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  1. Article ; Online: Self-care of medical staff in primary care: An issue that needs attention during the COVID-19 outbreak.

    Xu, Zhongqing

    Australian journal of general practice

    2020  Volume 49

    Abstract: Self-care is essential for primary care professionals who are at risk of COVID-19. ...

    Abstract Self-care is essential for primary care professionals who are at risk of COVID-19.
    Keywords covid19
    Language English
    Publishing date 2020-04-17
    Publishing country Australia
    Document type Journal Article
    ZDB-ID 2924889-9
    ISSN 2208-7958 ; 2208-794X
    ISSN (online) 2208-7958
    ISSN 2208-794X
    DOI 10.31128/AJGP-COVID-11
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Consequences of abolishing the COVID-19 zero-tolerance policy in Shanghai: Lessons for future responses.

    Xu, Zhongqing / Shi, Dandan / Ding, Jingjing / Lu, Hong / Shen, Xiaoyi / Hambly, Brett / Bao, Shisan

    Australian journal of general practice

    2024  Volume 53, Issue 1-2, Page(s) 78–80

    MeSH term(s) Humans ; COVID-19 ; China/epidemiology ; Policy
    Language English
    Publishing date 2024-02-05
    Publishing country Australia
    Document type Journal Article
    ZDB-ID 2924889-9
    ISSN 2208-7958 ; 2208-794X
    ISSN (online) 2208-7958
    ISSN 2208-794X
    DOI 10.31128/AJGP/05-23-6830
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article: Self-care of medical staff in primary care: An issue that needs attention during the COVID-19 outbreak

    Xu, Zhongqing

    Aust. J. Gen. Pract

    Abstract: Self-care is essential for primary care professionals who are at risk of COVID-19. ...

    Abstract Self-care is essential for primary care professionals who are at risk of COVID-19.
    Keywords covid19
    Publisher WHO
    Document type Article
    Note WHO #Covidence: #72443
    Database COVID19

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  4. Article ; Online: CKLF1 interference alleviates IL‑1β‑induced inflammation, apoptosis and degradation of the extracellular matrix in chondrocytes via CCR5.

    Wang, Haoran / Wu, Zhongqing / Xu, Kanna

    Experimental and therapeutic medicine

    2023  Volume 25, Issue 6, Page(s) 303

    Abstract: Osteoarthritis (OA) is a type of joint disease with a rising prevalence and incidence among the elderly across the global population. Chemokine-like factor 1 (CKLF1) is a human cytokine, which has been demonstrated to be involved in the progression of ... ...

    Abstract Osteoarthritis (OA) is a type of joint disease with a rising prevalence and incidence among the elderly across the global population. Chemokine-like factor 1 (CKLF1) is a human cytokine, which has been demonstrated to be involved in the progression of multiple human diseases. However, little attention has been paid to the impact of CKLF1 on OA. The present study was designed to identify the role of CKLF1 in OA and to clarify the regulatory mechanism. The expression levels of CKLF1 and its receptor CC chemokine receptor 5 (CCR5) were examined by reverse transcription-quantitative PCR (RT-qPCR) and western blotting. A Cell Counting Kit-8 assay was used to estimate cell viability. The levels and expression of inflammatory factors were determined by ELISA and RT-qPCR, respectively. Apoptosis was investigated by TUNEL assays and the protein levels of apoptosis-related factors were analyzed by western blotting. RT-qPCR and western blotting were used to examine the expression of extracellular matrix (ECM) degradation-associated proteins and ECM components. Dimethylmethylene blue analysis was used to analyze the production of soluble glycosamine sulfate additive. A co-immunoprecipitation assay was used to confirm the protein interaction between CKLF1 and CCR5. The results revealed that CKLF1 expression was increased in IL-1β-exposed murine chondrogenic ATDC5 cells. Furthermore, CKLF1 silencing enhanced the viability of IL-1β-induced ATDC5 cells, while inflammation, apoptosis and degradation of the ECM were reduced. Additionally, CKLF1 knockdown led to decreased CCR5 expression in IL-1β-challenged ATDC5 cells, and CKLF1 bound with CCR5. The enhanced viability, as well as the suppressed inflammation, apoptosis and degradation of the ECM, following CKLF1 knockdown in the IL-1β-induced ATDC5 cells were all restored after CCR5 was overexpressed. In conclusion, CKLF1 might serve a detrimental role in the development of OA by targeting its receptor CCR5.
    Language English
    Publishing date 2023-05-09
    Publishing country Greece
    Document type Journal Article
    ZDB-ID 2683844-8
    ISSN 1792-1015 ; 1792-0981
    ISSN (online) 1792-1015
    ISSN 1792-0981
    DOI 10.3892/etm.2023.12002
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Targeting FOS attenuates malignant phenotypes of breast cancer: Evidence from in silico and in vitro studies.

    Chang, Defeng / Li, Lanlan / Xu, Zhongqing / Chen, Xiaohong

    Journal of biochemical and molecular toxicology

    2023  Volume 37, Issue 7, Page(s) e23358

    Abstract: Data retrieved from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases can reveal important information behind molecular biomarkers and their associated oncogenesis. Therefore, this study was based on in silico predictions and in ... ...

    Abstract Data retrieved from The Cancer Genome Atlas (TCGA) and Gene Expression Omnibus (GEO) databases can reveal important information behind molecular biomarkers and their associated oncogenesis. Therefore, this study was based on in silico predictions and in vitro experiments to explore regulatory network associated with breast carcinogenesis. The breast cancer (BC)-related data sets were retrieved from GEO database, followed by differential analysis and protein-protein interaction (PPI) analysis. Then, Fos proto-oncogene, AP-1 transcription factor subunit (FOS)-associated gene network was constructed, and the key gene-related genes in BC were screened by LinkedOmics. Finally, FOS expression was determined in BC tissues and cells, and gain-of-function assays were performed to define the role of FOS in BC cells. It was noted that seven differentially expressed genes (EGR1, RASSF9, FOSB, CDC20, KLF4, PTGS2, and FOS) were obtained from BC microarray data sets. FOS was the gene with the most nodes in PPI analysis. Poor FOS mRNA expression was identified in BC patients. Furthermore, FOS was mainly located in the extracellular matrix and was involved in cell processes. FOS was downregulated in BC tissues and cells, and FOS overexpression restrained the malignant phenotypes of BC cells. Collectively, ectopic expression of FOS curtails the development of BC.
    MeSH term(s) Humans ; Gene Expression Profiling ; Cell Cycle Proteins/genetics ; Biomarkers, Tumor/genetics ; Neoplasms ; Phenotype ; Gene Expression Regulation, Neoplastic
    Chemical Substances Cell Cycle Proteins ; Biomarkers, Tumor
    Language English
    Publishing date 2023-04-04
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1410020-4
    ISSN 1099-0461 ; 1095-6670
    ISSN (online) 1099-0461
    ISSN 1095-6670
    DOI 10.1002/jbt.23358
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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2201: Show issues Location:
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  6. Article: Genkwanin suppresses mitochondrial dysfunction to alleviate IL-1β-elicited inflammation, apoptosis, and degradation of extracellular matrix in chondrocytes through upregulating DUSP1.

    Xu, Kanna / Wang, Haoran / Wu, Zhongqing

    The Chinese journal of physiology

    2023  Volume 66, Issue 4, Page(s) 284–293

    Abstract: Osteoarthritis (OA) is a form of chronic degenerative disease contributing to elevated disability rate among the elderly. Genkwanin is an active component extracted from Daphne genkwa possessing pharmacologic effects. Here, this study is designed to ... ...

    Abstract Osteoarthritis (OA) is a form of chronic degenerative disease contributing to elevated disability rate among the elderly. Genkwanin is an active component extracted from Daphne genkwa possessing pharmacologic effects. Here, this study is designed to expound the specific role of genkwanin in OA and elaborate the probable downstream mechanism. First, the viability of chondrocytes in the presence or absence of interleukin-1 beta (IL-1β) treatment was detected by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling assay was used to assess cell apoptosis. Inflammatory response was estimated through enzyme-linked immunosorbent assay and Western blot. In addition, immunofluorescence staining and Western blot were utilized to measure the expression of extracellular matrix (ECM)-associated proteins. Dual-specificity protein phosphatase-1 (DUSP1) expression was tested by reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and Western blot. Following DUSP1 elevation in genkwanin-treated chondrocytes exposed to IL-1β, inflammatory response and ECM-associated factors were evaluated as forementioned. In addition, 5,5',6,6'-tetrachloro-1,1',3,3'-tetraethylbenzimidazolocarbocyanine iodide staining was to assess the mitochondrial membrane potential. Adenosine triphosphate (ATP) level was examined with ATP assay kit, and RT-qPCR was used to test mitochondrial DNA expression. Results indicated that genkwanin administration enhanced the viability while ameliorated the apoptosis, inflammatory response, and ECM degradation in IL-1β-induced chondrocytes. Besides, genkwanin treatment fortified DUSP1 expression in IL-1β-exposed chondrocytes. DUSP1 interference further offsets the impacts of genkwanin on the inflammation, ECM degradation, and mitochondrial dysfunction in IL-1β-challenged chondrocytes. In short, genkwanin enhanced DUSP1 expression to mitigate mitochondrial dysfunction, thus ameliorating IL-1β-elicited inflammation, apoptosis, and degradation of ECM in chondrocytes.
    MeSH term(s) Humans ; Aged ; Chondrocytes/metabolism ; Interleukin-1beta/pharmacology ; Interleukin-1beta/metabolism ; Inflammation/drug therapy ; Extracellular Matrix/metabolism ; Osteoarthritis/drug therapy ; Osteoarthritis/metabolism ; Apoptosis ; Mitochondria ; Adenosine Triphosphate/metabolism ; Adenosine Triphosphate/pharmacology ; Adenosine Triphosphate/therapeutic use ; MicroRNAs/genetics ; Dual Specificity Phosphatase 1/metabolism ; Dual Specificity Phosphatase 1/pharmacology
    Chemical Substances genkwanin (5K3I5D6B2B) ; Interleukin-1beta ; Adenosine Triphosphate (8L70Q75FXE) ; MicroRNAs ; DUSP1 protein, human (EC 3.1.3.48) ; Dual Specificity Phosphatase 1 (EC 3.1.3.48)
    Language English
    Publishing date 2023-08-27
    Publishing country India
    Document type Journal Article
    ZDB-ID 966112-8
    ISSN 0304-4920 ; 0300-8525
    ISSN 0304-4920 ; 0300-8525
    DOI 10.4103/cjop.CJOP-D-23-00031
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    Zs.B 309: Show issues Location:
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  7. Article: A novel peptide HSP-17 ameliorates oxidative stress injury and apoptosis in H9c2 cardiomyocytes by activating the PI3K/Akt pathway.

    Chen, Xiaofang / Zhang, Hao / Feng, Mengwen / Xu, Zhongqing / Qian, Lingmei

    Annals of translational medicine

    2023  Volume 10, Issue 24, Page(s) 1357

    Abstract: Background: Oxidative stress and cell apoptosis play pivotal roles in the pathogenesis of doxorubicin (DOX)-induced myocardial injury. Heat shock protein-derived peptide (HSP-17) is a peptide which is low-expressed in DOX treated mouse heart tissue. It ... ...

    Abstract Background: Oxidative stress and cell apoptosis play pivotal roles in the pathogenesis of doxorubicin (DOX)-induced myocardial injury. Heat shock protein-derived peptide (HSP-17) is a peptide which is low-expressed in DOX treated mouse heart tissue. It has high bioactivity and interspecies sequence consistency, and is predicted to have myocardial protective effect.
    Methods: Firstly, we added 1 µM DOX to H9c2 cell culture medium for 24 hours to construct the myocardial cytotoxicity model. Then we detected the effect of HSP-17 on DOX induced H9c2 cardiomyocyte injury by measuring cell viability and lactate dehydrogenase (LDH) level. In addition, reactive oxygen species (ROS) and tetraethylbenzimidazolylcarbocyanine iodide kits are used to evaluate the effect of the HSP-17 peptide on DOX-induced oxidative stress injury to cardiomyocytes, and the detection of apoptosis related proteins and flow cytometry were applied to detect the level of apoptosis. Furthermore, the protein expression levels [phosphorylated Akt (p-Akt) and phosphorylated PI3K (p-PI3K)] of the PI3K/Akt pathway were also detected by western blotting.
    Results: We found that the HSP-17 peptide can increase cell viability, protect mitochondrial potential, reduce LDH levels, and reduce ROS and cardiomyocyte apoptosis. In addition, we also observed that HSP-17 upregulated the expression level of p-Akt, and LY294002, a typical inhibitor of PI3K/Akt, was found to eliminate the protective roles of HSP-17.
    Conclusions: In conclusion, this study demonstrated that the HSP-17 peptide protected H9c2 cells against oxidative stress and apoptosis via PI3K/Akt pathway activation, which provides a new idea for the treatment of DOX-induced myocardial injury.
    Language English
    Publishing date 2023-01-09
    Publishing country China
    Document type Journal Article
    ZDB-ID 2893931-1
    ISSN 2305-5847 ; 2305-5839
    ISSN (online) 2305-5847
    ISSN 2305-5839
    DOI 10.21037/atm-22-6007
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article ; Online: Network Pharmacology and Molecular Docking Analysis Exploring the Mechanism of

    Huang, Wenkai / Huang, Xu / Yang, Lin / Han, Wenjia / Zhu, Zhongqing / Wang, Yuanyin / Chen, Ran

    Medicina (Kaunas, Lithuania)

    2023  Volume 59, Issue 8

    Abstract: ... ...

    Abstract Background
    MeSH term(s) Humans ; Molecular Docking Simulation ; Tripterygium ; Caspase 3 ; Network Pharmacology ; Cyclooxygenase 2 ; Lichen Planus, Oral/drug therapy
    Chemical Substances Caspase 3 (EC 3.4.22.-) ; Cyclooxygenase 2 (EC 1.14.99.1)
    Language English
    Publishing date 2023-08-10
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2188113-3
    ISSN 1648-9144 ; 1010-660X
    ISSN (online) 1648-9144
    ISSN 1010-660X
    DOI 10.3390/medicina59081448
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  9. Article ; Online: Mycobacterium tuberculosis PE_PGRS45 (Rv2615c) Promotes Recombinant Mycobacteria Intracellular Survival via Regulation of Innate Immunity, and Inhibition of Cell Apoptosis.

    Xu, Tao / Wang, Chutong / Li, Minying / Wei, Jing / He, Zixuan / Qian, Zhongqing / Wang, Xiaojing / Wang, Hongtao

    Journal of microbiology (Seoul, Korea)

    2024  Volume 62, Issue 1, Page(s) 49–62

    Abstract: Tuberculosis (TB), a bacterial infectious disease caused by Mycobacterium tuberculosis (M. tuberculosis), is a significant global public health problem. Mycobacterium tuberculosis expresses a unique family of PE_PGRS proteins that have been implicated in ...

    Abstract Tuberculosis (TB), a bacterial infectious disease caused by Mycobacterium tuberculosis (M. tuberculosis), is a significant global public health problem. Mycobacterium tuberculosis expresses a unique family of PE_PGRS proteins that have been implicated in pathogenesis. Despite numerous studies, the functions of most PE_PGRS proteins in the pathogenesis of mycobacterium infections remain unclear. PE_PGRS45 (Rv2615c) is only found in pathogenic mycobacteria. In this study, we successfully constructed a recombinant Mycobacterium smegmatis (M. smegmatis) strain which heterologously expresses the PE_PGRS45 protein. We found that overexpression of this cell wall-associated protein enhanced bacterial viability under stress in vitro and cell survival in macrophages. MS_PE_PGRS45 decreased the secretion of pro-inflammatory cytokines such as IL-1β, IL-6, IL-12p40, and TNF-α. We also found that MS_PE_PGRS45 increased the expression of the anti-inflammatory cytokine IL-10 and altered macrophage-mediated immune responses. Furthermore, PE_PGRS45 enhanced the survival rate of M. smegmatis in macrophages by inhibiting cell apoptosis. Collectively, our findings show that PE_PGRS45 is a virulent factor actively involved in the interaction with the host macrophage.
    MeSH term(s) Humans ; Mycobacterium tuberculosis/genetics ; Bacterial Proteins/genetics ; Bacterial Proteins/metabolism ; Immunity, Innate ; Cytokines/metabolism ; Apoptosis ; Tuberculosis ; Mycobacterium smegmatis/genetics
    Chemical Substances Bacterial Proteins ; Cytokines
    Language English
    Publishing date 2024-02-09
    Publishing country Korea (South)
    Document type Journal Article
    ZDB-ID 2012399-1
    ISSN 1976-3794 ; 1225-8873
    ISSN (online) 1976-3794
    ISSN 1225-8873
    DOI 10.1007/s12275-023-00101-0
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  10. Article ; Online: Mycobacterium tuberculosis

    Xu, Tao / Wang, Chutong / Li, Minying / Yuan, Meili / Wei, Jing / Li, Baiqing / Qian, Zhongqing / Wang, Ting / Wang, Xiaojing / Wang, Hongtao

    DNA and cell biology

    2023  Volume 42, Issue 5, Page(s) 254–264

    Abstract: Tuberculosis is an important chronic and often fatal infectious disease mainly caused by the ... ...

    Abstract Tuberculosis is an important chronic and often fatal infectious disease mainly caused by the bacterium
    MeSH term(s) Cytokines/genetics ; Cytokines/metabolism ; Mycobacterium tuberculosis/metabolism ; Bacterial Proteins/genetics ; Host-Pathogen Interactions ; Mycobacterium smegmatis/genetics ; Mycobacterium smegmatis/metabolism ; Apoptosis
    Chemical Substances Cytokines ; Bacterial Proteins
    Language English
    Publishing date 2023-04-18
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1024454-2
    ISSN 1557-7430 ; 0198-0238 ; 1044-5498
    ISSN (online) 1557-7430
    ISSN 0198-0238 ; 1044-5498
    DOI 10.1089/dna.2022.0316
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