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  1. Article ; Online: A study of the storage and custody system for semi-critical medical items in the respiratory support category based on eight disciplines problem solving.

    Li, Wen / Li, Yanjie / Wu, Qinli / Kang, Huifang / Jia, Yunhui

    Minerva medica

    2024  

    Language English
    Publishing date 2024-01-10
    Publishing country Italy
    Document type Journal Article
    ZDB-ID 123586-2
    ISSN 1827-1669 ; 0026-4806
    ISSN (online) 1827-1669
    ISSN 0026-4806
    DOI 10.23736/S0026-4806.23.09038-9
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Modulators of MicroRNA Function in the Immune System.

    Jia, Yunhui / Wei, Yuanyuan

    International journal of molecular sciences

    2020  Volume 21, Issue 7

    Abstract: MicroRNAs (miRNAs) play a key role in fine-tuning host immune homeostasis and responses through the negative regulation of mRNA stability and translation. The pathways regulated by miRNAs are well characterized, but the precise mechanisms that control ... ...

    Abstract MicroRNAs (miRNAs) play a key role in fine-tuning host immune homeostasis and responses through the negative regulation of mRNA stability and translation. The pathways regulated by miRNAs are well characterized, but the precise mechanisms that control the miRNA-mediated regulation of gene expression during immune cell-development and immune responses to invading pathogens are incompletely understood. Context-specific interactions of miRNAs with other RNA species or proteins may modulate the function of a given miRNA. Dysregulation of miRNA function is associated with various human diseases, such as cardiovascular diseases and cancers. Here, we review the potential modulators of miRNA function in the immune system, including the transcription regulators of miRNA genes, miRNA-processing enzymes, factors affecting miRNA targeting, and intercellular communication.
    MeSH term(s) Animals ; Epigenesis, Genetic ; Gene Expression Regulation ; Homeostasis ; Humans ; Immune System/immunology ; Immune System/metabolism ; Immunomodulation/genetics ; Lymphocytes/immunology ; Lymphocytes/metabolism ; MicroRNAs/genetics ; RNA Interference ; RNA-Binding Proteins ; Signal Transduction ; Transcription, Genetic
    Chemical Substances MicroRNAs ; RNA-Binding Proteins
    Language English
    Publishing date 2020-03-29
    Publishing country Switzerland
    Document type Journal Article ; Review
    ZDB-ID 2019364-6
    ISSN 1422-0067 ; 1422-0067 ; 1661-6596
    ISSN (online) 1422-0067
    ISSN 1422-0067 ; 1661-6596
    DOI 10.3390/ijms21072357
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: miR-223-3p Prevents Necroptotic Macrophage Death by Targeting Ripk3 in a Negative Feedback Loop and Consequently Ameliorates Advanced Atherosclerosis.

    Jia, Yunhui / Cheng, Lianping / Yang, Jiaxuan / Mao, Jiaqi / Xie, Yuhuai / Yang, Xian / Zhang, Xin / Wang, Dingxin / Zhao, Zhen / Schober, Andreas / Wei, Yuanyuan

    Arteriosclerosis, thrombosis, and vascular biology

    2023  Volume 44, Issue 1, Page(s) 218–237

    Abstract: Background: The formation of large necrotic cores results in vulnerable atherosclerotic plaques, which can lead to severe cardiovascular diseases. However, the specific regulatory mechanisms underlying the development of necrotic cores remain unclear.!## ...

    Abstract Background: The formation of large necrotic cores results in vulnerable atherosclerotic plaques, which can lead to severe cardiovascular diseases. However, the specific regulatory mechanisms underlying the development of necrotic cores remain unclear.
    Methods: To evaluate how the modes of lesional cell death are reprogrammed during the development of atherosclerosis, the expression levels of key proteins that are involved in the necroptotic, apoptotic, and pyroptotic pathways were compared between different stages of plaques in humans and mice. Luciferase assays and loss-of-function studies were performed to identify the microRNA-mediated regulatory mechanism that protects foamy macrophages from necroptotic cell death. The role of this mechanism in atherosclerosis was determined by using a knockout mouse model with perivascular drug administration and tail vein injection of microRNA inhibitors in
    Results: Here, we demonstrate that the necroptotic, rather than the apoptotic or pyroptotic, pathway is more activated in advanced unstable plaques compared with stable plaques in both humans and mice, which closely correlates with necrotic core formation. The upregulated expression of Ripk3 (receptor-interacting protein kinase 3) promotes the C/EBPβ (CCAAT/enhancer binding protein beta)-dependent transcription of the microRNA miR-223-3p, which conversely inhibits Ripk3 expression and forms a negative feedback loop to regulate the necroptosis of foamy macrophages. The knockout of the
    Conclusions: Our study suggests that miR-223-3p expression in macrophages protects against atherosclerotic plaque rupture by limiting the formation of necrotic cores, thus providing a potential microRNA therapeutic candidate for atherosclerosis.
    MeSH term(s) Humans ; Animals ; Mice ; Feedback ; Atherosclerosis/genetics ; Atherosclerosis/prevention & control ; Atherosclerosis/metabolism ; Plaque, Atherosclerotic/metabolism ; Macrophages/metabolism ; Necrosis/metabolism ; MicroRNAs/genetics ; MicroRNAs/metabolism ; Mice, Knockout ; Apolipoproteins E ; Mice, Inbred C57BL ; Receptor-Interacting Protein Serine-Threonine Kinases/genetics ; Receptor-Interacting Protein Serine-Threonine Kinases/metabolism
    Chemical Substances MicroRNAs ; Apolipoproteins E ; MIRN223 microRNA, human ; Ripk3 protein, mouse (EC 2.7.11.1) ; Receptor-Interacting Protein Serine-Threonine Kinases (EC 2.7.11.1) ; MIRN223 microRNA, mouse
    Language English
    Publishing date 2023-11-16
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1221433-4
    ISSN 1524-4636 ; 1079-5642
    ISSN (online) 1524-4636
    ISSN 1079-5642
    DOI 10.1161/ATVBAHA.123.319776
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Erratum for Xu et al., "A Single Amino Acid at Position 431 of the PB2 Protein Determines the Virulence of H1N1 Swine Influenza Viruses in Mice".

    Xu, Chengzhi / Xu, Bangfeng / Wu, Yunpu / Yang, Shiman / Jia, Yunhui / Liang, Wenhua / Yang, Dawei / He, Likun / Zhu, Wenfei / Chen, Yan / Yang, Huanliang / Yu, Benliang / Wang, Dayan / Qiao, Chuanling

    Journal of virology

    2020  Volume 94, Issue 13

    Language English
    Publishing date 2020-06-16
    Publishing country United States
    Document type Journal Article ; Published Erratum
    ZDB-ID 80174-4
    ISSN 1098-5514 ; 0022-538X
    ISSN (online) 1098-5514
    ISSN 0022-538X
    DOI 10.1128/JVI.00653-20
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: A Single Amino Acid at Position 431 of the PB2 Protein Determines the Virulence of H1N1 Swine Influenza Viruses in Mice.

    Xu, Chengzhi / Xu, Bangfeng / Wu, Yunpu / Yang, Shiman / Jia, Yunhui / Liang, Wenhua / Yang, Dawei / He, Likun / Zhu, Wenfei / Chen, Yan / Yang, Huanliang / Yu, Benliang / Wang, Dayan / Qiao, Chuanling

    Journal of virology

    2020  Volume 94, Issue 8

    Abstract: Genetic reassortments occurred continuously among multiple subtypes or genotypes of influenza viruses prevalent in pigs. Of note, some reassortant viruses bearing the internal genes of the 2009 pandemic H1N1 (2009/H1N1) virus sporadically caused human ... ...

    Abstract Genetic reassortments occurred continuously among multiple subtypes or genotypes of influenza viruses prevalent in pigs. Of note, some reassortant viruses bearing the internal genes of the 2009 pandemic H1N1 (2009/H1N1) virus sporadically caused human infection, which highlights their potential threats to human public health. In this study, we performed phylogenetic analysis on swine influenza viruses (SIVs) circulating in Liaoning Province, China. A total of 22 viruses, including 18 H1N1 and 4 H1N2 viruses, were isolated from 5,750 nasal swabs collected from pigs in slaughterhouses from 2014 to 2016. H1N1 viruses formed four genotypes, which included Eurasian avian-like H1N1 (EA H1N1) and double/triple reassortant H1N1 derived from EA H1N1, 2009/H1N1, and triple reassortant H1N2 (TR H1N2) viruses. H1N1 SIVs with different genotypes and even those within the same genotypes represented different pathogenicities in mice. We further characterized two naturally isolated H1N1 SIVs that had similar viral genomes but differed substantially in their virulence in mice and found that a single amino acid at position 431 in the basic polymerase 2 (PB2) protein significantly affected the viral replication capacity and virulence of these two viruses. Taken together, our findings revealed the diverse genomic origins and virulence of the SIVs prevalent in Liaoning Province during 2014 to 2016, which highlights that continuous surveillance is essential to monitor the evolution of SIVs. We identified a naturally occurring amino acid mutation in the PB2 protein of H1N1 SIVs that impacts the viral replication and virulence in mice by altering the viral polymerase activity.
    MeSH term(s) Amino Acids/genetics ; Animals ; China ; Disease Models, Animal ; Female ; Genes, Viral/genetics ; Genome, Viral ; Genotype ; Influenza A Virus, H1N1 Subtype/classification ; Influenza A Virus, H1N1 Subtype/genetics ; Influenza A Virus, H1N1 Subtype/growth & development ; Influenza A Virus, H1N2 Subtype/genetics ; Kinetics ; Mice ; Mice, Inbred BALB C ; Mutation ; Phylogeny ; Reassortant Viruses/genetics ; Sequence Analysis, Protein ; Swine ; Swine Diseases/virology ; Virulence/genetics ; Virus Replication ; Whole Genome Sequencing
    Chemical Substances Amino Acids
    Language English
    Publishing date 2020-03-31
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 80174-4
    ISSN 1098-5514 ; 0022-538X
    ISSN (online) 1098-5514
    ISSN 0022-538X
    DOI 10.1128/JVI.01930-19
    Database MEDical Literature Analysis and Retrieval System OnLINE

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