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  1. TI=Microvascular disease in diabetes and severe COVID 19 outcomes
  2. TI=Despair in the time of COVID: A look at suicidal ingestions reported to the California Poison Control System during the pandemic

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  1. Article ; Online: Microvascular disease in diabetes and severe COVID-19 outcomes - Authors' reply.

    Colhoun, Helen M / McGurnaghan, Stuart J / McKeigue, Paul M

    The lancet. Diabetes & endocrinology

    2021  Volume 9, Issue 4, Page(s) 201

    MeSH term(s) COVID-19 ; Cohort Studies ; Diabetes Mellitus ; Humans ; Risk Factors ; SARS-CoV-2 ; Scotland
    Language English
    Publishing date 2021-03-19
    Publishing country England
    Document type Letter ; Comment
    ISSN 2213-8595
    ISSN (online) 2213-8595
    DOI 10.1016/S2213-8587(21)00055-3
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Microvascular disease in diabetes and severe COVID-19 outcomes.

    Corcillo, Antonella / Whyte, Martin B / Vas, Prashanth / Karalliedde, Janaka

    The lancet. Diabetes & endocrinology

    2021  Volume 9, Issue 4, Page(s) 200–201

    MeSH term(s) COVID-19 ; Cohort Studies ; Diabetes Mellitus ; Humans ; Risk Factors ; SARS-CoV-2 ; Scotland
    Language English
    Publishing date 2021-03-19
    Publishing country England
    Document type Letter ; Comment
    ISSN 2213-8595
    ISSN (online) 2213-8595
    DOI 10.1016/S2213-8587(21)00053-X
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: What is the impact of microvascular complications of diabetes on severe COVID-19?

    Basra, Ruman / Whyte, Martin / Karalliedde, Janaka / Vas, Prashanth

    Microvascular research

    2021  Volume 140, Page(s) 104310

    Abstract: ... retinopathy and nephropathy, in individuals with COVID-19 and diabetes. Future insights gained from exploring ... Evidence suggests severe coronavirus disease-19 (COVID-19) infection is characterised by pulmonary ... endothelial dysfunction and microvascular disease in diabetes will exacerbate the vascular insults associated ...

    Abstract Evidence suggests severe coronavirus disease-19 (COVID-19) infection is characterised by pulmonary and systemic microvasculature dysfunction, specifically, acute endothelial injury, hypercoagulation and increased capillary permeability. Diabetes, which is also characterised by vascular injury in itself, confers an increased risk of adverse COVID-19 outcomes. It has been suggested that pre-existing endothelial dysfunction and microvascular disease in diabetes will exacerbate the vascular insults associated with COVID-19 and thus lead to increased severity of COVID-19 infection. In this article, we evaluate the current evidence exploring the impact of microvascular complications, in the form of diabetic retinopathy and nephropathy, in individuals with COVID-19 and diabetes. Future insights gained from exploring the microvascular injury patterns and clinical outcomes may come to influence care delivery algorithms for either of these conditions.
    MeSH term(s) Albuminuria/etiology ; COVID-19/complications ; COVID-19/physiopathology ; Capillary Permeability ; Delivery of Health Care ; Diabetic Angiopathies/complications ; Diabetic Angiopathies/physiopathology ; Diabetic Nephropathies/complications ; Diabetic Nephropathies/physiopathology ; Diabetic Neuropathies/complications ; Diabetic Neuropathies/physiopathology ; Diabetic Retinopathy/complications ; Diabetic Retinopathy/physiopathology ; Endothelium, Vascular/injuries ; Endothelium, Vascular/pathology ; Humans ; Microcirculation ; Obesity/complications ; Obesity/physiopathology ; Pandemics ; Pulmonary Circulation ; Pulmonary Edema/etiology ; Pulmonary Edema/physiopathology ; SARS-CoV-2 ; Severity of Illness Index ; Thrombophilia/etiology ; Thrombophilia/physiopathology ; Treatment Outcome
    Language English
    Publishing date 2021-12-31
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 80307-8
    ISSN 1095-9319 ; 0026-2862
    ISSN (online) 1095-9319
    ISSN 0026-2862
    DOI 10.1016/j.mvr.2021.104310
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

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    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  4. Article ; Online: Endothelial glycocalyx damage as a systemic inflammatory microvascular endotheliopathy in COVID-19.

    Yamaoka-Tojo, Minako

    Biomedical journal

    2020  Volume 43, Issue 5, Page(s) 399–413

    Abstract: ... of COVID-19, binds to ACE2, which is abundantly present not only in human epithelia of the lung and ... the small intestine, but also in vascular endothelial cells and arterial smooth muscle cells. Moreover, COVID-19 ... of the vascular endothelial glycocalyx. In the current review, we propose new concepts and therapeutic goals for COVID-19 ...

    Abstract In atherosclerosis patients, vascular endothelial dysfunction is commonly observed alongside damage of the vascular endothelial glycocalyx, an extracellular matrix bound to and encapsulating the endothelial cells lining the blood vessel wall. Although atherosclerotic risk factors have been reported in severe patients with coronavirus disease 2019 (COVID-19), the exact mechanisms are unclear. The mortality associated with the COVID-19 outbreak is increased by comorbidities, including hypertension, diabetes, obesity, chronic obstructive pulmonary disease (COPD), and cardiovascular disease. Besides, older individuals and smokers have significantly worse outcomes. Interestingly, these comorbidities and risk factors are consistent with the pathophysiology that causes vascular endothelial glycocalyx damage. Moreover, vascular glycocalyx dysfunction causes microvascular leakage, which results in interstitial pulmonary abnormal shadows (multiple patchy shadows with a ground glass inter-pneumonic appearance). This is frequently followed by severe acute respiratory distress syndrome (ARDS), closely related to coagulo-fibrinolytic changes contributing to disseminated intravascular coagulation (DIC) and Kawasaki disease shock syndrome, as well as inducing activation of the coagulation cascade, leading to thromboembolism and multiple organ failure. Notably, SARS-CoV-2, the causative virus of COVID-19, binds to ACE2, which is abundantly present not only in human epithelia of the lung and the small intestine, but also in vascular endothelial cells and arterial smooth muscle cells. Moreover, COVID-19 can induce severe septic shock, and sepsis can easily lead to systemic degradation of the vascular endothelial glycocalyx. In the current review, we propose new concepts and therapeutic goals for COVID-19-related vascular endothelial glycocalyx damage, based on previous vascular endothelial medicine research.
    MeSH term(s) COVID-19/virology ; Endothelial Cells/metabolism ; Glycocalyx/virology ; Humans ; Lung/virology ; Respiratory Distress Syndrome/complications ; Respiratory Distress Syndrome/virology ; SARS-CoV-2/pathogenicity
    Keywords covid19
    Language English
    Publishing date 2020-08-24
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't ; Review
    ZDB-ID 2698541-X
    ISSN 2320-2890 ; 2320-2890
    ISSN (online) 2320-2890
    ISSN 2320-2890
    DOI 10.1016/j.bj.2020.08.007
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  5. Article ; Online: Endothelial glycocalyx damage as a systemic inflammatory microvascular endotheliopathy in COVID-19

    Minako Yamaoka-Tojo

    Biomedical Journal, Vol 43, Iss 5, Pp 399-

    2020  Volume 413

    Abstract: ... of COVID-19, binds to ACE2, which is abundantly present not only in human epithelia of the lung and ... the small intestine, but also in vascular endothelial cells and arterial smooth muscle cells. Moreover, COVID-19 ... of the vascular endothelial glycocalyx. In the current review, we propose new concepts and therapeutic goals for COVID-19 ...

    Abstract In atherosclerosis patients, vascular endothelial dysfunction is commonly observed alongside damage of the vascular endothelial glycocalyx, an extracellular matrix bound to and encapsulating the endothelial cells lining the blood vessel wall. Although atherosclerotic risk factors have been reported in severe patients with coronavirus disease 2019 (COVID-19), the exact mechanisms are unclear. The mortality associated with the COVID-19 outbreak is increased by comorbidities, including hypertension, diabetes, obesity, chronic obstructive pulmonary disease (COPD), and cardiovascular disease. Besides, older individuals and smokers have significantly worse outcomes. Interestingly, these comorbidities and risk factors are consistent with the pathophysiology that causes vascular endothelial glycocalyx damage. Moreover, vascular glycocalyx dysfunction causes microvascular leakage, which results in interstitial pulmonary abnormal shadows (multiple patchy shadows with a ground glass inter-pneumonic appearance). This is frequently followed by severe acute respiratory distress syndrome (ARDS), closely related to coagulo-fibrinolytic changes contributing to disseminated intravascular coagulation (DIC) and Kawasaki disease shock syndrome, as well as inducing activation of the coagulation cascade, leading to thromboembolism and multiple organ failure. Notably, SARS-CoV-2, the causative virus of COVID-19, binds to ACE2, which is abundantly present not only in human epithelia of the lung and the small intestine, but also in vascular endothelial cells and arterial smooth muscle cells. Moreover, COVID-19 can induce severe septic shock, and sepsis can easily lead to systemic degradation of the vascular endothelial glycocalyx. In the current review, we propose new concepts and therapeutic goals for COVID-19-related vascular endothelial glycocalyx damage, based on previous vascular endothelial medicine research.
    Keywords Vascular endothelial dysfunction ; Systemic inflammatory response ; Cytokine storm ; ARDS ; Kawasaki disease shock syndrome ; Medicine (General) ; R5-920 ; Biology (General) ; QH301-705.5
    Subject code 610
    Language English
    Publishing date 2020-10-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  6. Article: Endothelial glycocalyx damage as a systemic inflammatory microvascular endotheliopathy in COVID-19

    Yamaoka-Tojo, Minako

    Biomed. j. (Mumbai.Online)

    Abstract: ... of COVID-19, binds to ACE2, which is abundantly present not only in human epithelia of the lung and ... the small intestine, but also in vascular endothelial cells and arterial smooth muscle cells. Moreover, COVID-19 ... of the vascular endothelial glycocalyx. In the current review, we propose new concepts and therapeutic goals for COVID-19 ...

    Abstract In atherosclerosis patients, vascular endothelial dysfunction is commonly observed alongside damage of the vascular endothelial glycocalyx, an extracellular matrix bound to and encapsulating the endothelial cells lining the blood vessel wall. Although atherosclerotic risk factors have been reported in severe patients with coronavirus disease 2019 (COVID-19), the exact mechanisms are unclear. The mortality associated with the COVID-19 outbreak is increased by comorbidities, including hypertension, diabetes, obesity, chronic obstructive pulmonary disease (COPD), and cardiovascular disease. Besides, older individuals and smokers have significantly worse outcomes. Interestingly, these comorbidities and risk factors are consistent with the pathophysiology that causes vascular endothelial glycocalyx damage. Moreover, vascular glycocalyx dysfunction causes microvascular leakage, which results in interstitial pulmonary abnormal shadows (multiple patchy shadows with a ground glass inter-pneumonic appearance). This is frequently followed by severe acute respiratory distress syndrome (ARDS), closely related to coagulo-fibrinolytic changes contributing to disseminated intravascular coagulation (DIC) and Kawasaki disease shock syndrome, as well as inducing activation of the coagulation cascade, leading to thromboembolism and multiple organ failure. Notably, SARS-CoV-2, the causative virus of COVID-19, binds to ACE2, which is abundantly present not only in human epithelia of the lung and the small intestine, but also in vascular endothelial cells and arterial smooth muscle cells. Moreover, COVID-19 can induce severe septic shock, and sepsis can easily lead to systemic degradation of the vascular endothelial glycocalyx. In the current review, we propose new concepts and therapeutic goals for COVID-19-related vascular endothelial glycocalyx damage, based on previous vascular endothelial medicine research.
    Keywords covid19
    Publisher WHO
    Document type Article
    Note WHO #Covidence: #726411
    Database COVID19

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