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  1. Article ; Online: Exploring Artificial Intelligence and the Future of Primary Care.

    Gilfoyle, Meghan / Bosworth, K Taylor / Adesanya, T M Ayodele / Chisholm, Ashley / Ohioma, Minika / Ringwald, Bryce / Warpinski, Chloe L / Kueper, Jacqueline K / Liaw, Winston

    Annals of family medicine

    2024  Volume 22, Issue 2, Page(s) 174–175

    MeSH term(s) Humans ; Artificial Intelligence ; Forecasting ; Primary Health Care
    Language English
    Publishing date 2024-03-25
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2171425-3
    ISSN 1544-1717 ; 1544-1709
    ISSN (online) 1544-1717
    ISSN 1544-1709
    DOI 10.1370/afm.3112
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  2. Article ; Online: C1 Esterase Inhibition: Targeting Multiple Systems in COVID-19.

    Adesanya, T M Ayodele / Campbell, Courtney M / Cheng, Lijun / Ogbogu, Princess U / Kahwash, Rami

    Journal of clinical immunology

    2021  Volume 41, Issue 4, Page(s) 729–732

    MeSH term(s) Blood Coagulation/drug effects ; Blood Coagulation/immunology ; COVID-19/blood ; COVID-19/drug therapy ; COVID-19/immunology ; COVID-19/virology ; Complement Activation/drug effects ; Complement Activation/immunology ; Complement C1 Inhibitor Protein/metabolism ; Complement C1s/antagonists & inhibitors ; Complement C1s/metabolism ; Complement Inactivating Agents/pharmacology ; Complement Inactivating Agents/therapeutic use ; Humans ; Immunity, Innate/drug effects ; SARS-CoV-2/immunology ; SARS-CoV-2/metabolism ; Thrombosis/blood ; Thrombosis/immunology ; Thrombosis/prevention & control
    Chemical Substances Complement C1 Inhibitor Protein ; Complement Inactivating Agents ; Complement C1s (EC 3.4.21.42)
    Language English
    Publishing date 2021-01-21
    Publishing country Netherlands
    Document type Letter ; Review
    ZDB-ID 779361-3
    ISSN 1573-2592 ; 0271-9142
    ISSN (online) 1573-2592
    ISSN 0271-9142
    DOI 10.1007/s10875-021-00972-1
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    Zs.A 1640: Show issues Location:
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  3. Article: Dealing with a Porcelain Aorta during Coronary Artery Bypass Grafting.

    Adesanya, T M Ayodele / Kilic, Ahmet

    Case reports in surgery

    2014  Volume 2014, Page(s) 582425

    Abstract: We report a complex case of multivessel CAD in a patient with a porcelain aorta and high-grade left subclavian artery stenosis. Utilizing a staged left subclavian artery stent placement with a next-day plan for a four-vessel, on-pump CABG and ascending ... ...

    Abstract We report a complex case of multivessel CAD in a patient with a porcelain aorta and high-grade left subclavian artery stenosis. Utilizing a staged left subclavian artery stent placement with a next-day plan for a four-vessel, on-pump CABG and ascending aortic replacement, this case highlights an organized approach to diagnosing and dealing with a heavily calcified aorta while describing a stepwise algorithm to deal with aortic calcifications prior to initiating cardiac surgery.
    Language English
    Publishing date 2014-12-24
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2657697-1
    ISSN 2090-6919 ; 2090-6900
    ISSN (online) 2090-6919
    ISSN 2090-6900
    DOI 10.1155/2014/582425
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  4. Article ; Online: Dealing with a Porcelain Aorta during Coronary Artery Bypass Grafting

    T. M. Ayodele Adesanya / Ahmet Kilic

    Case Reports in Surgery, Vol

    2014  Volume 2014

    Keywords Surgery ; RD1-811 ; Medicine ; R
    Language English
    Publishing date 2014-01-01T00:00:00Z
    Publisher Hindawi Publishing Corporation
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  5. Article ; Online: MG53 suppresses interferon-β and inflammation via regulation of ryanodine receptor-mediated intracellular calcium signaling

    Matthew Sermersheim / Adam D. Kenney / Pei-Hui Lin / Temet M. McMichael / Chuanxi Cai / Kristyn Gumpper / T. M. Ayodele Adesanya / Haichang Li / Xinyu Zhou / Ki-Ho Park / Jacob S. Yount / Jianjie Ma

    Nature Communications, Vol 11, Iss 1, Pp 1-

    2020  Volume 12

    Abstract: TRIM proteins are known to play critical roles in the context of viral infection. Here the authors establish MG53 (TRIM72) suppresses IFN and inflammation by modulation of ryanodine receptor related intracellular calcium induction. ...

    Abstract TRIM proteins are known to play critical roles in the context of viral infection. Here the authors establish MG53 (TRIM72) suppresses IFN and inflammation by modulation of ryanodine receptor related intracellular calcium induction.
    Keywords Science ; Q
    Language English
    Publishing date 2020-07-01T00:00:00Z
    Publisher Nature Portfolio
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  6. Article ; Online: MG53 suppresses interferon-β and inflammation via regulation of ryanodine receptor-mediated intracellular calcium signaling.

    Sermersheim, Matthew / Kenney, Adam D / Lin, Pei-Hui / McMichael, Temet M / Cai, Chuanxi / Gumpper, Kristyn / Adesanya, T M Ayodele / Li, Haichang / Zhou, Xinyu / Park, Ki-Ho / Yount, Jacob S / Ma, Jianjie

    Nature communications

    2020  Volume 11, Issue 1, Page(s) 3624

    Abstract: TRIM family proteins play integral roles in the innate immune response to virus infection. MG53 (TRIM72) is essential for cell membrane repair and is believed to be a muscle-specific TRIM protein. Here we show human macrophages express MG53, and MG53 ... ...

    Abstract TRIM family proteins play integral roles in the innate immune response to virus infection. MG53 (TRIM72) is essential for cell membrane repair and is believed to be a muscle-specific TRIM protein. Here we show human macrophages express MG53, and MG53 protein expression is reduced following virus infection. Knockdown of MG53 in macrophages leads to increases in type I interferon (IFN) upon infection. MG53 knockout mice infected with influenza virus show comparable influenza virus titres to wild type mice, but display increased morbidity accompanied by more accumulation of CD45+ cells and elevation of IFNβ in the lung. We find that MG53 knockdown results in activation of NFκB signalling, which is linked to an increase in intracellular calcium oscillation mediated by ryanodine receptor (RyR). MG53 inhibits IFNβ induction in an RyR-dependent manner. This study establishes MG53 as a new target for control of virus-induced morbidity and tissue injury.
    MeSH term(s) Animals ; Calcium Signaling/immunology ; Cell Line, Tumor ; Disease Models, Animal ; Gene Knockdown Techniques ; Gene Knockout Techniques ; Humans ; Immunity, Innate ; Influenza A Virus, H1N1 Subtype/immunology ; Influenza, Human/immunology ; Influenza, Human/virology ; Interferon-beta/immunology ; Interferon-beta/metabolism ; Macrophages/immunology ; Macrophages/metabolism ; Male ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Mice ; Mice, Knockout ; NF-kappa B/metabolism ; RNA, Small Interfering ; Ryanodine Receptor Calcium Release Channel/metabolism ; Signal Transduction/immunology ; Tripartite Motif Proteins/genetics ; Tripartite Motif Proteins/metabolism
    Chemical Substances MG53 protein, mouse ; Membrane Proteins ; NF-kappa B ; RNA, Small Interfering ; Ryanodine Receptor Calcium Release Channel ; TRIM72 protein, human ; Tripartite Motif Proteins ; Interferon-beta (77238-31-4)
    Language English
    Publishing date 2020-07-17
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Video-Audio Media
    ZDB-ID 2553671-0
    ISSN 2041-1723 ; 2041-1723
    ISSN (online) 2041-1723
    ISSN 2041-1723
    DOI 10.1038/s41467-020-17177-6
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  7. Article ; Online: A systematic study of gene expression variation at single-nucleotide resolution reveals widespread regulatory roles for uAUGs.

    Yun, Yue / Adesanya, T M Ayodele / Mitra, Robi D

    Genome research

    2012  Volume 22, Issue 6, Page(s) 1089–1097

    Abstract: Regulatory single-nucleotide polymorphisms (rSNPs) alter gene expression. Common approaches for identifying rSNPs focus on sequence variants in conserved regions; however, it is unknown what fraction of rSNPs is undetectable using this approach. We ... ...

    Abstract Regulatory single-nucleotide polymorphisms (rSNPs) alter gene expression. Common approaches for identifying rSNPs focus on sequence variants in conserved regions; however, it is unknown what fraction of rSNPs is undetectable using this approach. We present a systematic analysis of gene expression variation at the single-nucleotide level in the Saccharomyces cerevisiae GAL1-10 regulatory region. We exhaustively mutated nearly every base and measured the expression of each variant with a sensitive dual reporter assay. We observed an expression change for 7% (43/582) of the bases in this region, most of which (35/43, 81%) reside in conserved positions. The most dramatic changes were caused by variants that produced AUGs upstream of the translation start (uAUGs), and we sought to understand the consequences and molecular mechanisms underlying this class of mutations. A genome-wide analysis showed that genes with uAUGs display significantly lower mRNA and protein levels than genes without uAUGs. To determine the generality of this mechanism, we introduced uAUGs into S. cerevisiae genes and observed significantly reduced expression in 17/21 instances (p < 0.01), suggesting that uAUGs are functional in a wide variety of sequence contexts. Quantification of mRNA and protein levels for uAUG mutants showed that uAUGs affect both transcription and translation. Expression of uAUG mutants under the upf1Δ strain demonstrated that uAUGs stimulate the nonsense-mediated decay pathway. Our results suggest that uAUGs are potent and widespread regulators of gene expression that act by attenuating both protein and RNA levels.
    MeSH term(s) 5' Untranslated Regions ; Base Sequence ; Conserved Sequence ; Gene Expression Regulation, Fungal ; Molecular Sequence Data ; Mutation ; Peptide Chain Initiation, Translational ; Polymorphism, Single Nucleotide ; RNA, Messenger ; Regulatory Sequences, Nucleic Acid ; Saccharomyces cerevisiae/genetics ; Saccharomyces cerevisiae Proteins/genetics ; Saccharomyces cerevisiae Proteins/metabolism
    Chemical Substances 5' Untranslated Regions ; RNA, Messenger ; Saccharomyces cerevisiae Proteins
    Language English
    Publishing date 2012-03-27
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1284872-4
    ISSN 1549-5469 ; 1088-9051 ; 1054-9803
    ISSN (online) 1549-5469
    ISSN 1088-9051 ; 1054-9803
    DOI 10.1101/gr.117366.110
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    Zs.A 3729: Show issues Location:
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    Zs.MG 8: Show issues

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  8. Article ; Online: MG 53 Protein Protects Aortic Valve Interstitial Cells From Membrane Injury and Fibrocalcific Remodeling.

    Adesanya, T M Ayodele / Russell, Melanie / Park, Ki Ho / Zhou, Xinyu / Sermersheim, Matthew A / Gumpper, Kristyn / Koenig, Sara N / Tan, Tao / Whitson, Bryan A / Janssen, Paul M L / Lincoln, Joy / Zhu, Hua / Ma, Jianjie

    Journal of the American Heart Association

    2019  Volume 8, Issue 4, Page(s) e009960

    Abstract: Background The aortic valve of the heart experiences constant mechanical stress under physiological conditions. Maladaptive valve injury responses contribute to the development of valvular heart disease. Here, we test the hypothesis that MG 53 ( ... ...

    Abstract Background The aortic valve of the heart experiences constant mechanical stress under physiological conditions. Maladaptive valve injury responses contribute to the development of valvular heart disease. Here, we test the hypothesis that MG 53 (mitsugumin 53), an essential cell membrane repair protein, can protect valvular cells from injury and fibrocalcific remodeling processes associated with valvular heart disease. Methods and Results We found that MG 53 is expressed in pig and human patient aortic valves and observed aortic valve disease in aged Mg53-/- mice. Aortic valves of Mg53-/- mice showed compromised cell membrane integrity. In vitro studies demonstrated that recombinant human MG 53 protein protects primary valve interstitial cells from mechanical injury and that, in addition to mediating membrane repair, recombinant human MG 53 can enter valve interstitial cells and suppress transforming growth factor-β-dependent activation of fibrocalcific signaling. Conclusions Together, our data characterize valve interstitial cell membrane repair as a novel mechanism of protection against valvular remodeling and assess potential in vivo roles of MG 53 in preventing valvular heart disease.
    MeSH term(s) Animals ; Aortic Valve/metabolism ; Aortic Valve/pathology ; Aortic Valve Stenosis/diagnosis ; Aortic Valve Stenosis/metabolism ; Aortic Valve Stenosis/physiopathology ; Biomarkers/metabolism ; Blotting, Western ; Calcinosis/diagnosis ; Calcinosis/metabolism ; Calcinosis/physiopathology ; Cells, Cultured ; Disease Models, Animal ; Echocardiography ; Humans ; Immunohistochemistry ; Male ; Mice ; Signal Transduction ; Stress, Mechanical ; Swine ; Tripartite Motif Proteins/biosynthesis ; Ventricular Remodeling
    Chemical Substances Biomarkers ; TRIM72 protein, human ; Tripartite Motif Proteins
    Language English
    Publishing date 2019-02-13
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2653953-6
    ISSN 2047-9980 ; 2047-9980
    ISSN (online) 2047-9980
    ISSN 2047-9980
    DOI 10.1161/JAHA.118.009960
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  9. Article ; Online: MG53 promotes corneal wound healing and mitigates fibrotic remodeling in rodents

    Heather L. Chandler / Tao Tan / Chunlin Yang / Anne J. Gemensky-Metzler / Rita F. Wehrman / Qiwei Jiang / Cornelia M. W. Peterson / Bingchuan Geng / Xinyu Zhou / Qiang Wang / Denis Kaili / T. M. Ayodele Adesanya / Frank Yi / Hua Zhu / Jianjie Ma

    Communications Biology, Vol 2, Iss 1, Pp 1-

    2019  Volume 10

    Abstract: Heather Chandler, Tao Tan, Chunlin Yang et al. find that the cell membrane repair protein MG53 plays a key role in repairing cornea injury. Using mouse and rat models, they show that recombinant human MG53 protects the cornea against injury and enhances ... ...

    Abstract Heather Chandler, Tao Tan, Chunlin Yang et al. find that the cell membrane repair protein MG53 plays a key role in repairing cornea injury. Using mouse and rat models, they show that recombinant human MG53 protects the cornea against injury and enhances healing.
    Keywords Biology (General) ; QH301-705.5
    Language English
    Publishing date 2019-02-01T00:00:00Z
    Publisher Nature Publishing Group
    Document type Article ; Online
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  10. Article ; Online: MG53 promotes corneal wound healing and mitigates fibrotic remodeling in rodents.

    Chandler, Heather L / Tan, Tao / Yang, Chunlin / Gemensky-Metzler, Anne J / Wehrman, Rita F / Jiang, Qiwei / Peterson, Cornelia M W / Geng, Bingchuan / Zhou, Xinyu / Wang, Qiang / Kaili, Denis / Adesanya, T M Ayodele / Yi, Frank / Zhu, Hua / Ma, Jianjie

    Communications biology

    2019  Volume 2, Page(s) 71

    Abstract: The cornea plays an important role in transmitting light and providing protection to the eye, but is susceptible to injury and infection. Standard treatments for corneal wounds include topical lubricants, antibiotics, bandage contact lens, and surgery. ... ...

    Abstract The cornea plays an important role in transmitting light and providing protection to the eye, but is susceptible to injury and infection. Standard treatments for corneal wounds include topical lubricants, antibiotics, bandage contact lens, and surgery. However, these measures are often ineffective. Here we show that MG53, a protein with an essential role in cell membrane repair, contributes to the corneal injury-repair process. Native MG53 is present in the corneal epithelia, tear film, and aqueous humor, suggesting its potential function in corneal homeostasis. Knockout of MG53 in mice causes impaired healing and regenerative capacity following injury. Exogenous recombinant human MG53 (rhMG53) protein protects the corneal epithelia against mechanical injury and enhances healing by promoting migration of corneal fibroblasts. Using in vivo alkaline-induced injury to the rat cornea, we show that rhMG53 promotes re-epithelialization and reduces post-injury fibrosis and vascularization. Finally, we show that rhMG53 modulates TGF-β-mediated fibrotic remodeling associated with corneal injury. Overall, our data support the bi-functional role of MG53 in facilitating corneal healing and maintaining corneal transparency by reducing fibrosis and vascularization associated with corneal injuries.
    MeSH term(s) Animals ; Cell Movement/drug effects ; Cell Movement/genetics ; Cornea/drug effects ; Cornea/metabolism ; Cornea/pathology ; Corneal Injuries/genetics ; Corneal Injuries/metabolism ; Corneal Injuries/physiopathology ; Epithelium, Corneal/drug effects ; Epithelium, Corneal/metabolism ; Fibroblasts/cytology ; Fibroblasts/drug effects ; Fibroblasts/metabolism ; Fibrosis ; Humans ; Membrane Proteins/genetics ; Membrane Proteins/metabolism ; Mice, Knockout ; Rats ; Recombinant Proteins/pharmacology ; Regeneration/drug effects ; Regeneration/genetics ; Rodentia/genetics ; Rodentia/metabolism ; Transforming Growth Factor beta/pharmacology ; Wound Healing/drug effects ; Wound Healing/genetics ; Wound Healing/physiology
    Chemical Substances MG53 protein, mouse ; Membrane Proteins ; Recombinant Proteins ; Transforming Growth Factor beta
    Language English
    Publishing date 2019-02-20
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ISSN 2399-3642
    ISSN (online) 2399-3642
    DOI 10.1038/s42003-019-0316-7
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