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  1. Article: In Memoriam: Aubrey E. Taylor (1933-2015).

    Granger, D Neil / Townsley, Mary I

    The Physiologist

    2016  Volume 59, Issue 2, Page(s) 117–118

    MeSH term(s) History, 20th Century ; History, 21st Century ; Physiology/history
    Language English
    Publishing date 2016-03
    Publishing country United States
    Document type Biography ; Historical Article ; Journal Article
    ZDB-ID 208883-6
    ISSN 1522-1202 ; 0031-9376
    ISSN (online) 1522-1202
    ISSN 0031-9376
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    Zs.B 380: Show issues Location:
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  2. Article: Reperfusion therapy-What's with the obstructed, leaky and broken capillaries?

    Granger, D Neil / Kvietys, Peter R

    Pathophysiology : the official journal of the International Society for Pathophysiology

    2017  Volume 24, Issue 4, Page(s) 213–228

    Abstract: Microvascular dysfunction is well established as an early and rate-determining factor in the injury response of tissues to ischemia and reperfusion (I/R). Severe endothelial cell dysfunction, which can develop without obvious morphological cell injury, ... ...

    Abstract Microvascular dysfunction is well established as an early and rate-determining factor in the injury response of tissues to ischemia and reperfusion (I/R). Severe endothelial cell dysfunction, which can develop without obvious morphological cell injury, is a major underlying cause of the microvascular abnormalities that accompany I/R. While I/R-induced microvascular dysfunction is manifested in different ways, two responses that have received much attention in both the experimental and clinical setting are impaired capillary perfusion (no-reflow) and endothelial barrier failure with a transition to hemorrhage. These responses are emerging as potentially important determinants of the severity of the tissue injury response, and there is growing clinical evidence that they are predictive of clinical outcome following reperfusion therapy. This review provides a summary of animal studies that have focused on the mechanisms that may underlie the genesis of no-reflow and hemorrhage following reperfusion of ischemic tissues, and addresses the clinical evidence that implicates these vascular events in the responses of the ischemic brain (stroke) and heart (myocardial infarction) to reperfusion therapy. Inasmuch as reactive oxygen species (ROS) and matrix metalloproteinases (MMP) are frequently invoked as triggers of the microvascular dysfunction elicited by I/R, the potential roles and sources of these mediators are also discussed. The available evidence in the literature justifies the increased interest in the development of no-reflow and hemorrhage in heart and brain following reperfusion therapy, and suggests that these vascular events may be predictive of poor clinical outcome and warrant the development of targeted treatment strategies.
    Language English
    Publishing date 2017-09-21
    Publishing country Netherlands
    Document type Journal Article ; Review
    ZDB-ID 1212740-1
    ISSN 0928-4680
    ISSN 0928-4680
    DOI 10.1016/j.pathophys.2017.09.003
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    Zs.A 4137: Show issues Location:
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  3. Article: Blood cells and endothelial barrier function.

    Rodrigues, Stephen F / Granger, D Neil

    Tissue barriers

    2015  Volume 3, Issue 1-2, Page(s) e978720

    Abstract: The barrier properties of endothelial cells are critical for the maintenance of water and protein balance between the intravascular and extravascular compartments. An impairment of endothelial barrier function has been implicated in the genesis and/or ... ...

    Abstract The barrier properties of endothelial cells are critical for the maintenance of water and protein balance between the intravascular and extravascular compartments. An impairment of endothelial barrier function has been implicated in the genesis and/or progression of a variety of pathological conditions, including pulmonary edema, ischemic stroke, neurodegenerative disorders, angioedema, sepsis and cancer. The altered barrier function in these conditions is often linked to the release of soluble mediators from resident cells (e.g., mast cells, macrophages) and/or recruited blood cells. The interaction of the mediators with receptors expressed on the surface of endothelial cells diminishes barrier function either by altering the expression of adhesive proteins in the inter-endothelial junctions, by altering the organization of the cytoskeleton, or both. Reactive oxygen species (ROS), proteolytic enzymes (e.g., matrix metalloproteinase, elastase), oncostatin M, and VEGF are part of a long list of mediators that have been implicated in endothelial barrier failure. In this review, we address the role of blood borne cells, including, neutrophils, lymphocytes, monocytes, and platelets, in the regulation of endothelial barrier function in health and disease. Attention is also devoted to new targets for therapeutic intervention in disease states with morbidity and mortality related to endothelial barrier dysfunction.
    Language English
    Publishing date 2015
    Publishing country United States
    Document type Journal Article
    ISSN 2168-8362
    ISSN 2168-8362
    DOI 10.4161/21688370.2014.978720
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Reperfusion injury and reactive oxygen species: The evolution of a concept.

    Granger, D Neil / Kvietys, Peter R

    Redox biology

    2015  Volume 6, Page(s) 524–551

    Abstract: Reperfusion injury, the paradoxical tissue response that is manifested by blood flow-deprived and oxygen-starved organs following the restoration of blood flow and tissue oxygenation, has been a focus of basic and clinical research for over 4-decades. ... ...

    Abstract Reperfusion injury, the paradoxical tissue response that is manifested by blood flow-deprived and oxygen-starved organs following the restoration of blood flow and tissue oxygenation, has been a focus of basic and clinical research for over 4-decades. While a variety of molecular mechanisms have been proposed to explain this phenomenon, excess production of reactive oxygen species (ROS) continues to receive much attention as a critical factor in the genesis of reperfusion injury. As a consequence, considerable effort has been devoted to identifying the dominant cellular and enzymatic sources of excess ROS production following ischemia-reperfusion (I/R). Of the potential ROS sources described to date, xanthine oxidase, NADPH oxidase (Nox), mitochondria, and uncoupled nitric oxide synthase have gained a status as the most likely contributors to reperfusion-induced oxidative stress and represent priority targets for therapeutic intervention against reperfusion-induced organ dysfunction and tissue damage. Although all four enzymatic sources are present in most tissues and are likely to play some role in reperfusion injury, priority and emphasis has been given to specific ROS sources that are enriched in certain tissues, such as xanthine oxidase in the gastrointestinal tract and mitochondria in the metabolically active heart and brain. The possibility that multiple ROS sources contribute to reperfusion injury in most tissues is supported by evidence demonstrating that redox-signaling enables ROS produced by one enzymatic source (e.g., Nox) to activate and enhance ROS production by a second source (e.g., mitochondria). This review provides a synopsis of the evidence implicating ROS in reperfusion injury, the clinical implications of this phenomenon, and summarizes current understanding of the four most frequently invoked enzymatic sources of ROS production in post-ischemic tissue.
    MeSH term(s) Animals ; Cell Hypoxia ; Humans ; Oxidation-Reduction ; Oxidative Stress ; Reactive Oxygen Species/metabolism ; Reperfusion Injury/metabolism
    Chemical Substances Reactive Oxygen Species
    Language English
    Publishing date 2015-10-08
    Publishing country Netherlands
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ISSN 2213-2317
    ISSN (online) 2213-2317
    DOI 10.1016/j.redox.2015.08.020
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  5. Article ; Online: Novel Role of T Cells and IL-6 (Interleukin-6) in Angiotensin II-Induced Microvascular Dysfunction.

    Senchenkova, Elena Y / Russell, Janice / Yildirim, Alper / Granger, D Neil / Gavins, Felicity N E

    Hypertension (Dallas, Tex. : 1979)

    2019  Volume 73, Issue 4, Page(s) 829–838

    Abstract: Hypertension is an established risk factor for subsequent cardiovascular diseases, with Ang II (angiotensin II) playing a major role in mediating thrombotic and inflammatory abnormalities. Although T cells and IL-6 (interleukin-6) play an important role ... ...

    Abstract Hypertension is an established risk factor for subsequent cardiovascular diseases, with Ang II (angiotensin II) playing a major role in mediating thrombotic and inflammatory abnormalities. Although T cells and IL-6 (interleukin-6) play an important role in adaptive immune responses, little is known about their role(s) in the thromboinflammatory responses associated with Ang II. Here we show using intravital microscopy coupled with the light/dye injury model that Rag-1 deficient (Rag-1
    MeSH term(s) Adaptive Immunity ; Angiotensin II/toxicity ; Animals ; Blood Pressure/physiology ; Disease Models, Animal ; Flow Cytometry ; Hypertension/complications ; Hypertension/immunology ; Hypertension/metabolism ; Hypertension/physiopathology ; Interleukin-6/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Microcirculation/drug effects ; Signal Transduction ; T-Lymphocytes/immunology ; Thrombosis/chemically induced ; Thrombosis/immunology ; Thrombosis/metabolism
    Chemical Substances Interleukin-6 ; Angiotensin II (11128-99-7)
    Language English
    Publishing date 2019-03-11
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 423736-5
    ISSN 1524-4563 ; 0194-911X ; 0362-4323
    ISSN (online) 1524-4563
    ISSN 0194-911X ; 0362-4323
    DOI 10.1161/HYPERTENSIONAHA.118.12286
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    Zs.A 1488: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
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    Jg. 1995 - 2021: Lesesall (1.OG)
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  6. Article ; Online: Hypercholesterolemia blunts the oxidative stress elicited by hypertension in venules through angiotensin II type-2 receptors.

    Yildirim, Alper / Senchenkova, Elena / Granger, D Neil

    Microvascular research

    2016  Volume 105, Page(s) 54–60

    Abstract: Objective: Hypertension and hypercholesterolemia elicit inflammatory and thrombogenic responses in the microvasculature. However, little is known about whether and how risk factor combinations alter microvascular function. We examined how the actions of ...

    Abstract Objective: Hypertension and hypercholesterolemia elicit inflammatory and thrombogenic responses in the microvasculature. However, little is known about whether and how risk factor combinations alter microvascular function. We examined how the actions of HTN+HCh on the microvasculature differ from the responses elicited by either risk factor alone.
    Methods: Intravital microscopy was used to monitor the adhesion and emigration of leukocytes and dihydrorhodamine oxidation in cremaster muscle venules of wild type mice that were infused with angiotensin II for 2 weeks (HTN), placed on a high cholesterol diet (HCD), or both.
    Results: Either HTN or HCh alone enhanced the production of reactive oxygen species and promoted the recruitment of leukocytes in venules. However, the combination of HTN and HCh produced changes in ROS production and leukocyte recruitment that were greatly attenuated compared to HTN alone. The inhibitory effects of HCh on the AngII mediated responses were also observed in genetically-induced HCh (ApoE-deficient mice). Treating HCh+HTN mice with an antagonist to AT2r reversed the HCh-dependent protection against oxidative stress and inflammation during HTN.
    Conclusions: These findings indicate that HCh blunts the oxidative stress and inflammatory cell recruitment elicited by hypertension in venules through a mechanism that involves AT2 receptor activation.
    MeSH term(s) Angiotensin II ; Angiotensin II Type 2 Receptor Blockers/pharmacology ; Animals ; Apolipoproteins E/deficiency ; Apolipoproteins E/genetics ; Cell Adhesion ; Chemotaxis, Leukocyte ; Cholesterol, Dietary ; Disease Models, Animal ; Hypercholesterolemia/etiology ; Hypercholesterolemia/genetics ; Hypercholesterolemia/metabolism ; Hypercholesterolemia/physiopathology ; Hypertension/chemically induced ; Hypertension/metabolism ; Hypertension/physiopathology ; Leukocytes/metabolism ; Male ; Mice, Inbred C57BL ; Mice, Knockout ; Oxidative Stress ; Receptor, Angiotensin, Type 2/drug effects ; Receptor, Angiotensin, Type 2/metabolism ; Signal Transduction/drug effects ; Venules/drug effects ; Venules/metabolism ; Venules/physiopathology
    Chemical Substances Angiotensin II Type 2 Receptor Blockers ; Apolipoproteins E ; Cholesterol, Dietary ; Receptor, Angiotensin, Type 2 ; Angiotensin II (11128-99-7)
    Language English
    Publishing date 2016-05
    Publishing country United States
    Document type Comparative Study ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 80307-8
    ISSN 1095-9319 ; 0026-2862
    ISSN (online) 1095-9319
    ISSN 0026-2862
    DOI 10.1016/j.mvr.2016.01.002
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    Zs.A 746: Show issues Location:
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  7. Article ; Online: The Gastrointestinal Circulation: Physiology and Pathophysiology.

    Granger, D Neil / Holm, Lena / Kvietys, Peter

    Comprehensive Physiology

    2015  Volume 5, Issue 3, Page(s) 1541–1583

    Abstract: The gastrointestinal (GI) circulation receives a large fraction of cardiac output and this increases following ingestion of a meal. While blood flow regulation is not the intense phenomenon noted in other vascular beds, the combined responses of blood ... ...

    Abstract The gastrointestinal (GI) circulation receives a large fraction of cardiac output and this increases following ingestion of a meal. While blood flow regulation is not the intense phenomenon noted in other vascular beds, the combined responses of blood flow, and capillary oxygen exchange help ensure a level of tissue oxygenation that is commensurate with organ metabolism and function. This is evidenced in the vascular responses of the stomach to increased acid production and in intestine during periods of enhanced nutrient absorption. Complimenting the metabolic vasoregulation is a strong myogenic response that contributes to basal vascular tone and to the responses elicited by changes in intravascular pressure. The GI circulation also contributes to a mucosal defense mechanism that protects against excessive damage to the epithelial lining following ingestion of toxins and/or noxious agents. Profound reductions in GI blood flow are evidenced in certain physiological (strenuous exercise) and pathological (hemorrhage) conditions, while some disease states (e.g., chronic portal hypertension) are associated with a hyperdynamic circulation. The sacrificial nature of GI blood flow is essential for ensuring adequate perfusion of vital organs during periods of whole body stress. The restoration of blood flow (reperfusion) to GI organs following ischemia elicits an exaggerated tissue injury response that reflects the potential of this organ system to generate reactive oxygen species and to mount an inflammatory response. Human and animal studies of inflammatory bowel disease have also revealed a contribution of the vasculature to the initiation and perpetuation of the tissue inflammation and associated injury response.
    MeSH term(s) Animals ; Autonomic Nervous System/metabolism ; Autonomic Nervous System/physiology ; Gastrointestinal Tract/blood supply ; Gastrointestinal Tract/physiology ; Gastrointestinal Tract/physiopathology ; Humans ; Hyperemia/etiology ; Microvessels/metabolism ; Microvessels/physiology ; Oxygen Consumption ; Vasoconstriction
    Language English
    Publishing date 2015-07-01
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
    ISSN 2040-4603
    ISSN (online) 2040-4603
    DOI 10.1002/cphy.c150007
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  8. Article ; Online: Hypercoagulability and Platelet Abnormalities in Inflammatory Bowel Disease.

    Senchenkova, Elena / Seifert, Hilary / Granger, D Neil

    Seminars in thrombosis and hemostasis

    2015  Volume 41, Issue 6, Page(s) 582–589

    Abstract: Patients with inflammatory bowel disease (IBD) exhibit a threefold higher risk for development of systemic thrombosis than the general population. Although the underlying causes of the increased risk for thrombus development remain poorly understood, ... ...

    Abstract Patients with inflammatory bowel disease (IBD) exhibit a threefold higher risk for development of systemic thrombosis than the general population. Although the underlying causes of the increased risk for thrombus development remain poorly understood, there is a large body of evidence suggesting that abnormalities in coagulation, fibrinolysis, and platelet function may contribute to this response. Changes in hemostatic biomarkers are consistent with subclinical activation of coagulation system, including tissue factor activation, impaired protein C pathway, enhanced thrombin generation, and diminished fibrinolytic capacity. There is also evidence for an increased production and reactivity of platelets, with an enhanced formation of platelet-platelet and platelet-leukocyte aggregates. The altered coagulation and platelet function, and the predisposition to thrombus formation have also been demonstrated in animal models of IBD. The animal studies have revealed a major role for inflammatory cytokines, including tumor necrosis factor-α, interleukin (IL)-1β, and IL-6, as mediators of the platelet abnormalities and enhanced thrombus development in experimental IBD. These findings in animal models raise hope for the development of novel therapeutic strategies to reduce thrombosis-related mortality in IBD patients.
    MeSH term(s) Animals ; Blood Coagulation Factors/metabolism ; Blood Platelets/pathology ; Colitis/blood ; Colon/blood supply ; Cytokines/physiology ; Disease Models, Animal ; Fibrinolysis ; Humans ; Inflammatory Bowel Diseases/blood ; Inflammatory Bowel Diseases/complications ; Inflammatory Bowel Diseases/drug therapy ; Leukocytes/pathology ; Microcirculation ; Models, Biological ; Nitric Oxide/metabolism ; Platelet Activation ; Risk ; Thrombophilia/blood ; Thrombophilia/etiology ; Thrombophilia/prevention & control ; Thrombosis/epidemiology ; Thrombosis/etiology
    Chemical Substances Blood Coagulation Factors ; Cytokines ; Nitric Oxide (31C4KY9ESH)
    Language English
    Publishing date 2015-09
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 196901-8
    ISSN 1098-9064 ; 0094-6176
    ISSN (online) 1098-9064
    ISSN 0094-6176
    DOI 10.1055/s-0035-1556590
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    Zs.A 1259: Show issues Location:
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  9. Article ; Online: Platelets: a critical link between inflammation and microvascular dysfunction.

    Stokes, Karen Y / Granger, D Neil

    The Journal of physiology

    2011  Volume 590, Issue 5, Page(s) 1023–1034

    Abstract: Inflammation is an underlying feature of a variety of human diseases. An important manifestation of this pathophysiological response is microvascular dysfunction, which includes the activation of vascular endothelial cells, and circulating leucocytes and ...

    Abstract Inflammation is an underlying feature of a variety of human diseases. An important manifestation of this pathophysiological response is microvascular dysfunction, which includes the activation of vascular endothelial cells, and circulating leucocytes and platelets. While endothelial cells and leucocytes are widely accepted as critical players in the microvascular alterations induced by inflammation, recent attention has focused on the modulatory role of platelets, which act both as effector and target cells in inflamed microvessels. Evidence is presented to demonstrate the capacity for 'cross-talk' between platelets and other cells (endothelial cells, leucocytes) that contribute to an inflammatory response, and to illustrate the pathophysiological consequences of these interactions of platelets with other cells within the microvasculature.
    MeSH term(s) Animals ; Blood Platelets/physiology ; Endothelial Cells/physiology ; Endothelium, Vascular/physiopathology ; Humans ; Inflammation/physiopathology ; Leukocytes/physiology ; Microvessels/physiopathology
    Language English
    Publishing date 2011-12-19
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Review
    ZDB-ID 3115-x
    ISSN 1469-7793 ; 0022-3751
    ISSN (online) 1469-7793
    ISSN 0022-3751
    DOI 10.1113/jphysiol.2011.225417
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  10. Article ; Online: Blood and MRI biomarkers of mild traumatic brain injury in non-concussed collegiate football players.

    Cho, Eunhan / Granger, Joshua / Theall, Bailey / Lemoine, Nathan / Calvert, Derek / Marucci, Jack / Mullenix, Shelly / O'Neal, Hollis / Jacome, Tomas / Irving, Brian A / Johannsen, Neil M / Carmichael, Owen / Spielmann, Guillaume

    Scientific reports

    2024  Volume 14, Issue 1, Page(s) 665

    Abstract: Football has one of the highest incidence rates of mild traumatic brain injury (mTBI) among contact sports; however, the effects of repeated sub-concussive head impacts on brain structure and function remain under-studied. We assessed the association ... ...

    Abstract Football has one of the highest incidence rates of mild traumatic brain injury (mTBI) among contact sports; however, the effects of repeated sub-concussive head impacts on brain structure and function remain under-studied. We assessed the association between biomarkers of mTBI and structural and functional MRI scans over an entire season among non-concussed NCAA Division I linemen and non-linemen. Concentrations of S100B, GFAP, BDNF, NFL, and NSE were assessed in 48 collegiate football players (32 linemen; 16 non-linemen) before the start of pre-season training (pre-camp), at the end of pre-season training (pre-season), and at the end of the competitive season (post-season). Changes in brain structure and function were assessed in a sub-sample of 11 linemen and 6 non-linemen using structural and functional MRI during the execution of Stroop and attention network tasks. S100B, GFAP and BDNF concentrations were increased at post-season compared to pre-camp in linemen. White matter hyperintensities increased in linemen during pre-season camp training compared to pre-camp. This study showed that the effects of repeated head impacts are detectable in the blood of elite level non-concussed collegiate football players exposed to low-moderate impacts to the heads, which correlated with some neurological outcomes without translating to clinically-relevant changes in brain anatomy or function.
    MeSH term(s) Humans ; Football ; Brain Concussion/diagnostic imaging ; Brain-Derived Neurotrophic Factor ; Biomarkers ; Magnetic Resonance Imaging
    Chemical Substances Brain-Derived Neurotrophic Factor ; Biomarkers
    Language English
    Publishing date 2024-01-05
    Publishing country England
    Document type Journal Article
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-023-51067-3
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