showed that GA promoted inflammatory responses, reduced bacterial clearance, aggravated organ damage, and increased mortality in septic mice. GA increased apoptosis in peritoneal macrophages (PMs) and RAW 264.7 cells. Meanwhile, GA inhibited SUMOylation and increased the nuclear translocation of NF-κB p65 as well as its phosphorylation level. Conclusion Collectively, GA promotes inflammation and macrophage apoptosis in sepsis, which may be mediated by inhibiting the SUMOylation process and increasing NF-κB p65 activity.
    Type of Medium: Online Resource
    ISSN: 2296-858X
    URL: Article
    DOI: 10.3389/fmed.2022.1108882
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2023
    detail.hit.zdb_id: 2775999-4
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  • 6
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    Leupaxin Promotes Bladder Cancer Proliferation, Metastasis, and Angiogenesis Through the PI3K/AKT Pathway
    S. Karger AG ; 2018
    In:  Cellular Physiology and Biochemistry Vol. 47, No. 6 ( 2018), p. 2250-2260
    Details
    In: Cellular Physiology and Biochemistry, S. Karger AG, Vol. 47, No. 6 ( 2018), p. 2250-2260
    Abstract: Background/Aims: Leupaxin (LPXN) is a member of the paxillin protein family. Several studies have reported that LPXN regulates cancer development; however, the role of LPXN in bladder cancer remains unknown. Methods: The expression of LPXN in bladder cancer cells and tissues was determined by real-time PCR, western blotting, and immunohistochemistry, respectively. The biological role of LPXN in bladder cancer cell proliferation, invasion, and angiogenesis was explored both in vitro and in vivo. Results: LPXN expression was elevated in bladder cancer tissues and cell lines compared to adjacent non-tumor tissues and normal urothelial cells. High LPXN expression was correlated with large tumor size, advanced tumor stage, and poor survival in bladder cancer patients. Overexpression of LPXN significantly promoted the proliferation, invasion, and angiogenesis of bladder cancer cells, while suppressing LPXN had the opposite effects. The impact on tumor progression was abolished by inhibiting PI3K/ AKT signaling pathway. We further demonstrated that LPXN probably up-regulated S100P via the PI3K/AKT pathway. Conclusions: LPXN may facilitate bladder cancer progression by upregulating the expression of S100P via PI3K/AKT pathway. These results provide a novel insight into the role of LPXN in tumorigenesis and progression of bladder cancer and potential therapeutic target of bladder cancer.
    Type of Medium: Online Resource
    ISSN: 1015-8987 , 1421-9778
    URL: Article
    DOI: 10.1159/000491536
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2018
    detail.hit.zdb_id: 1482056-0
    SSG: 12
    SSG: 15,3
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  • 7
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    Th17/Treg balance: the bloom and wane in the pathophysiology of sepsis
    Frontiers Media SA ; 2024
    In:  Frontiers in Immunology Vol. 15 ( 2024-3-15)
    Details
    In: Frontiers in Immunology, Frontiers Media SA, Vol. 15 ( 2024-3-15)
    Abstract: Sepsis is a multi-organ dysfunction characterized by an unregulated host response to infection. It is associated with high morbidity, rapid disease progression, and high mortality. Current therapies mainly focus on symptomatic treatment, such as blood volume supplementation and antibiotic use, but their effectiveness is limited. Th17/Treg balance, based on its inflammatory property, plays a crucial role in determining the direction of the inflammatory response and the regression of organ damage in sepsis patients. This review provides a summary of the changes in T-helper (Th) 17 cell and regulatory T (Treg) cell differentiation and function during sepsis, the heterogeneity of Th17/Treg balance in the inflammatory response, and the relationship between Th17/Treg balance and organ damage. Th17/Treg balance exerts significant control over the bloom and wanes in host inflammatory response throughout sepsis.
    Type of Medium: Online Resource
    ISSN: 1664-3224
    URL: Article
    DOI: 10.3389/fimmu.2024.1356869
    Language: Unknown
    Publisher: Frontiers Media SA
    Publication Date: 2024
    detail.hit.zdb_id: 2606827-8
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  • 8
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    Emodin alleviates LPS ‐induced myocardial injury through inhibition of NLRP3 inflammasome activation
    Wiley ; 2021
    In:  Phytotherapy Research Vol. 35, No. 9 ( 2021-09), p. 5203-5213
    Details
    In: Phytotherapy Research, Wiley, Vol. 35, No. 9 ( 2021-09), p. 5203-5213
    Abstract: Myocardial injury and cardiovascular dysfunction are serious consequences of sepsis and contribute to high mortality. Currently, the pathogenesis of myocardial injury in sepsis is still unclear, and therapeutic approaches are limited. In this study, we investigated the protective effect of emodin on septic myocardial injury and the underlying mechanism. Lipopolysaccharide (LPS)‐induced C57BL/6 mice and cardiomyocytes were used as models of sepsis in vivo and in vitro, respectively. The results showed that emodin alleviated cardiac dysfunction, myocardial injury and improved survival rate in LPS‐induced septic mice. Emodin attenuated the levels of inflammatory cytokines and cardiac inflammation induced by LPS. Emodin reduced NOD‐like receptor protein 3 (NLRP3) and Gasdermin D (GSDMD) expression in the heart tissue of LPS‐induced septic mice. In vitro, emodin alleviated LPS‐induced cell injury and inflammation in cardiomyocytes by inhibiting NLRP3 inflammasome activation. In addition, an NLRP3 inhibitor was used to further confirm the function of the NLRP3 inflammasome in LPS‐induced myocardial injury. Taken together, our findings suggest that emodin improves LPS‐induced myocardial injury and cardiac dysfunction by alleviating the inflammatory response and cardiomyocyte pyroptosis by inhibiting NLRP3 inflammasome activation, which provides a feasible strategy for preventing and treating myocardial injury in sepsis.
    Type of Medium: Online Resource
    ISSN: 0951-418X , 1099-1573
    URL: Issue
    URL: Article
    DOI: 10.1002/ptr.v35.9
    DOI: 10.1002/ptr.7191
    Language: English
    Publisher: Wiley
    Publication Date: 2021
    detail.hit.zdb_id: 1493490-5
    SSG: 15,3
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  • 9
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    HBO1 promotes cell proliferation in bladder cancer via activation of Wnt/β‐catenin signaling
    Wiley ; 2018
    In:  Molecular Carcinogenesis Vol. 57, No. 1 ( 2018-01), p. 12-21
    Details
    In: Molecular Carcinogenesis, Wiley, Vol. 57, No. 1 ( 2018-01), p. 12-21
    Abstract: Histone acetyltransferase binding to ORC1 (HBO1), a histone acetyltransferase, was recently identified as an oncoprotein; however, its role in bladder cancer remains unknown. In this study, we showed that HBO1 was highly expressed at both the mRNA and the protein levels in bladder cancer. HBO1 expression was associated with the clinical features of human bladder cancer, including tumor size ( P  = 0.018) and T ( P  = 0.007) classifications. Patients with higher HBO1 expression had shorter recurrence‐free survival time, whereas patients with lower HBO1 expression had better survival time. Moreover, we found that ectopic overexpression of HBO1 promoted, whereas HBO1 silencing inhibited tumor growth in bladder cancer cells both in vitro and in vivo. We further demonstrated that upregulation of HBO1 activated the Wnt/β‐catenin signaling pathway and led to nuclear localization of β‐catenin and upregulation of downstream targets of of Wnt/β‐catenin signaling. These findings suggest that HBO1 plays a key role in the progression of bladder cancer via the Wnt/β‐catenin pathway, and may serve as a potential therapeutic target for the treatment of bladder cancer.
    Type of Medium: Online Resource
    ISSN: 0899-1987 , 1098-2744
    URL: Issue
    URL: Article
    DOI: 10.1002/mc.v57.1
    DOI: 10.1002/mc.22715
    Language: English
    Publisher: Wiley
    Publication Date: 2018
    detail.hit.zdb_id: 2001984-1
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  • 10
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    Loss of Fezf2 promotes malignant progression of bladder cancer by regulating the NF-κB signaling pathway
    Elsevier BV ; 2018
    In:  Laboratory Investigation Vol. 98, No. 9 ( 2018-09), p. 1225-1236
    Details
    In: Laboratory Investigation, Elsevier BV, Vol. 98, No. 9 ( 2018-09), p. 1225-1236
    Type of Medium: Online Resource
    ISSN: 0023-6837
    URL: Article
    DOI: 10.1038/s41374-018-0077-9
    RVK:
    WA 15000
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2018
    detail.hit.zdb_id: 2041329-4
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