• They are divided into techniques including reperfusion of the ischemic tissue (transient focal cerebral ischemia) and those without reperfusion (permanent focal cerebral ischemia). (wikipedia.org)
  • Transient middle cerebral artery occlusion was induced for 1 hour followed by 12-hour to 7-day reperfusion in C57/BL6 mice. (scienceopen.com)
  • Adeno-associated viral (AAV)-NRP-1 was stereotaxically inoculated into the cortex and ipsilateral striatum posterior of adult male Sprague-Dawley (SD) rats before a 90-min transient middle cerebral artery occlusion (tMCAO) and subsequent reperfusion. (biomedcentral.com)
  • The effect of moderate whole body hypothermia (300 C) on transient focal cerebral ischemia induced inflammatory injury was investigated. (banglajol.info)
  • Experimental stroke (transient focal cerebral ischemia) was induced by a 2-hour middle cerebral artery occlusion (MCAO) with the use of a suture inserting into the lumen of the internal carotid artery (ICA) in male Wistar rats. (banglajol.info)
  • Our results indicate that moderate hypothermia has a significant protective effect on the inflammatory injury induced by transient focal cerebral ischemia. (banglajol.info)
  • Pre-stroke surgery is not beneficial to normotensive rats undergoing sixty minutes of transient focal cerebral ischemia PLOS ONE. (nottingham.ac.uk)
  • Ischemic tolerance defines transient resistance to lethal ischemia gained by a prior sublethal noxious stimulus (i.e., preconditioning). (biomedcentral.com)
  • Transient global cerebral ischemia, such as that which occurs during cardiac arrest and resuscitation, is a major cause of serious neurologic morbidity. (silverchair.com)
  • Animals underwent either permanent MCAO or transient MCAO with 80-min reperfusion. (omicsdi.org)
  • Here we further assess this refined surgical approach on reperfusion characteristics following transient MCAO in mice. (omicsdi.org)
  • Furthermore, we demonstrated that PT enhanced brain inflammation and aggravated stroke severity in middle cerebral artery occlusion mouse model. (bmj.com)
  • Primary cortical neurons were subjected to glucose deprivation (GD), oxygen-glucose deprivation (OGD) or simulated ischemia-reperfusion (I/R). Ischemic stroke was induced in C57BL/6J mice by middle cerebral artery occlusion, followed by reperfusion. (scienceopen.com)
  • In adult male Sprague-Dawley rats, the focal cerebral ischemic injury was induced by middle cerebral artery occlusion (MCAO) models for 1.5 h. (biomedcentral.com)
  • Middle Cerebral Artery Occlusion Allowing Reperfusion via Common Carotid Artery Repair in Mice JOVE-JOURNAL OF VISUALIZED EXPERIMENTS. (nottingham.ac.uk)
  • Ischemia-reperfusion injured rat model was induced by middle cerebral artery occlusion and reperfusion (MCAO/R). EA treatment at the DU 20 and DU 24 acupoints treatment were conducted to rats from the 12 h after MCAO/R injury for consecutive 7 days. (biomedcentral.com)
  • We previously reported that a surgical refinement in the middle cerebral artery occlusion (MCAO) model of stroke, via repair of the common carotid artery (CCA), removes the reliance on the Circle of Willis for reperfusion and reduced infarct variability. (omicsdi.org)
  • However, they are less immediately relevant to human stroke than the focal stroke models, because global ischemia is not a common feature of human stroke. (wikipedia.org)
  • Male C57Bl/6 mice were subjected to focal cerebral ischemia and periods of reperfusion (0, 8 and 24 h). (biomedcentral.com)
  • Microglia were both hyper- and de-ramified in striatal and cortical brain regions (respectively) after 60 min of focal cerebral ischemia. (biomedcentral.com)
  • The clinical presentation of cerebral reperfusion syndrome varies but generally includes components of the following triad: 1) ipsilateral headache, 2) contralateral focal neurologic deficits, and/or 3) seizures. (medscape.com)
  • Cerebral reperfusion syndrome presents with ipsilateral headache, contralateral focal neurologic deficits, and/or seizures, but a complete triad is not required for diagnosis. (medscape.com)
  • Focal neurologic deficits are usually due to cortical injury or irritation and depend on the vascular territory involved. (medscape.com)
  • Our previous studies have reported that EA could relieve neurological disorders, reduce infarct volumes after focal cerebral ischemia (Wang et al. (biomedcentral.com)
  • Re: 'Protective Effect of Focal Adhesion Kinase against Skeletal Muscle Reperfusion Injury after Acute Limb Ischemia': Exciting Questions about Ischemia Reperfusion Injury. (safasatoglu.com)
  • The fate of the brain tissue after focal cerebral ischemia is determined by the degree and duration of ischemia, and even without preconditioning, resident brain cells naturally respond to brain ischemia by mobilizing a host of defences and counter responses to mitigate cell injury and death [ 5 ]. (biomedcentral.com)
  • When injecting spheres into the cerebral circulation, their size determines the pattern of brain infarction: Macrospheres (300-400 µm) induce infarcts similar to those achieved by occlusion of the proximal MCA [5], whereas microsphere (~ 50 µm) injection results in distal, diffuse embolism [6]. (wikipedia.org)
  • This study aimed to investigate whether resuscitation after a hemorrhagic shock (HS) and/or mild cerebral ischemia caused by a unilateral common carotid artery occlusion (UCCAO) can cause brain injury and concomitant neurological dysfunction, and explore the potential mechanisms. (medsci.org)
  • Both the occlusion of a blood vessel supplying the brain and the rupture of a cerebral vessel occur suddenly and mostly unexpectedly. (symptoma.mt)
  • Comment on the article "Symptomatic carotid near-occlusion causes a high risk of recurrent ipsilateral ischemic stroke" by Gu et al. (renevas.es)
  • However, the increasing clinical evidences supported that reperfusion even within 6-24?h may salvage ischemic tissue and improve neurological outcomes in selected large vessel occlusion patients, without inducing serious ischemia/reperfusion injury and hemorrhagic transformation. (omicsdi.org)
  • Animal models of ischemic stroke are procedures inducing cerebral ischemia. (wikipedia.org)
  • Exogenous endothelin-1 can also be used to induce stroke and cell death after sustained vasoconstriction with reperfusion. (wikipedia.org)
  • Although ideally positioned for immediate response to ischemic stroke (IS) and reperfusion, their progressive morphological transformation into activated cells has not been quantified. (biomedcentral.com)
  • CD11b expression, but not iNOS expression, was increased in regions of hyper- and de-ramified microglia during the course of ischemic stroke and 24 h of reperfusion. (biomedcentral.com)
  • Emerging evidences indicate that systemic inflammatory cascades after stroke contribute to brain damage. (bmj.com)
  • However, the direct effects and features of systemic inflammation on brain injury, especially comparing between ischaemic and haemorrhagic stroke, are still obscure. (bmj.com)
  • The neurodeficits, stroke lesion, immune response and blood-brain barrier (BBB) destruction were assessed. (bmj.com)
  • Conclusions Our results suggest that PT increases inflammatory response that exacerbates brain injury after ICH or ischaemic stroke in mouse model. (bmj.com)
  • 1 2 At present, although progress has been made in understanding the molecular and cellular pathways leading to brain injury after stroke, the current clinical treatments remain poorly effective. (bmj.com)
  • NLRP1 and NLRP3 inflammasome components were also analyzed in postmortem brain tissue samples from stroke patients. (scienceopen.com)
  • Similarly, levels of NLRP1 and NLRP3 inflammasome proteins, IL-1 β and IL-18 were elevated in ipsilateral brain tissues of cerebral I/R mice and stroke patients. (scienceopen.com)
  • Caspase-1 inhibitor treatment protected cultured cortical neurons and brain cells in vivo in experimental stroke models. (scienceopen.com)
  • NRP-1 can produce neuroprotective effects against I/R injury to the brain by activating the Wnt/β-catenin signaling pathway and promoting mitochondrial structural repair and functional recovery, which may serve as a promising candidate target in treating ischemic stroke. (biomedcentral.com)
  • Leukotrienes derived from 5-lipoxygenase (5-LOX) cause inflammation and are thus involved in the pathobiology of stroke injury. (biomedcentral.com)
  • The objective of the present study was to determine whether an alternate MMP activatable probe with a shorter optical imaging time, MMPSense ™ 750 FAST (MMPSense750), could be used for visualization of MMP activity in the early stages of ischemia reperfusion in a mouse model of stroke. (biomedcentral.com)
  • In stroke, the ischemic crisis activates a series of events, including the inflammatory reactions that are potentiated by reperfusion, eventually leading to neuronal damage. (banglajol.info)
  • Acute vestibular syndrome can be due to stroke, and bedside neurologic testing has been shown to be highly sensitive for detection of a central etiology, even in the setting of a negative brain MRI. (medlink.com)
  • I am particularly interested in developing novel MRI methodologies for examining brain function, investigating the role of sex and steroid hormones in ischaemic stroke/cognitive decline and increasing the translational relevance of experimental models of CNS injury and disease. (nottingham.ac.uk)
  • A cerebrovascular accident, more commonly known as a stroke, occurs when the blood supply to determined parts of the brain suddenly ceases. (symptoma.mt)
  • Despite the fact that stroke therapy aims at recanalization and restoration of blood flow to affected brain regions, it can't currently be excluded that tissue reperfusion contributes to neuroinflammation and neuronal death. (symptoma.mt)
  • Although molecular and cellular events following tissue reperfusion are well described, evidence regarding possibly detrimental effects of reperfusion in stroke patients is still scarce [7]. (symptoma.mt)
  • Depending on which area of the brain is affected, a stroke can cause speech impairments, paralysis, unconsciousness , or even death. (symptoma.mt)
  • Other effects that may result from brain ischemia are stroke, cardiorespiratory arrest, and irreversible brain damage. (symptoma.mt)
  • Treatments that can reperfuse the ischemic brain regions as early as possible after stroke onset are critical for the prevention of brain-cell death. (en-journal.org)
  • Intra- and extra-hospital improvement in ischemic stroke patients: influence of reperfusion therapy and molecular mechanisms. (renevas.es)
  • Intravenous delivery of adipose tissue-derived mesenchymal stem cells improves brain repair in hyperglycemic stroke rats. (renevas.es)
  • Ongoing projects are focused on understanding how inflammatory responses are regulated after a stroke and how they affect short-term brain injury and long term outcomes like dementia and depression. (stanford.edu)
  • Ongoing projects focus on glial cells (astrocytes and microglia) and how they coordinate with immune cells from the blood to affect bystander brain injury in the days after stroke. (stanford.edu)
  • We also study the brain blood vessel response to stroke in aging, and in longer term models of dementia. (stanford.edu)
  • Reperfusion exceeded time window may induce ischemia/reperfusion injury, increase hemorrhagic transformation, and deteriorate neurological outcomes in ischemic stroke models. (omicsdi.org)
  • Improved reperfusion following alternative surgical approach for experimental stroke in mice. (omicsdi.org)
  • Following ischemic stroke, recanalisation and restoration of blood flow to the affected area of the brain is critical and directly correlates with patient recovery. (omicsdi.org)
  • models of ischemic stroke show high variability in outcomes, which may be due to variability in reperfusion. (omicsdi.org)
  • Accumulating evidence indicates that immune cells, especially brain-resident microglia and infiltrated circulating macrophages, are intimately involved in the pathological development of ischemic stroke [ 2 , 3 ]. (thno.org)
  • However, the phenotypes of T lymphocytes and their functions in peripheral immune organs and the brain have not been well analyzed in the acute and chronic phases of stroke. (en-journal.org)
  • Increased numbers of CD4 - CD8 - CD3 + double-negative T cells were observed in the mouse brain during the early stages of stroke, whereas interleukin (IL)-10 + Foxp3 + regulatory T lymphocytes increased from two weeks during the chronic phase. (en-journal.org)
  • This study provides fundamental information regarding the T lymphocyte alterations from the brain to the peripheral immune organs following stroke. (en-journal.org)
  • Ischemic stroke occurs when blood flow to the brain is blocked. (en-journal.org)
  • The process of cell death in the brain following a stroke leads to the activation of local immune cells, causing inflammation of the brain tissue. (en-journal.org)
  • Her main interests are in brain hemorrhage, unusual and rare causes of stroke, cerebral venous thrombosis, anticoagulation management after strokes and use of technology for improving outcomes in the neurological ICU. (stanford.edu)
  • Therefore, our data support the hypothesis that EA could exert its anti-inflammatory effect via inhibiting the astroglial and microglial/macrophage P2 purinoceptors (P2X7R and P2Y1R)-mediated neuroinflammation after MCAO/R injury. (biomedcentral.com)
  • Adoptive transfer of Sig-1R intact bone marrow-derived macrophages (BMDMs) to Sig-1R knockout mice restored the clearance activity of dead/dying neurons, reduced infarct area and neuroinflammation, and improved long-term functional recovery after cerebral ischemia. (thno.org)
  • Excessive neuroinflammation further promotes neuronal and glial cell damage and impairs brain repair and functional recovery. (thno.org)
  • We use this new tool to track microglia during embryonic development and in the context of ischemic injury and neuroinflammation. (elifesciences.org)
  • When combined with an HS, an UCCAO is associated with ischemic neuronal injury in the ipsilateral hemisphere of adult rat brain, which can be attenuated by therapeutic hypothermia. (medsci.org)
  • The increase in ipsilateral signal intensity was attenuated by hypothermia. (biomedcentral.com)
  • Evidence supporting the use of therapeutic hypothermia after brain ischemia, however, is limited. (symptoma.mt)
  • We examined the effects of the anesthetics isoflurane and pentobarbital, or hypothermia (30 degrees C), on the ability of rabbits to acquire an eyeblink conditioned response after 6.5 min of cerebral ischemia. (silverchair.com)
  • Animals in the hypothermia group were cooled to 30 degrees C before ischemia. (silverchair.com)
  • 2013 ). In addition, we demonstrated that EA could attenuate cerebral ischemic injury via regulation of α7nAChR-mediated inhibition of HMGB1 release in rats (Wang et al. (biomedcentral.com)
  • MCAO induced inflammatory injury, involving the ipsilateral cortex and basal ganglia with massive infiltration of neutrophils, macrophages and microvascular proliferation, was exhibited in all normothermic rats. (banglajol.info)
  • Three-month-old female Sprague-Dawley rats received L3 spinal compression injury. (biomedcentral.com)
  • The expression of NLRP3 inflammasome in the penumbral tissue following reperfusion was assessed by western blotting and immunoflourescent staining. (biomedcentral.com)
  • However, it is not known whether resuscitation after a [ 10 - 12 ] HS can cause cerebral injury and concomitant neurological dysfunction, and its potential mechanisms. (medsci.org)
  • Several mechanisms have been proposed for the pathogenesis of cerebral reperfusion injury. (medscape.com)
  • Since the first landmark experimental demonstration of ischemic tolerance in the gerbil brain in early 1990's, basic scientific knowledge on the mechanisms of cerebral ischemic tolerance increased substantially. (biomedcentral.com)
  • Danger signal evoked in the brain by the stressing preconditioning stimulus induces complex endogenous protective mechanisms resulting to a latent protective phenotype. (biomedcentral.com)
  • High mortality rates, in turn, make reliable conclusions difficult, in particular if a study focuses on mechanisms of secondary brain damage and neuroprotection (Lee et al, 2009). (openaccessjournals.com)
  • [ 11 , 12 ] Hyperperfusion is defined as a major increase in ipsilateral cerebral blood flow (CBF) that is well above the metabolic demands of the brain tissue. (medscape.com)
  • This model creates a unilateral infarct in the hemisphere ipsilateral to the ligation, since the hypoxia alone is subthreshold for injury at this age. (wikipedia.org)
  • Quantitative analysis reveals a significant spatiotemporal relationship between microglia morphology and evolving cerebral injury in the ipsilateral hemisphere after IS and reperfusion. (biomedcentral.com)
  • Images were acquired starting at 2 or 24 hours after reperfusion over the ipsilateral and contralateral cortex before and for 3 hours after, MMPSense750 was injected. (biomedcentral.com)
  • miR-22-3p (hereafter miR-22), a conserved miRNA that is expressed throughout the body, including the brain [ 14 , 15 ], was previously identified among upregulated miRNAs within the mouse hippocampus contralateral to the epileptogenic zone in the intraamygdala kainic acid model of status epilepticus [ 16 ]. (researchsquare.com)
  • Therefore, over the past several years, research has been directed to limit the brain lesions produced by acute ischemia (neuroprotection) and to increase the recovery, plasticity and neuroregenerative processes that complement rehabilitation and enhance the possibility of recovery and return to normal functions (neurorepair). (mdpi.com)
  • 2012 ). Our team has proposed a new approach of electroacupuncture (EA) neuroprotection for the prevention of cerebral ischemia injury. (biomedcentral.com)
  • However, the quality of MCAO - and thus the volume of brain infarcts - is very variable, a fact which is further aggravated by a certain rate of spontaneous lysis of injected blood clots. (wikipedia.org)
  • Activated phagocytic microglia/macrophages were examined by immunohistochemistry in post-mortem brains (n=6 MCAO, n=2 controls) at 3 and 24 hours (acute stage), 2 and 4 weeks (subacute stage), and 4, and 20 months (chronic stage) following MCAO. (en-journal.org)
  • if MCAO is applied during this phase, mainly cortical areas are spared (early ischemia-tolerant phenotype). (biomedcentral.com)
  • Mice underwent 60 min of MCAO, followed by either CCA repair or ligation at reperfusion. (omicsdi.org)
  • Live cell morphology and process activity were measured from movies acquired in acute brain slices from GFP-CX3CR1 transgenic mice after IS and 24-h reperfusion. (biomedcentral.com)
  • We also found that female mice sustained smaller infarcts than males three months post- ischemia . (nih.gov)
  • Mice lacking miR-22 displayed normal behaviour and brain structure and developed similar status epilepticus after intraamygdala kainic acid compared to wildtype animals. (researchsquare.com)
  • Depletion of Sig-1R greatly impaired the phagocytic activity of macrophages/microglia, accordingly with worsened brain damage and neurological defects in Sig-1R knockout mice subjected to tMCAO. (thno.org)
  • Acute tamoxifen administration in Cx3cr1-CreER mice also labels circulating monocytes, which can infiltrate the CNS in the context of injury or disease, thus complicating interpretation. (elifesciences.org)
  • The damage from ICH includes the primary tissue injury due to the mechanical effects of the haemorrhage and also the development of perihaematomal oedema (PHO), which induces a severe secondary injury and/or destruction of the adjacent tissue, in addition to an impairment in the integrity of the blood-brain barrier (BBB). (bmj.com)
  • We recently reported that neonatal ischemia induces microglia/macrophage activation three days post- ischemia . (nih.gov)
  • A resuscitation from an HS regards as a reperfusion insult which may induce neurological injury in patients with an UCCAO disease. (medsci.org)
  • Microglia cells continuously survey the healthy brain in a ramified morphology and, in response to injury, undergo progressive morphological and functional changes that encompass microglia activation. (biomedcentral.com)
  • As such, the dichotomous nature of these cells continues to confound our understanding of microglia-mediated injury after IS and reperfusion. (biomedcentral.com)
  • The purpose of this study was to quantitatively characterize the spatiotemporal pattern of microglia morphology during the evolution of cerebral injury after IS and reperfusion. (biomedcentral.com)
  • The microglia process length/cell and number of endpoints/cell was quantified from immunofluorescent confocal images of brain regions using a skeleton analysis method developed for this study. (biomedcentral.com)
  • Live microglia were de-ramified, and, in addition, process activity was severely blunted proximal to the necrotic core after IS and 24 h of reperfusion. (biomedcentral.com)
  • Immunohistochemical study of brain sections showed IR-mediated increased expression of 5-LOX in the neurons and microglia. (biomedcentral.com)
  • As the resident macrophages of the brain and spinal cord, microglia are crucial for the phagocytosis of infectious agents, apoptotic cells and synapses. (elifesciences.org)
  • During brain injury or infection, bone-marrow derived macrophages invade neural tissue, making it difficult to distinguish between invading macrophages and resident microglia. (elifesciences.org)
  • Microglia, the resident macrophages of the neural parenchyma, regulate a wide variety of processes in the brain, from development and synapse remodeling, to inflammatory insult and antigen presentation. (elifesciences.org)
  • The infarct size, neurological deficit score, TUNEL staining and the expression of proinflammatory factors or anti-inflammatory cytokines were evaluated at 72 h after reperfusion in the presence or absence of either α7nAChR antagonist (α-BGT) or agonist (PHA-543,613). (biomedcentral.com)
  • A sudden drop in systemic blood pressure could lead to cerebral ischemia, while, on the other hand, a sudden rise in systemic blood pressure could lead to edema or hemorrhage. (medscape.com)
  • Risk of traumatic intracranial hemorrhage in patients with head injury and preinjury warfarin or clopidogrel use. (medscape.com)
  • Her research focuses on the study of intracerebral hemorrhage using brain imaging with CT and MRI. (stanford.edu)
  • I am interested in the study of the radiological characteristics and temporal profile of edema/ tissue injury in the perihematomal area around spontaneous intracerebral hemorrhage. (stanford.edu)
  • Lentivirus (LV)-NRP-1 was transfected into rat primary cortical neuronal cultures before a 2-h oxygen-glucose deprivation and reoxygenation (OGD/R) injury to neurons. (biomedcentral.com)
  • Therefore, we speculate that purinergic receptors might play dualistic roles in response to EA effects treating inflammatory injury induced by ischemia. (biomedcentral.com)
  • The patient had severe cardiac dysfunction and atrial fibrillation and presented with acute ischemia in the right lower limb 24 h after receiving an inferior vena cava filter. (medscape.com)
  • 30%) with acute symptoms of right lower-extremity ischemia. (medscape.com)
  • Here we characterized the effect of intraspinal grafting of clinical grade human fetal spinal cord-derived neural stem cells (HSSC) on the recovery of neurological function in a rat model of acute lumbar (L3) compression injury. (biomedcentral.com)
  • Peri-acute intraspinal grafting of HSSC can represent an effective therapy which ameliorates motor and sensory deficits after traumatic spinal cord injury. (biomedcentral.com)
  • The area of injury is typically concentrated in periventricular regions of the brain, especially cortical and hippocampal areas. (wikipedia.org)
  • Ischemia-like conditions increased the levels of NLRP1 and NLRP3 inflammasome proteins, and IL-1 β and IL-18, in primary cortical neurons. (scienceopen.com)
  • As an integrated platform for triggering inflammation, inflammasome contributes to the pathogenesis of initiating innate immune response after cerebral ischemia/reperfusion (I/R)(Ismael et al. (biomedcentral.com)
  • We also identified NLRP1 and NLRP3 inflammasome inhibition as a novel mechanism by which IVIg can protect brain cells against ischemic damage, suggesting a potential clinical benefit of therapeutic interventions that target inflammasome assembly and activity. (scienceopen.com)
  • An UCCAO caused a slight cerebral ischemia (cerebral blood flow [CBF] 70%) without hypotension (MABP 85 mmHg), systemic inflammation, multiple organs injuries, or neurological injury. (medsci.org)
  • An HS caused a moderate cerebral ischemia (52% of the original CBF levels), a moderate hypotension (MABP downed to 22 mmHg), systemic inflammation, and peripheral organs injuries. (medsci.org)
  • However, combined an UCCAO and an HS caused a severe cerebral ischemia (18% of the original CBF levels), a moderate hypotension (MABP downed to 17 mmHg), systemic inflammation, peripheral organs damage, and neurological injury, which can be attenuated by whole body cooling. (medsci.org)
  • Although deliberate hypotension during surgery may potentially cause organ ischaemia, in particular of the myocardium and cerebrum, it is widely used as an adjuvant. (annals.edu.sg)
  • 2009 ) and regulate the Reperfusion Injury Salvage Kinase (RISK) signaling pathway (ERKε, PKC, GSK-3β, STAT3) via cannabinoid receptor 1 (CB1R)(Wang et al. (biomedcentral.com)
  • It is well-documented that extracellular ATP triggers surrounding glial purinergic receptors signaling pathway and pro-inflammatory cytokines release to aggravate neural injury in cerebral ischemia [ 8 , 9 ]. (biomedcentral.com)
  • Patient outcomes following a minor polytrauma are often worse than those with a single severe injury. (medsci.org)
  • Damage to Myelin and Oligodendrocytes: A Role in Chronic Outcomes Following Traumatic Brain Injury? (mdpi.com)
  • Cerebral reperfusion, or hyperperfusion, syndrome is a rare but serious complication that can occur following rapid revascularization of a partially or completely occluded artery with successful thrombolytic therapy, successful thrombectomy, carotid enterectomy (CEA), or carotid artery stenting (CAS). (medscape.com)
  • Space-occupying brain edema is a serious and potentially fatal complication of cerebrovascular accidents. (symptoma.mt)
  • Brain edema is accompanied by an increase of intracranial pressure and thus, edema-mediated brain damage is not necessarily restricted to those brain regions originally affected by the cerebrovascular accident. (symptoma.mt)
  • Both in vitro and in vivo models of cerebral ischemia/reperfusion (I/R) injury presented a sharp increase in NRP-1 expression. (biomedcentral.com)
  • Matrix-metalloproteinase upregulation in ischemia reperfusion can be imaged acutely in-vivo with NIRF using MMPSense750. (biomedcentral.com)
  • The IMPROVE Guidelines (Ischaemia Models: Procedural Refinements Of in Vivo Experiments). (nottingham.ac.uk)
  • Positron emission tomography (PET) is a powerful imaging technique which enables in vivo examination of brain functions. (bmj.com)
  • Importantly, quantitative analyses of microglial morphology and activity are feasible and, in future studies, would assist in the comprehensive identification and stratification of their dichotomous contribution toward cerebral injury and recovery during IS and reperfusion. (biomedcentral.com)
  • Symptom severity is not necessarily proportional to degree of reperfusion - both reperfusion and hyperperfusion can result in cerebral injury with similar clinical presentations. (medscape.com)
  • Mediterranean Diet and Physical Activity Protect from Silent Brain Infarcts in a Cohort of Patients with Atrial Fibrillation. (renevas.es)
  • The resuscitation after an HS causes a reperfusion or reoxygenation insult [ 2 - 4 ], gut injury, and multiple organ dysfunctions [ 5 , 6 ]. (medsci.org)
  • Polytrauma can be defined as a combination of multiple, simultaneous injuries to more than one body part or organ system. (medsci.org)
  • Which Model Yields More Ischemia-Reperfusion Organ Injury? (safasatoglu.com)
  • Assessment of protective effects of pheniramine maleate on reperfusion injury in lung after distant organ ischemia: a rat model. (safasatoglu.com)
  • However, in various settings global ischemia is also relevant, e.g. in global anoxic brain damage due to cardiac arrest. (wikipedia.org)
  • Prolonged or repeated seizures are damaging to the brain and can establish lasting states of hyperexcitability that produce recurrent spontaneous seizures (epilepsy) [ 1 , 2 ]. (researchsquare.com)
  • Our previous research confirmed that electroacupuncture (EA) stimulus elicits neuroprotective effects against cerebral ischemic injury through α7 nicotinic acetylcholine receptor (α7nAChR)-mediated inhibition of high-mobility group box 1 release mechanism. (biomedcentral.com)
  • The contents of inflammasome proteins were gradually increased after cerebral ischemia/reperfusion (I/R). EA stimulus attenuated NLRP3 inflammasome mediated inflammatory reaction and regulated the balance between proinflammatory factors and anti-inflammatory cytokines. (biomedcentral.com)
  • In the scenario of IT, PC stimulus primes the brain for subsequent injurious ischemic injury. (biomedcentral.com)
  • Seven days after ischemia, eyeblink training was started using an audible tone presented for 100 ms as the conditioned stimulus. (silverchair.com)
  • Magnetic resonance imaging volume reconstruction and immunofluorescence analysis of grafted cell survival showed near complete injury-cavity-filling by grafted cells and development of putative GABA-ergic synapses between grafted and host neurons. (biomedcentral.com)
  • A separate group of experimental treatment modalities is aimed at improving the local neurotrophic activity at and around the injury epicenter with the primary goal of increasing the survival of partially injured axons and/or neurons. (biomedcentral.com)
  • Neurological assessment was performed, brain tissue damage was quantified, and NLRP1 and NLRP3 inflammasome protein levels were evaluated. (scienceopen.com)
  • Visual processing speed in hemianopia patients secondary to acquired brain injury: a new assessment methodology. (renevas.es)
  • The extent of reperfusion injury likely depends on the extent of initial hypoperfusion, the time to collateral collapse, the volume of irreversible tissue damage, and the degree of autoregulatory and pro-inflammatory responses. (medscape.com)
  • When the lethal ischemic insult is applied onto this latent protective phenotype, a separate set of responses are triggered that constitute ischemia-tolerant phenotype, which strikingly differs from the unprimed or unpreconditioned brain's phenotype (Figure 1 ). (biomedcentral.com)
  • A typical feature is the patient's inability to stand or walk due to gait and truncal ataxia as well as ipsilateral lateropulsion. (medlink.com)
  • However, whether NRP-1 can repair mitochondrial structure and promote functional recovery after cerebral ischemia is still unknown. (biomedcentral.com)
  • Therefore, promoting the mitochondrial structural repair and functional recovery is the crucial for the amelioration of the neurological damage after cerebral ischemia. (biomedcentral.com)
  • This study demonstrates that a brief episode of cerebral ischemia results in the impairment of associative learning. (silverchair.com)