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  1. Article: Virtual education revolution during the COVID-19 pandemic: the introduction of national educational rounds in sport and exercise medicine.

    Gelber, Nitai / Dilworth, Neil / Elliott, Wade / Bradley, Lindsay

    Canadian medical education journal

    2021  Volume 12, Issue 2, Page(s) e120–e121

    Language English
    Publishing date 2021-04-30
    Publishing country Canada
    Document type Journal Article
    ZDB-ID 2689512-2
    ISSN 1923-1202
    ISSN 1923-1202
    DOI 10.36834/cmej.70949
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Virtual education revolution during the COVID-19 pandemic

    Nitai Gelber / Neil Dilworth / Wade Elliott / Lindsay Bradley

    Canadian Medical Education Journal, Vol 12, Iss

    the introduction of national educational rounds in sport and exercise medicine

    2020  Volume 2

    Keywords Education (General) ; L7-991 ; Medicine (General) ; R5-920
    Language English
    Publishing date 2020-10-01T00:00:00Z
    Publisher Canadian Medical Education Journal
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  3. Article ; Online: Virtual education revolution during the COVID-19 pandemic

    Gelber, Nitai / Dilworth, Neil / Elliott, Wade / Bradley, Lindsay

    Canadian Medical Education Journal; In Press ; 1923-1202 ; 10.36834/cmej.vi0

    The introduction of national educational rounds in sport and exercise medicine: Une révolution de l’éducation virtuelle pendant la pandémie de la COVID-19 : l’introduction des séminaires nationaux en médecine du sport et de l’exercice

    2020  

    Keywords covid19
    Language English
    Publishing date 2020-10-23
    Publisher Canadian Medical Education Journal
    Publishing country ca
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  4. Article ; Online: Virtual education revolution during the COVID-19 pandemic

    Gelber, Nitai / Dilworth, Neil / Elliott, Wade / Bradley, Lindsay

    Canadian Medical Education Journal; In Press ; 1923-1202 ; 10.36834/cmej.vi0

    The introduction of national educational rounds in sport and exercise medicine: Une révolution de l’éducation virtuelle pendant la pandémie de la COVID-19 : l’introduction des séminaires nationaux en médecine du sport et de l’exercice

    2020  

    Keywords covid19
    Language English
    Publishing date 2020-10-23
    Publisher Canadian Medical Education Journal
    Publishing country ca
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  5. Article ; Online: Acute, delayed and chronic remote ischemic conditioning is associated with downregulation of mTOR and enhanced autophagy signaling.

    Sagar Rohailla / Nadia Clarizia / Michel Sourour / Wesam Sourour / Nitai Gelber / Can Wei / Jing Li / Andrew N Redington

    PLoS ONE, Vol 9, Iss 10, p e

    2014  Volume 111291

    Abstract: BACKGROUND:Remote ischemic conditioning (RIC), induced by brief periods of limb ischemia has been shown to decrease acute myocardial injury and chronic responses after acute coronary syndromes. While several signaling pathways have been implicated, our ... ...

    Abstract BACKGROUND:Remote ischemic conditioning (RIC), induced by brief periods of limb ischemia has been shown to decrease acute myocardial injury and chronic responses after acute coronary syndromes. While several signaling pathways have been implicated, our understanding of the cardioprotection and its underlying mediators and mechanisms remains incomplete. In this study we examine the effect of RIC on pro-autophagy signaling as a possible mechanism of benefit. METHODS AND RESULTS:We examined the role of autophagy in the acute/first window (15 minutes after RIC), delayed/second window (24 hours after RIC) and chronic (24 hours after 9 days of repeated RIC) phases of cardioprotection. C57BL/6 mice (N = 69) were allocated to each treatment phase and further stratified to receive RIC, induced by four cycles of 5 minutes of limb ischemia followed by 5 minutes of reperfusion, or control treatment consisting solely of handling without transient ischemia. The groups included, group 1 (1W control), group 2 (1W RIC), group 3 (2W control), group 4 (2W RIC), group 5 (3W control) and group 6 (3W RIC). Hearts were isolated for assessment of cardiac function and infarct size after global ischemia using a Langendorff preparation. Infarct size was reduced in all three phases of cardioprotection, in association with improvements in post-ischemic left ventricular end diastolic pressure (LVEDP) and developed pressure (LVDP) (P<0.05). The pattern of autophagy signaling varied; 1W RIC increased AMPK levels and decreased the activation of mammalian target of rapamycin (mTOR), whereas chronic RIC was associated with persistent mTOR suppression and increased levels of autophagosome proteins, LC3II/I and Atg5. CONCLUSIONS:Cardioprotection following transient ischemia exists in both the acute and delayed/chronic phases of conditioning. RIC induces pro-autophagy signaling but the pattern of responses varies depending on the phase, with the most complete portfolio of responses observed when RIC is administered chronically.
    Keywords Medicine ; R ; Science ; Q
    Subject code 630
    Language English
    Publishing date 2014-01-01T00:00:00Z
    Publisher Public Library of Science (PLoS)
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  6. Article ; Online: (with research data) Acute, delayed and chronic remote ischemic conditioning is associated with downregulation of mTOR and enhanced autophagy signaling.

    Rohailla, Sagar / Clarizia, Nadia / Sourour, Michel / Sourour, Wesam / Gelber, Nitai / Wei, Can / Li, Jing / Redington, Andrew N

    PloS one

    2014  Volume 9, Issue 10, Page(s) e111291

    Abstract: Background: Remote ischemic conditioning (RIC), induced by brief periods of limb ischemia has been shown to decrease acute myocardial injury and chronic responses after acute coronary syndromes. While several signaling pathways have been implicated, our ...

    Abstract Background: Remote ischemic conditioning (RIC), induced by brief periods of limb ischemia has been shown to decrease acute myocardial injury and chronic responses after acute coronary syndromes. While several signaling pathways have been implicated, our understanding of the cardioprotection and its underlying mediators and mechanisms remains incomplete. In this study we examine the effect of RIC on pro-autophagy signaling as a possible mechanism of benefit.
    Methods and results: We examined the role of autophagy in the acute/first window (15 minutes after RIC), delayed/second window (24 hours after RIC) and chronic (24 hours after 9 days of repeated RIC) phases of cardioprotection. C57BL/6 mice (N = 69) were allocated to each treatment phase and further stratified to receive RIC, induced by four cycles of 5 minutes of limb ischemia followed by 5 minutes of reperfusion, or control treatment consisting solely of handling without transient ischemia. The groups included, group 1 (1W control), group 2 (1W RIC), group 3 (2W control), group 4 (2W RIC), group 5 (3W control) and group 6 (3W RIC). Hearts were isolated for assessment of cardiac function and infarct size after global ischemia using a Langendorff preparation. Infarct size was reduced in all three phases of cardioprotection, in association with improvements in post-ischemic left ventricular end diastolic pressure (LVEDP) and developed pressure (LVDP) (P<0.05). The pattern of autophagy signaling varied; 1W RIC increased AMPK levels and decreased the activation of mammalian target of rapamycin (mTOR), whereas chronic RIC was associated with persistent mTOR suppression and increased levels of autophagosome proteins, LC3II/I and Atg5.
    Conclusions: Cardioprotection following transient ischemia exists in both the acute and delayed/chronic phases of conditioning. RIC induces pro-autophagy signaling but the pattern of responses varies depending on the phase, with the most complete portfolio of responses observed when RIC is administered chronically.
    MeSH term(s) AMP-Activated Protein Kinases/genetics ; AMP-Activated Protein Kinases/metabolism ; Animals ; Autophagy ; Autophagy-Related Protein 5 ; Down-Regulation ; Extremities/blood supply ; Ischemic Preconditioning/methods ; Mice ; Mice, Inbred C57BL ; Microtubule-Associated Proteins/metabolism ; Myocardial Reperfusion Injury/metabolism ; Myocardial Reperfusion Injury/prevention & control ; Myocardium/metabolism ; Myocardium/pathology ; Signal Transduction ; TOR Serine-Threonine Kinases/genetics ; TOR Serine-Threonine Kinases/metabolism
    Chemical Substances Atg5 protein, mouse ; Autophagy-Related Protein 5 ; Microtubule-Associated Proteins ; TOR Serine-Threonine Kinases (EC 2.7.1.1) ; AMP-Activated Protein Kinases (EC 2.7.11.31)
    Language English
    Publishing date 2014-10-27
    Publishing country United States
    Document type Journal Article
    ISSN 1932-6203
    ISSN (online) 1932-6203
    DOI 10.1371/journal.pone.0111291
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: MicroRNA-144 is a circulating effector of remote ischemic preconditioning.

    Li, Jing / Rohailla, Sagar / Gelber, Nitai / Rutka, James / Sabah, Nesrin / Gladstone, Rachel A / Wei, Can / Hu, Pingzhao / Kharbanda, Rajesh K / Redington, Andrew N

    Basic research in cardiology

    2014  Volume 109, Issue 5, Page(s) 423

    Abstract: Remote ischemic preconditioning (rIPC) induced by cycles of transient limb ischemia and reperfusion is a powerful cardioprotective strategy with additional pleiotropic effects. However, our understanding of its underlying mediators and mechanisms remains ...

    Abstract Remote ischemic preconditioning (rIPC) induced by cycles of transient limb ischemia and reperfusion is a powerful cardioprotective strategy with additional pleiotropic effects. However, our understanding of its underlying mediators and mechanisms remains incomplete. We examined the role of miR-144 in the cardioprotection induced by rIPC. Microarray studies first established that rIPC increases, and IR injury decreases miR-144 levels in mouse myocardium, the latter being rescued by both rIPC and intravenous administration of miR-144. Going along with this systemic treatment with miR-144 increased P-Akt, P-GSK3β and P-p44/42 MAPK, decreased p-mTOR level and induced autophagy signaling, and induced early and delayed cardioprotection with improved functional recovery and reduction in infarct size similar to that achieved by rIPC. Conversely, systemic administration of a specific antisense oligonucleotide reduced myocardial levels of miR-144 and abrogated cardioprotection by rIPC. We then showed that rIPC increases plasma miR-144 levels in mice and humans, but there was no change in plasma microparticle (50-400 nM) numbers or their miR-144 content. However, there was an almost fourfold increase in miR-144 precursor in the exosome pellet, and a significant increase in miR-144 levels in exosome-poor serum which, in turn, was associated with increased levels of the miR carriage protein Argonaute-2. Systemic release of microRNA 144 plays a pivotal role in the cardioprotection induced by rIPC. Future studies should assess the potential for plasma miR-144 as a biomarker of the effectiveness of rIPC induced by limb ischemia, and whether miR-144 itself may represent a novel therapy to reduce clinical ischemia-reperfusion injury.
    MeSH term(s) Animals ; Blotting, Western ; Humans ; Immunoprecipitation ; Ischemic Preconditioning, Myocardial ; Mice ; Mice, Inbred C57BL ; MicroRNAs/blood ; Myocardial Reperfusion Injury/metabolism ; Myocardial Reperfusion Injury/prevention & control ; Oligonucleotide Array Sequence Analysis ; Reverse Transcriptase Polymerase Chain Reaction
    Chemical Substances MIRN144 microRNA, human ; MIRN144 microRNA, mouse ; MicroRNAs
    Language English
    Publishing date 2014
    Publishing country Germany
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 189755-x
    ISSN 1435-1803 ; 0300-8428 ; 0175-9418
    ISSN (online) 1435-1803
    ISSN 0300-8428 ; 0175-9418
    DOI 10.1007/s00395-014-0423-z
    Database MEDical Literature Analysis and Retrieval System OnLINE

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