Results 51 to 60 of about 1,336,017 (348)

AG490 protects cerebral ischemia/reperfusion injury via inhibiting the JAK2/3 signaling pathway

open access: yesBrain and Behavior, 2021
Background Cerebral ischemia/reperfusion injury is a severe problem in patients with brain ischemia. Brain injury caused by the immune response is important in the pathogenesis of cerebral ischemia/reperfusion injury and immune pathways.
Lichao Fan, Lichun Zhou
doaj   +1 more source

Protective effect of platinum nano-antioxidant and nitric oxide against hepatic ischemia-reperfusion injury

open access: yesNature Communications, 2021
Therapeutic interventions of hepatic ischemia-reperfusion injury to attenuate liver dysfunction or multiple organ failure following liver surgery and transplantation remain limited.
Jing Mu   +11 more
semanticscholar   +1 more source

Application of a novel method for subsequent evaluation of sinusoids and postsinusoidal venules after ischemia-reperfusion injury of rat liver [PDF]

open access: yes, 1998
Although several intravital fluorescence microscopic studies demonstrated that microcirculatory derangement is induced during liver ischemia-reperfusion, these data were obtained from randomly selected microvascular areas and microvessels, Repeated ...
Todoroki, T.   +5 more
core   +1 more source

The roles of microRNAs in spinal cord ischemia-reperfusion injury

open access: yesNeural Regeneration Research, 2022
Spinal cord ischemia/reperfusion injury is a devastating medical disorder with poor prognosis that is associated with several pathophysiological conditions. However, multiple stimuli can trigger SCII, so the underlying mechanism of this pathology has not
Feng-Shou Chen   +5 more
doaj   +1 more source

The role of prostaglandin and antioxidant availability in recovery from forearm ischemia-reperfusion injury in humans [PDF]

open access: yes, 2014
This article is made available through the Brunel Open Access Publishing Fund. It is shared under the Creative Commons License Attribution-Noncommercial No Derivative 3.0 (CCBY NCND).
Carter, SE   +10 more
core   +1 more source

Macrophage Polarization and Liver Ischemia-Reperfusion Injury

open access: yesInternational Journal of Medical Sciences, 2021
Ischemia-reperfusion injury refers to organ damage caused by the previous insufficient supply of oxygen and nutrients and the involvement of metabolic by-products after blood flow is restored.
Hai Wang   +5 more
semanticscholar   +1 more source

The uncoordinated-5 homolog B receptor affects hepatic ischemia reperfusion injury [PDF]

open access: yes, 2012
Recent evidence has demonstrated additional roles for the neuronal guidance protein receptor UNC5B outside the nervous system. Given the fact that ischemia reperfusion injury (IRI) of the liver is a common source of liver dysfunction and the role of ...
Tiago Granja (147967)   +33 more
core   +2 more sources

Targeting Oxidative Stress and Inflammation to Prevent Ischemia-Reperfusion Injury

open access: yesFrontiers in Molecular Neuroscience, 2020
The cerebral ischemia injury can result in neuronal death and/or functional impairment, which leads to further damage and dysfunction after recovery of blood supply.
Li-Quan Wu   +6 more
semanticscholar   +1 more source

ACE-inhibition prevents postischemic coronary leukocyte adhesion and leukocyte-dependent reperfusion injury [PDF]

open access: yes, 1997
Objective: Polymorphonuclear leukocytes (PMN), retained in the microvascular bed, can contribute to postischemic myocardial reperfusion injury. Since a beneficial effect of ACE-inhibition on reperfusion injury has been reported, we investigated the ...
Weber, Christian   +7 more
core   +1 more source

Tumor Necrosis Factor-α Contributes to Ischemia- and Reperfusion-Induced Endothelial Activation in Isolated Hearts [PDF]

open access: yes, 1999
During myocardial reperfusion, polymorphonuclear neutrophil (PMN) adhesion involving the intercellular adhesion molecule-1 (ICAM-1) may lead to aggravation and prolongation of reperfusion injury.
Kelly, Ralph A.   +15 more
core   +1 more source

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