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  1. Article ; Online: MitoWave: Spatiotemporal analysis of mitochondrial membrane potential fluctuations during I/R.

    Ashok, Deepthi / O'Rourke, Brian

    Biophysical journal

    2021  Volume 120, Issue 16, Page(s) 3261–3271

    Abstract: Mitochondria exhibit unstable inner membrane potentials ( ... ...

    Abstract Mitochondria exhibit unstable inner membrane potentials (ΔΨ
    MeSH term(s) Animals ; Ischemia/metabolism ; Membrane Potential, Mitochondrial ; Mice ; Mitochondria, Heart/metabolism ; Myocytes, Cardiac/metabolism ; Reperfusion ; Spatio-Temporal Analysis
    Language English
    Publishing date 2021-07-21
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 218078-9
    ISSN 1542-0086 ; 0006-3495
    ISSN (online) 1542-0086
    ISSN 0006-3495
    DOI 10.1016/j.bpj.2021.05.033
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Response to redefining health technology assessment: a comment on "the new definition of health technology assessment: a milestone in international collaboration".

    O'Rourke, Brian / Oortwijn, Wija / Schuller, Tara

    International journal of technology assessment in health care

    2022  Volume 38, Issue 1, Page(s) e55

    MeSH term(s) Biomedical Technology ; Technology Assessment, Biomedical
    Language English
    Publishing date 2022-07-05
    Publishing country England
    Document type Letter ; Comment
    ZDB-ID 632573-7
    ISSN 1471-6348 ; 0266-4623
    ISSN (online) 1471-6348
    ISSN 0266-4623
    DOI 10.1017/S0266462322000344
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  3. Article ; Online: Distinct Effects of Mitochondrial Na

    Velmurugan, Sathya / Liu, Ting / Chen, Kuey C / Despa, Florin / O'Rourke, Brian / Despa, Sanda

    Journal of the American Heart Association

    2023  Volume 12, Issue 14, Page(s) e029997

    Abstract: Background Mitochondrial dysfunction contributes to the cardiac remodeling triggered by type 2 diabetes (T2D). Mitochondrial ... ...

    Abstract Background Mitochondrial dysfunction contributes to the cardiac remodeling triggered by type 2 diabetes (T2D). Mitochondrial Ca
    MeSH term(s) Rats ; Humans ; Animals ; Myocytes, Cardiac/metabolism ; Diabetes Mellitus, Type 2/complications ; Diabetes Mellitus, Type 2/metabolism ; Sodium-Calcium Exchanger/metabolism ; Diabetes Mellitus, Experimental/metabolism ; Arrhythmias, Cardiac/metabolism ; Sarcoplasmic Reticulum/metabolism ; Calcium Signaling/physiology ; Mitochondria/metabolism ; Calcium/metabolism
    Chemical Substances Sodium-Calcium Exchanger ; Calcium (SY7Q814VUP)
    Language English
    Publishing date 2023-07-08
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2653953-6
    ISSN 2047-9980 ; 2047-9980
    ISSN (online) 2047-9980
    ISSN 2047-9980
    DOI 10.1161/JAHA.123.029997
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  4. Article: Cardiac sympathetic denervation prevents sudden cardiac arrest and improves cardiac function by enhancing mitochondrial-antioxidant capacity.

    Dey, Swati / Joshi, Pooja / O'Rourke, Brian / Estes, Shanea / DeMazumder, Deeptankar

    bioRxiv : the preprint server for biology

    2023  

    Abstract: Rationale: Sudden cardiac arrest (SCA) and heart failure (HF) are leading causes of death. The underlying mechanisms are incompletely understood, limiting the design of new therapies. Whereas most autonomic modulation therapies have not shown clear ... ...

    Abstract Rationale: Sudden cardiac arrest (SCA) and heart failure (HF) are leading causes of death. The underlying mechanisms are incompletely understood, limiting the design of new therapies. Whereas most autonomic modulation therapies have not shown clear benefit in HF patients, growing evidence indicates cardiac sympathetic denervation (CSD) exerts cardioprotective effects. The underlying molecular and cellular mechanisms remain unexplored.
    Objective: Based on the hypothesis that mitochondrial reactive oxygen species (mROS) drive the pathogenesis of HF and SCA, we investigated whether CSD prevents SCA and HF by improving mitochondrial antioxidant capacity and redox balance, to correct impaired Ca2+ handling and repolarization reserve.
    Methods and results: We interrogated CSD-specific responses in pressure-overload HF models with spontaneous SCA using in vivo echocardiographic and electrocardiographic studies and in vitro biochemical and functional studies including ratiometric measures of mROS, Ca2+ and sarcomere dynamics in left ventricular myocytes. Pressure-overloaded HF reduced mitochondrial antioxidant capacity and increased mROS, which impaired β-adrenergic signaling and caused SR Ca2+ leak, reducing SR Ca2+ and increasing diastolic Ca2+, impaired myofilament contraction and further increased the sympathetic stress response. CSD improved contractile function and mitigated mROS-mediated diastolic Ca2+ overload, dispersion of repolarization, triggered activity and SCA by upregulating mitochondrial antioxidant and NADPH-producing enzymes.
    Conclusions: Our findings support a fundamental role of sympathetic stress-induced downregulation of mROS scavenging enzymes and RyR-leak mediated diastolic Ca2+ overload in HF and SCA pathogenesis that are mitigated by CSD. This first report on the molecular and cellular mechanisms of CSD supports its evaluation in additional high-risk patient groups.
    Language English
    Publishing date 2023-10-28
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2023.01.29.526082
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  5. Article ; Online: Top-level leaders and implementation strategies to support organizational diversity, equity, inclusion, and belonging (DEIB) interventions: a qualitative study of top-level DEIB leaders in healthcare organizations.

    Hogan, Tory H / O'Rourke, Brian P / Weeks, Eddie / Silvera, Geoffrey A / Choi, Seongwon

    Implementation science : IS

    2023  Volume 18, Issue 1, Page(s) 59

    Abstract: Background: The Black Lives Matter movement and COVID-19 pandemic motivated the wide-scale adoption of diversity, equity, inclusion, and belonging (DEIB) initiatives within healthcare organizations and the creation of DEIB top-level leader positions. ... ...

    Abstract Background: The Black Lives Matter movement and COVID-19 pandemic motivated the wide-scale adoption of diversity, equity, inclusion, and belonging (DEIB) initiatives within healthcare organizations and the creation of DEIB top-level leader positions. The next step is to understand how these leaders contribute to the implementation of DEIB interventions, a task with notable salience due to not only the historical difficulties associated with DEIB strategy execution, but also the substantial evidence that leadership plays a significant role in implementation processes. Therefore, the objective of this qualitative study is to understand the role of top-level DEIB leaders in the implementation of healthcare organizational DEIB interventions.
    Methods: A qualitative research approach which used an in-depth semi-structured interview approach was employed. We conducted thirty-one 60-90-min semi-structured interviews with DEIB top-level leaders between February 2022 and October 2022 over Zoom. An iterative coding process was used to identify the key implementation strategies and activities of DEIB top-level leaders.
    Results: Interviewees were mostly Black, majority female, and mostly heterosexual and had a variety of educational backgrounds. We identified the DEIB top-level leader as the DEIB strategy implementation champion. These leaders drive five DEIB implementation strategies: (1) People, (2) Health Equity, (3) Monitoring and Feedback, (4) Operational Planning and Communication, and (5) External Partners. Within these, we identified 19 significant activities that describe the unique implementation strategies supported by the DEIB top-level leaders.
    Conclusions: To move toward sustained commitment to DEIB, the organization must focus on not only establishing DEIB interventions, but on their successful implementation. Our findings help explicate the implementation activities that drive the DEIB initiatives of healthcare organizations and the role of DEIB leaders. Our work can help healthcare organizations systematically identify how to support the success of DEIB organizational interventions.
    MeSH term(s) Humans ; Female ; Diversity, Equity, Inclusion ; Pandemics ; Qualitative Research ; Delivery of Health Care ; Leadership
    Chemical Substances N-(2-(diethylamino)ethyl)-4-iodobenzamide (106790-96-9)
    Language English
    Publishing date 2023-11-07
    Publishing country England
    Document type Journal Article
    ZDB-ID 2225822-X
    ISSN 1748-5908 ; 1748-5908
    ISSN (online) 1748-5908
    ISSN 1748-5908
    DOI 10.1186/s13012-023-01319-7
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  6. Article: Innate Immune Activation and Mitochondrial ROS Invoke Persistent Cardiac Conduction System Dysfunction after COVID-19.

    Ashok, Deepthi / Liu, Ting / Criscione, Joseph / Prakash, Meghana / Kim, Byunggik / Chow, Julian / Craney, Morgan / Papanicolaou, Kyriakos N / Sidor, Agnieszka / Brian Foster, D / Pekosz, Andrew / Villano, Jason / Kim, Deok-Ho / O'Rourke, Brian

    bioRxiv : the preprint server for biology

    2024  

    Abstract: Background: Cardiac risk rises during acute SARS-CoV-2 infection and in long COVID syndrome in humans, but the mechanisms behind COVID-19-linked arrhythmias are unknown. This study explores the acute and long term effects of SARS-CoV-2 on the cardiac ... ...

    Abstract Background: Cardiac risk rises during acute SARS-CoV-2 infection and in long COVID syndrome in humans, but the mechanisms behind COVID-19-linked arrhythmias are unknown. This study explores the acute and long term effects of SARS-CoV-2 on the cardiac conduction system (CCS) in a hamster model of COVID-19.
    Methods: Radiotelemetry in conscious animals was used to non-invasively record electrocardiograms and subpleural pressures after intranasal SARS-CoV-2 infection. Cardiac cytokines, interferon-stimulated gene expression, and macrophage infiltration of the CCS, were assessed at 4 days and 4 weeks post-infection. A double-stranded RNA mimetic, polyinosinic:polycytidylic acid (PIC), was used in vivo and in vitro to activate viral pattern recognition receptors in the absence of SARS-CoV-2 infection.
    Results: COVID-19 induced pronounced tachypnea and severe cardiac conduction system (CCS) dysfunction, spanning from bradycardia to persistent atrioventricular block, although no viral protein expression was detected in the heart. Arrhythmias developed rapidly, partially reversed, and then redeveloped after the pulmonary infection was resolved, indicating persistent CCS injury. Increased cardiac cytokines, interferon-stimulated gene expression, and macrophage remodeling in the CCS accompanied the electrophysiological abnormalities. Interestingly, the arrhythmia phenotype was reproduced by cardiac injection of PIC in the absence of virus, indicating that innate immune activation was sufficient to drive the response. PIC also strongly induced cytokine secretion and robust interferon signaling in hearts, human iPSC-derived cardiomyocytes (hiPSC-CMs), and engineered heart tissues, accompanied by alterations in electrical and Ca
    Conclusions: The findings indicate that long term dysfunction and immune cell remodeling of the CCS is induced by COVID-19, arising indirectly from oxidative stress and excessive activation of cardiac innate immune responses during infection, with implications for long COVID Syndrome.
    Language English
    Publishing date 2024-01-08
    Publishing country United States
    Document type Preprint
    DOI 10.1101/2024.01.05.574280
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  7. Article ; Online: Metabolism: Beyond the power of mitochondria.

    O'Rourke, Brian

    Nature reviews. Cardiology

    2016  Volume 13, Issue 7, Page(s) 386–388

    MeSH term(s) Animals ; Cardiovascular Diseases/metabolism ; Energy Metabolism ; Humans ; Mitochondria, Heart/metabolism ; Oxidative Stress
    Language English
    Publishing date 2016-06-15
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural
    ZDB-ID 2490375-9
    ISSN 1759-5010 ; 1759-5002
    ISSN (online) 1759-5010
    ISSN 1759-5002
    DOI 10.1038/nrcardio.2016.95
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  8. Article ; Online: Mitochondria Do Not Survive Calcium Overload During Transplantation.

    Bertero, Edoardo / O'Rourke, Brian / Maack, Christoph

    Circulation research

    2020  Volume 126, Issue 6, Page(s) 784–786

    MeSH term(s) Calcium ; Calcium, Dietary ; Mitochondria
    Chemical Substances Calcium, Dietary ; Calcium (SY7Q814VUP)
    Language English
    Publishing date 2020-02-06
    Publishing country United States
    Document type Letter ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 80100-8
    ISSN 1524-4571 ; 0009-7330 ; 0931-6876
    ISSN (online) 1524-4571
    ISSN 0009-7330 ; 0931-6876
    DOI 10.1161/CIRCRESAHA.119.316291
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  9. Article ; Online: Correction to: Multiscale Modeling of the Mitochondrial Origin of Cardiac Reentrant and Fibrillatory Arrhythmias.

    Solhjoo, Soroosh / Kim, Seulhee / Plank, Gernot / O'Rourke, Brian / Zhou, Lufang

    Methods in molecular biology (Clifton, N.J.)

    2022  Volume 2399, Page(s) C1

    Language English
    Publishing date 2022-07-27
    Publishing country United States
    Document type Published Erratum
    ISSN 1940-6029
    ISSN (online) 1940-6029
    DOI 10.1007/978-1-0716-1831-8_18
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  10. Article ; Online: Response by Bertero et al to Letter Regarding Article, "Mitochondria Do Not Survive Calcium Overload".

    Bertero, Edoardo / O'Rourke, Brian / Maack, Christoph

    Circulation research

    2020  Volume 126, Issue 8, Page(s) e58–e59

    MeSH term(s) Calcium ; Calcium, Dietary ; Mitochondria
    Chemical Substances Calcium, Dietary ; Calcium (SY7Q814VUP)
    Language English
    Publishing date 2020-04-09
    Publishing country United States
    Document type Letter ; Comment
    ZDB-ID 80100-8
    ISSN 1524-4571 ; 0009-7330 ; 0931-6876
    ISSN (online) 1524-4571
    ISSN 0009-7330 ; 0931-6876
    DOI 10.1161/CIRCRESAHA.120.316843
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