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  • 1
    Online Resource
    Online Resource
    Antibacterial Fusion Protein BPI21/LL-37 Modification Enhances the Therapeutic Efficacy of hUC-MSCs in Sepsis
    Elsevier BV ; 2020
    In:  Molecular Therapy Vol. 28, No. 8 ( 2020-08), p. 1806-1817
    Details
    In: Molecular Therapy, Elsevier BV, Vol. 28, No. 8 ( 2020-08), p. 1806-1817
    Type of Medium: Online Resource
    ISSN: 1525-0016
    URL: Article
    DOI: 10.1016/j.ymthe.2020.05.014
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2020
    detail.hit.zdb_id: 2001818-6
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  • 2
    Online Resource
    Online Resource
    Analysis on the Problems Existing in China's College Classes and Management Strategies
    Synergy Publishing Pte. Ltd. ; 2017
    In:  Journal of Educational Theory and Management Vol. 1, No. 1 ( 2017-10-16), p. 158-
    Details
    In: Journal of Educational Theory and Management, Synergy Publishing Pte. Ltd., Vol. 1, No. 1 ( 2017-10-16), p. 158-
    Abstract: Class is a place where all kinds of teaching activities are carried out and is a space where the teachers and students gather to study and grow up together. The scientific and reasonable college class management methods not only can effectively maintain the teaching order in class, but also can improve the students' learning initiative and increase the teaching efficiency, thus improving the quality of higher education. However, the situation of college class management is not optimistic at present. This paper is aimed at analyzing the problems existing in China's college classes and exploring the relevant solutions based on them to provide the reference for the quality of China's higher education.
    Type of Medium: Online Resource
    ISSN: 2591-7102 , 2591-7099
    URL: Article
    DOI: 10.26549/jetm.v1i1.593
    Language: Unknown
    Publisher: Synergy Publishing Pte. Ltd.
    Publication Date: 2017
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  • 3
    Online Resource
    Online Resource
    HDAC2 inhibits EMT-mediated cancer metastasis by downregulating the long noncoding RNA H19 in colorectal cancer
    Springer Science and Business Media LLC ; 2020
    In:  Journal of Experimental & Clinical Cancer Research Vol. 39, No. 1 ( 2020-12)
    Details
    In: Journal of Experimental & Clinical Cancer Research, Springer Science and Business Media LLC, Vol. 39, No. 1 ( 2020-12)
    Abstract: Emerging evidence suggests that epithelial mesenchymal transition (EMT) and epigenetic mechanisms promote metastasis . Histone deacetylases (HDACs) and noncoding RNAs (ncRNAs) are important epigenetic regulators. Here, we elucidated a novel role of histone deacetylase 2 ( HDAC2 ) in regulating EMT and CRC metastasis via ncRNA. Methods The expression of HDACs in CRC was analyzed using the public databases and matched primary and metastatic tissues, and CRC cells with different metastatic potentials (DLD1, HCT116, SW480 and SW620). Microarray analysis was used to identify differential genes in parental and HDAC2 knockout CRC cells. EMT and histone modifications were determined using western blot and immunofluorescence. Migration ability was assessed by transwell assay, and metastasis was assessed in vivo using a tail vain injection. Gene expression and regulation was assessed by RT-PCR, chromatin immunoprecipitation and reporter assays. Protein interaction was assessed by immunoprecipitation. Specific siRNAs targeting H19 , SP1 and MMP14 were used to validate their role in HDAC2 loss induced EMT and metastasis. Results Reduced HDAC2 expression was associated with poor prognosis in CRC patients and found in CRC metastasis. HDAC2 deletion or knockdown induced EMT and metastasis by upregulating the long noncoding RNA H19 ( LncRNA H19 ). HDAC2 inhibited LncRNA H19 expression by histone H3K27 deacetylation in its promoter via binding with SP1. LncRNA H19 functioned as a miR-22-3P sponge to increase the expression of MMP14. HDAC2 loss strongly promoted CRC lung metastasis, which was suppressed LncRNA H19 knockdown. Conclusion Our study supports HDAC2 as a CRC metastasis suppressor through the inhibition of EMT and the expression of H19 and MMP14.
    Type of Medium: Online Resource
    ISSN: 1756-9966
    URL: Article
    DOI: 10.1186/s13046-020-01783-9
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2020
    detail.hit.zdb_id: 2430698-8
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  • 4
    Online Resource
    Online Resource
    Low‐concentration DMSO accelerates skin wound healing by Akt / mTOR ‐mediated cell proliferation and migration in diabetic mice
    Wiley ; 2020
    In:  British Journal of Pharmacology Vol. 177, No. 14 ( 2020-07), p. 3327-3341
    Details
    In: British Journal of Pharmacology, Wiley, Vol. 177, No. 14 ( 2020-07), p. 3327-3341
    Abstract: DMSO has been found to promote tissue repair. However, the role of DMSO in diabetic skin wound healing and the underlying molecular mechanisms are still unclear. Experimental Approach The effects of DMSO on wound healing were evaluated by HE staining, immunohistochemistry and collagen staining using a wound model of full‐thickness skin resection on the backs of non‐diabetic or diabetic mice. Real‐time cell analysis and 5‐ethynyl‐2′‐deoxyuridine incorporation assays were used to study the effect of DMSO on primary fibroblast proliferation. A transwell assay was used to investigate keratinocyte migration. The associated signalling pathway was identified by western blotting and inhibitor blocking. The effect of DMSO on the translation rate of downstream target genes was studied by RT‐qPCR of polyribosome mRNA . Key Results We found that low‐concentration DMSO significantly accelerated skin wound closure by promoting fibroblast proliferation in both nondiabetic and diabetic mice. In addition, increased migration of keratinocytes may also contribute to accelerated wound healing, which was stimulated by increased TGF‐β1 secretion from fibroblasts. Furthermore, we demonstrated that this effect of DMSO depends on Akt/mTOR‐mediated translational control and the promotion of the translation of a set of cell proliferation‐related genes. As expected, DMSO‐induced wound healing and cell proliferation were impaired by rapamycin, an inhibitor of Akt/mTOR signalling. Conclusion and Implications DMSO can promote skin wound healing in diabetic mice by activating the Akt/mTOR pathway. Low‐concentration DMSO presents an alternative medication for chronic cutaneous wounds, especially for diabetic patients.
    Type of Medium: Online Resource
    ISSN: 0007-1188 , 1476-5381
    URL: Issue
    URL: Article
    DOI: 10.1111/bph.v177.14
    DOI: 10.1111/bph.15052
    Language: English
    Publisher: Wiley
    Publication Date: 2020
    detail.hit.zdb_id: 2029728-2
    SSG: 15,3
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  • 5
    Online Resource
    Online Resource
    METTL3/IGF2BP3 axis inhibits tumor immune surveillance by upregulating N6-methyladenosine modification of PD-L1 mRNA in breast cancer
    Springer Science and Business Media LLC ; 2022
    In:  Molecular Cancer Vol. 21, No. 1 ( 2022-12)
    Details
    In: Molecular Cancer, Springer Science and Business Media LLC, Vol. 21, No. 1 ( 2022-12)
    Abstract: Continual expression of PD-L1 in tumor cells is critical for tumor immune escape and host T cell exhaustion, however, knowledge on its clinical benefits through inhibition is limited in breast cancer. N 6 -methyladenosine (m 6 A) plays a crucial role in multiple biological activities. Our study aimed to investigate the regulatory role of the m 6 A modification in PD-L1 expression and immune surveillance in breast cancer. Methods MeRIP-seq and epitranscriptomic microarray identified that PD-L1 is the downstream target of METTL3. MeRIP-qPCR, absolute quantification of m 6 A modification assay, and RIP-qPCR were used to examine the molecular mechanism underlying METTL3/m 6 A/IGF2BP3 signaling axis in PD-L1 expression. B-NDG and BALB/c mice were used to construct xenograft tumor models to verify the phenotypes upon METTL3 and IGF2BP3 silencing. In addition, breast cancer tissue microarray was used to analyze the correlation between PD-L1 and METTL3 or IGF2BP3 expression. Results We identified that PD-L1 was a downstream target of METTL3-mediated m 6 A modification in breast cancer cells. METTL3 knockdown significantly abolished m 6 A modification and reduced stabilization of PD-L1 mRNA. Additionally, METTL3-mediated PD-L1 mRNA activation was m 6 A-IGF2BP3-dependent. Moreover, inhibition of METTL3 or IGF2BP3 enhanced anti-tumor immunity through PD-L1-mediated T cell activation, exhaustion, and infiltration both in vitro and in vivo. PD-L1 expression was also positively correlated with METTL3 and IGF2BP3 expression in breast cancer tissues. Conclusion Our study suggested that METTL3 could post-transcriptionally upregulate PD-L1 expression in an m 6 A-IGF2BP3-dependent manner to further promote stabilization of PD-L1 mRNA, which may have important implications for new and efficient therapeutic strategies in the tumor immunotherapy.
    Type of Medium: Online Resource
    ISSN: 1476-4598
    URL: Article
    DOI: 10.1186/s12943-021-01447-y
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2022
    detail.hit.zdb_id: 2091373-4
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  • 6
    Online Resource
    Online Resource
    Interferon-gamma and tumor necrosis factor-alpha synergistically enhance the immunosuppressive capacity of human umbilical-cord-derived mesenchymal stem cells by increasing PD-L1 expression
    Baishideng Publishing Group Inc. ; 2023
    In:  World Journal of Stem Cells Vol. 15, No. 8 ( 2023-8-26), p. 787-806
    Details
    In: World Journal of Stem Cells, Baishideng Publishing Group Inc., Vol. 15, No. 8 ( 2023-8-26), p. 787-806
    Abstract: The art of constructing an insightful literature review manuscript has witnessed an exemplar in the work of Oz et al (2023), wherein concept progression harmoniously merges with figures and tables. Reflecting on retrospective data science, it is evident that well-cited articles can wield a transformative influence on the Journal Citation Reports Impact Factor score, as exemplified by Robert Weinberg’s landmark on cancer (Hanahan and Weinberg, 2011). Here, we aim to spotlight a commendable contribution by Tuba Oz, Ajeet Kaushik, and Małgorzata Kujawska in this issue while pivoting towards identifying the hallmarks of a subpar literature review-elements that hinder rather than promote advancement. The hurdles and roadblocks encountered within subpar literature reviews are multifold. Anticipation of emerging trends, identification of challenges, and exploration of solutions remain conspicuously absent. Original Contributions fail to surface amidst the vast sea of pre-existing literature, with noticeable gaps amplified by the lack of illustrative figures and tables. The manuscript, at times, assumes a skeletal form, reflecting an attempt to accommodate an excess of references, leading to convoluted sentences laden with citations. In contrast, a potent solution lies in adopting a comprehensive approach. A nuanced and critical evaluation of sources can culminate in a robust discussion, surpassing the mere summarization of conclusions drawn by others. This approach, often dismissed, holds the potential to elevate clarity, coherence, and logical flow, ultimately inviting engaged readership and coveted citations. The critical necessity of integrating visionary insights is underscored and achieved through a rigorous analysis of pivotal concepts and innovative ideas. Examples can be harnessed to elucidate the application of these solutions. We advocate a paradigm shift, urging literature review writers to embrace the readers’ perspective. A literature review’s purpose extends beyond providing a comprehensive panorama; it should illuminate avenues for concept development within a specific field of interest. By achieving this balance, literature reviews stand to captivate a devoted readership, paving the way for manuscripts that are both widely read and frequently cited. The pathway forward requires a fusion of astute analysis and visionary insights, shaping the future of literature review composition.
    Type of Medium: Online Resource
    ISSN: 1948-0210
    URL: Article
    DOI: 10.4252/wjsc.v15.i8.787
    Language: Unknown
    Publisher: Baishideng Publishing Group Inc.
    Publication Date: 2023
    detail.hit.zdb_id: 2583482-4
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  • 7
    Online Resource
    Online Resource
    Lavender essential oil accelerates lipopolysaccharide‐induced chronic wound healing by inhibiting caspase‐11‐mediated macrophage pyroptosis
    Wiley ; 2023
    In:  The Kaohsiung Journal of Medical Sciences Vol. 39, No. 5 ( 2023-05), p. 511-521
    Details
    In: The Kaohsiung Journal of Medical Sciences, Wiley, Vol. 39, No. 5 ( 2023-05), p. 511-521
    Abstract: Chronic wounds seriously affect the quality of life of the elderly, obese people, and diabetic patients. The excessive inflammatory response is a key driver of delayed chronic wound healing. Although lavender essential oil (EO [lav]) has been proven to have anti‐inflammatory and accelerate wound curative effects, the specific molecular mechanism involved is still ambiguous. The results showed that the wounds treated with lipopolysaccharide (LPS) not only had delayed healing, but also the expression levels of pro‐inflammatory cytokines, such as tumor necrosis factor‐α (TNF‐α), interleukin‐6 (IL‐6), interleukin‐1β (IL‐1β), and the inflammatory mediator protein, high‐mobility group box 1 protein (HMGB‐1), in the wound tissues were significantly increased. However, treatment of LPS‐induced chronic wounds with EO (lav) accelerated wound healing and decreased IL‐1β and HMGB‐1 expression levels. It was further found that LPS induced macrophage pyroptosis to produce IL‐1β. After treatment with EO (lav), the expression level of macrophage pyroptosis marker Gasdermin D (GSDMD) and pyroptosis‐related cytotoxic effects were significantly reduced. Immunofluorescence results also directly indicate that EO (lav) can protect macrophages from LPS‐induced pyroptosis. Moreover, EO (lav) can down‐regulate expression levels of IL‐1β, GSDMD, and nucleotide‐binding oligomerization domain‐like receptor protein 3 (NLRP3) in the caspase‐11‐related pyroptotic signaling pathway. This study demonstrates that EO (lav) can reduce proinflammatory factor production and ameliorate inflammatory response by inhibiting macrophage pyroptosis, which accelerates LPS‐induced chronic wound healing.
    Type of Medium: Online Resource
    ISSN: 1607-551X , 2410-8650
    URL: Issue
    URL: Article
    DOI: 10.1002/kjm2.v39.5
    DOI: 10.1002/kjm2.12654
    Language: English
    Publisher: Wiley
    Publication Date: 2023
    detail.hit.zdb_id: 2202782-8
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  • 8
    Online Resource
    Online Resource
    TNF-α augments CXCL10/CXCR3 axis activity to induce Epithelial-Mesenchymal Transition in colon cancer cell
    Ivyspring International Publisher ; 2021
    In:  International Journal of Biological Sciences Vol. 17, No. 11 ( 2021), p. 2683-2702
    Details
    In: International Journal of Biological Sciences, Ivyspring International Publisher, Vol. 17, No. 11 ( 2021), p. 2683-2702
    Type of Medium: Online Resource
    ISSN: 1449-2288
    URL: Article
    DOI: 10.7150/ijbs.61350
    Language: English
    Publisher: Ivyspring International Publisher
    Publication Date: 2021
    detail.hit.zdb_id: 2179208-2
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  • 9
    Online Resource
    Online Resource
    Anti-αFR CAR-engineered NK-92 Cells Display Potent Cytotoxicity Against αFR-positive Ovarian Cancer
    Ovid Technologies (Wolters Kluwer Health) ; 2019
    In:  Journal of Immunotherapy Vol. 42, No. 8 ( 2019-10), p. 284-296
    Details
    In: Journal of Immunotherapy, Ovid Technologies (Wolters Kluwer Health), Vol. 42, No. 8 ( 2019-10), p. 284-296
    Abstract: Folate receptor alpha (αFR) is overexpressed in 90% of ovarian cancers, one of the most lethal gynecologic cancers. Recent studies have suggested that natural killer (NK) cells may be better chimeric antigen receptor (CAR) drivers because of their favorable innate characteristics, such as directly recognizing and killing tumor cells. However, the therapeutic effects of CAR-engineered NK cells targeting αFR in ovarian cancer have not been reported. In this research, 3 generations of anti-αFR CAR were constructed, namely αFR-ζ (first generation), αFR-28ζ (second generation), and αFR-28BBζ (third generation), and were highly expressed on the surface of NK-92 cells by lentivirus gene transfection. Three anti-αFR CAR-engineered NK-92 cells can specifically kill αFR-positive tumor cells in vitro, especially ovarian cancer cells with high αFR expression. Compared with NK-92 cells expressing αFR-ζ or αFR-28ζ, NK-92 cells expressing αFR-28BBζ showed not only higher antigen-specific cytotoxicity and proliferation but also lower antigen-induced apoptosis. Moreover, stronger degranulation and cytokine secretion were detected in NK-92 cells expressing αFR-28BBζ cocultured with αFR-positive tumor cells. Real-time cell analysis and live cell imaging recorded the process of NK-92 cells expressing αFR-28BBζ killing ovarian cancer cells in vitro. Furthermore, NK-92 cells expressing αFR-28BBζ can effectively eliminate cancer cells in a mouse xenograft model of ovarian cancer and significantly prolong the survival of tumor-bearing mice. These results demonstrate that the anti-αFR CARs redirect NK-92 cells with specific antitumor activity, and the third-generation anti-αFR CAR-engineered NK-92 cells display more potent cytotoxicity against αFR-positive ovarian cancer, laying the foundation for future clinical research.
    Type of Medium: Online Resource
    ISSN: 1524-9557
    URL: Article
    DOI: 10.1097/CJI.0000000000000286
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2019
    detail.hit.zdb_id: 2048797-6
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  • 10
    Online Resource
    Online Resource
    Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition) 1
    Informa UK Limited ; 2021
    In:  Autophagy Vol. 17, No. 1 ( 2021-01-02), p. 1-382
    Details
    In: Autophagy, Informa UK Limited, Vol. 17, No. 1 ( 2021-01-02), p. 1-382
    Type of Medium: Online Resource
    ISSN: 1554-8627 , 1554-8635
    URL: Article
    DOI: 10.1080/15548627.2020.1797280
    Language: English
    Publisher: Informa UK Limited
    Publication Date: 2021
    detail.hit.zdb_id: 2262043-6
    SSG: 12
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