• Expression of SOX9 did not decrease during aging and was instead upregulated by reactive astrocytes in a number of settings, including a murine model of amyotrophic lateral sclerosis (SOD1G93A), middle cerebral artery occlusion, and multiple mini-strokes. (jneurosci.org)
  • 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)
  • Global cerebral ischemia was performed via 10 min of four-vessel occlusion. (springer.com)
  • i.p) or vehicle administered 24 hours after permanent middle cerebral artery occlusion (pMCAO) on behavior, angiogenesis, ultra-structural integrity of brain capillary endothelial cells, and expression of EPO and VEGF were assessed. (researchgate.net)
  • The right middle cerebral artery occlusion model was used in the study. (biomedcentral.com)
  • Female rats with intact ovaries and ovariectomized (OVX) females treated with 17β-estradiol, progesterone, or placebo were subjected to transient, unilateral middle cerebral artery occlusion followed by reperfusion (I/R). The maximum contractile response, measured my wire myography, in response to the endothelin B receptor agonist sarafotoxin 6c was increased in female arteries after I/R, but the maximum response was significantly lower in arteries from OVX females. (lu.se)
  • 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)
  • Healthy adult Sprague‑Dawley (SD) male rats were used to establish a control group, sham‑operated group, middle cerebral artery occlusion (MCAO) group, empty virus group and lentivirus group. (spandidos-publications.com)
  • Temporary occlusion (120 min) of the right middle cerebral artery was induced 4 days after preconditioning and the infarct volume was measured. (elsevierpure.com)
  • To determine if and the extent to which MPO-generated oxidants contribute to brain I/R injury, we treated mice subjected to middle cerebral artery occlusion (MCAO) with N -acetyl lysyltyrosylcysteine amide (KYC), a novel, specific and non-toxic inhibitor of MPO. (biomedcentral.com)
  • Cerebral collateral circulation is a subsidiary vascular network, which is dynamically recruited after arterial occlusion, and represents a powerful determinant of ischemic stroke outcome. (biomedcentral.com)
  • The most common type of stroke is ischemic stroke, which results from the occlusion of a cerebral vessel by a clot. (explorationpub.com)
  • Immunohistochemical analysis of protein expression after middle cerebral artery occlusion in mice. (mpg.de)
  • Proteomics of infarct evolution after transient middle cerebral artery occlusion in mice. (mpg.de)
  • Brain edema primarily occurs as a consequence of various cerebral injuries including ischemic stroke. (benthamscience.com)
  • Role of aquaporin-4 in cerebral edema and stroke. (benthamscience.com)
  • Intrinsically, ischemic stroke indicates the cascade of congesting events, i.e., thrombus formation and embolism, that ultimately decreases the local blood flow and cause oxygen deprivation in affected brain tissue. (hindawi.com)
  • Therefore, an effective therapeutic strategy is required to prevent the onset of acute stroke and manage the chronic symptoms associated with neural ischemia, i.e., long-term neuroinflammation and localized necrosis [ 8 , 9 ]. (hindawi.com)
  • Graphical presentation of the various stages of cerebral ischemia stroke, i.e., acute phase, subacute phase, and chronic phase and their contributing factors. (hindawi.com)
  • A deleterious consequence of cerebral ischemia is upregulation of vasoconstrictor receptors in cerebral arteries that exacerbate stroke injury. (lu.se)
  • An ischemic stroke consists of two related pathological injury processes: Primary ischemia-induced brain injury and secondary ischemia reperfusion injury ( 3 ). (spandidos-publications.com)
  • A study has shown that neurons in the ischemic penumbra may undergo apoptosis hours or days after ischemia and alleviating ischemia reperfusion injury is an achievable therapeutic goal in the early intervention of ischemic stroke aimed at limiting the amount of infarction ( 4 ). (spandidos-publications.com)
  • When ischemic stroke occurs, cerebral ischemia and hypoxia cause the release of excessive excitatory amino acids, mainly glutamic acid and aspartic acid, which exert excitotoxic effects on the central nervous system. (spandidos-publications.com)
  • Therefore, selective NR1/2B subtype antagonists are considered as potentially attractive drugs for the treatment of neurodegenerative disorders such as stroke, brain trauma, pain, and Parkinson's disease. (inteligand.com)
  • Oxidative stress plays an important and causal role in the mechanisms by which ischemia/reperfusion (I/R) injury increases brain damage after stroke. (biomedcentral.com)
  • Accordingly, reducing oxidative stress has been proposed as a therapeutic strategy for limiting damage in the brain after stroke. (biomedcentral.com)
  • MPO-generated oxidants play detrimental roles in causing brain damage after stroke which is effectively reduced by KYC. (biomedcentral.com)
  • Extensive studies have shown that the increase in oxidative stress induced by I/R after acute stroke plays a critical role in brain tissue injury. (biomedcentral.com)
  • Taken together, these reports strongly support the idea that ROS and RNS play important roles in the mechanisms by which stroke induces and propagates tissue injury and brain cell death after stroke. (biomedcentral.com)
  • When administered post-stroke, mesenchymal stromal cell-derived extracellular vesicles (MSC-EVs) induce neuroprotection, promote brain remodeling and plasticity, and enhance neurological recovery in rodents and non-human primates via mechanisms that involve immunomodulation and anti-inflammation. (explorationpub.com)
  • Ischemic stroke activates components of innate and/or adaptive immunity and induces brain inflammatory responses, which besides removing damaged tissue exacerbate ischemic brain injury [ 3 , 4 ]. (explorationpub.com)
  • Following a stroke, immune responses and neuroinflammation persist throughout all phases of injury, from early tissue damage to late brain tissue remodeling [ 3 , 4 ]. (explorationpub.com)
  • Specifically, polymorphonuclear neutrophils (PMNs) have been shown to play a critical role in the exacerbation of ischemic brain injury in the acute stroke phase and in the postischemic brain remodeling and angiogenesis in the post-acute phase [ 5 , 6 ]. (explorationpub.com)
  • In addition, morroniside could protect ischemia/reperfusion-induced brain injury by decreased the caspase-3 activity, reduced the infarction volume and minimized oxidative stress [ 7 ]. (ijpsonline.com)
  • Thus, we hypothesize that Cordyceps sinensis possess protective effect of against ischemia-induced brain infarction by modulating 17β-estradiol production. (biomedcentral.com)
  • Here we investigated whether remifentanil postconditioning exerts neuroprotective effects against global cerebral ischemia/reperfusion injury in rats and its potential mechanisms. (springer.com)
  • The results suggest that remifentanil postconditioning exhibits neuroprotective effects against global cerebral ischemia/reperfusion injury in rats, and its mechanisms might involve inhibition of neuronal apoptosis through the PI3K pathway. (springer.com)
  • Wang JY, Shen J, Gao Q et al (2008) Ischemic postconditioning protects against global cerebral ischemia/reperfusion-induced injury in rats. (springer.com)
  • Ren C, Yan Z, Wei D et al (2009) Limb remote ischemic postconditioning protects against focal ischemia in rats. (springer.com)
  • Ding ZM, Wu B, Zhang WQ et al (2012) Neuroprotective Effects of Ischemic Preconditioning and Postconditioning on Global Brain Ischemia in Rats through the same effect on inhibition of apoptosis. (springer.com)
  • Jeong S, Kim SJ, Jeong C et al (2012) Neuroprotective effects of remifentanil against transient focal cerebral ischemia in rats. (springer.com)
  • Esketamine activated the mature brain-derived neurotrophic factor/tropomyosin receptor kinase B/phosphatidylinositide 3-kinase (mBDNF/TrkB/PI3K) signaling pathway in propofol-administrated rats. (degruyter.com)
  • Overall, esketamine mitigates propofol-induced cognitive dysfunction and brain injury in rats by activating mBDNF/TrkB/PI3K signaling. (degruyter.com)
  • Cordyceps sinensis extract significantly improved the outcome in rats after cerebral ischemia and reperfusion in terms of neurobehavioral function. (biomedcentral.com)
  • Our results showed that NMN administration markedly attenuated histological damages, neuronal death, brain edema, and improved neurological and cognitive deficits in TBI rats. (medsci.org)
  • These results suggested that HSP90β is involved in the process of cerebral ischemia‑reperfusion injury in rats and that inhibition of HSP90β expression increases EAAT2 levels, conferring a neuroprotective effect in MCAO model rats. (spandidos-publications.com)
  • The aim of present study was to investigate the neuroprotective effect of agmatine (AGM) on cerebral ischemic damage in diabetic rats. (elsevierpure.com)
  • Methods: Normoglycemic (n=30) and streptozocine-induced diabetic rats (n=82) were subjected to 30 minutes of sutureocclusion of the middle cerebral artery (MCAO) with 24 or 72 hours of reperfusion. (elsevierpure.com)
  • Conclusions: AGM posttreatment reduced cerebral infarct size and neurological deficit expression in diabetic rats subjected to MCAO. (elsevierpure.com)
  • Transgenic mice overexpressing XIAP in neurons show better outcome after transient cerebral ischemia. (mpg.de)
  • A model of cerebral ischemia‑reperfusion was established using the MCAO method. (spandidos-publications.com)
  • Behavioral testing, ischemic damage, blood-brain-barrier disruption, apoptosis, neutrophils infiltration, microglia/macrophage activation, and MPO oxidation were analyzed within a 7-day period after MCAO. (biomedcentral.com)
  • Our studies show that KYC treatment significantly reduces neurological severity scores, infarct size, IgG extravasation, neutrophil infiltration, loss of neurons, apoptosis, and microglia/macrophage activation in the brains of MCAO mice. (biomedcentral.com)
  • Excessive activation of N-methyl-D-aspartate (NMDA) receptors and resulting calcium overload of neurons is thought to be a key contributor to neuronal cell death following acute cerebral ischaemia. (inteligand.com)
  • Humans may sustain a variety of forms of acute central nervous system injury including ischemia, trauma, vasospasm, and perinatal hypoxemia. (duke.edu)
  • The Multidisciplinary Neuroprotection Laboratories is dedicated to examining the pathophysiology of acute brain and spinal cord injury with particular reference to disease states managed in the perioperative or neurointensive care environments. (duke.edu)
  • Compelling experimental evidence indicates that both soluble A-beta and insoluble vascular deposits of A-beta (i.e. cerebral amyloid angiopathy) promote cerebral vessel dysfunction, which could heighten sensitivity to acute neurologic insults such as ischemic brain injury and/or subarachnoid hemorrhage. (wustl.edu)
  • TBM must be differentiated not only from other forms of acute and subacute meningitis, but also from conditions such as viral infections and cerebral abscesses (See Diagnosis ). (medscape.com)
  • Loss of cholinergic innervation differentially affects eNOS-mediated blood flow, drainage of Aβ and cerebral amyloid angiopathy in the cortex and hippocampus of adult mice. (open.ac.uk)
  • Additionally, ERK 1/2 activation and cyclooxygenase-2 (COX-2) expression in the cerebral cortex were examined by Western blotting analysis immediately after cessation of CSD, or at 1, 2, 4, 8, and 24 h after CSD. (elsevierpure.com)
  • It consists of the thalamus, the hypothalamus, and the cerebral cortex. (medscape.com)
  • The outer covering of the cerebral hemispheres is known as the cerebral cortex. (medscape.com)
  • The frontal lobe is the part of the cerebral cortex responsible for voluntary movement and attention as well as goal-directed behavior. (medscape.com)
  • The neuroprotective effects of remifentanil preconditioning against cerebral ischemia/reperfusion injury have been recently reported. (springer.com)
  • At the top of the pons, the basilar artery divides into 2 posterior cerebral arteries (PCAs). (medscape.com)
  • At the base of the brain, the carotid and basilar systems join to form a circle of large, communicating arteries known as the circle of Willis. (medscape.com)
  • Because of this arrangement of collateral vessels, even when one of the main arteries is occluded, adequate perfusion of the brain still may be possible. (medscape.com)
  • Vasospasm is defined by delayed narrowing of large cerebral arteries that often leads to ischemic brain injury. (wustl.edu)
  • The effect of moderate whole body hypothermia (300 C) on transient focal cerebral ischemia induced inflammatory injury was investigated. (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)
  • Protection of cerebral microvasculature after moderate hypothermia following experimental focal cerebral ischemia in mice. (mpg.de)
  • Burk J, Burggraf D, Vosko M, Dichgans M, Hamann G. Effects of hypothermia on focal cerebral ischemia in plasminogen knockout mice. (mpg.de)
  • Burk J, Burggraf D, Vosko M, Dichgans M, Hamann G. Hypothermia strengths inhibitors of matrix degrading proteases following experimental focal cerebral ischemia in mice. (mpg.de)
  • 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)
  • Charron C, Messier C, Plamondon H (2008) Neuroprotection and functional recovery conferred by administration of kappa- and delta 1-opioid agonists in a rat model of global ischemia. (springer.com)
  • Multiparametric analysis of brain injury following transient focal cerebral ischemia in mice. (mpg.de)
  • Propofol has been shown to attenuate brain injury in experimental ischemia models, but few studies have focused on the direct effect of propofol on mitochondrial dysfunction. (nih.gov)
  • These experimental results suggest that complement Cordyceps sinensis extract is protective after cerebral ischemia in specific way. (biomedcentral.com)
  • Burggraf D, Vosko MR, Schubert M, Stassen JM, Hamann GF Different therapy options protecting microvasculature after experimental cerebral ischaemia and reperfusion. (mpg.de)
  • Increasing doses of rt-PA reduce MMP3-activity following experimental focal cerebral ischemia. (mpg.de)
  • Microplasmin reduces dose-dependently microvascular basal lamina damage in experimental focal cerebral ischemia. (mpg.de)
  • Advancing brain barriers RNA sequencing: guidelines from experimental design to publication. (open.ac.uk)
  • The clinical correlates of these smaller lesions consist of a variety of focal neurologic deficits, depending on their location within the brainstem. (medscape.com)
  • Repeated treatments with Catalpol reduced neurological deficits and significantly improved angiogenesis, while significantly increasing brain levels of EPO and VEGF without worsening BBB edema. (researchgate.net)
  • Inhibition of HSP90β expression improved neurological deficits and alleviated brain injury by increasing EAAT2 expression. (spandidos-publications.com)
  • These results suggested that catalpol might contribute to infarcted-brain angiogenesis and ameliorate the edema of brain capillary endothelial cells (BCECs) by upregulating VEGF and EPO coordinately. (researchgate.net)
  • Mounting evidence has demonstrated that AQP4, a water channel protein, is closely correlated with brain edema and could be an optimal therapeutic target for the reduction of ischemic brain edema. (benthamscience.com)
  • Mechanisms of astrocyte-mediated cerebral edema. (benthamscience.com)
  • Igarashi H, Huber VJ, Tsujita M, Nakada T. Pretreatment with a novel aquaporin 4 inhibitor, TGN-020, significantly reduces ischemic cerebral edema. (benthamscience.com)
  • The brain infarct volume and edema volume were assessed. (elsevierpure.com)
  • Examination of the brain showed diffuse cerebral edema, and cerebellar arachnoid hemorrhages most likely due to the prolonged cerebral ischemia. (hawaii.edu)
  • Perhaps, the therapeutic effect was related to a reduction in releasing of cytotoxic products and improvement of the cerebral microcirculation. (banglajol.info)
  • Ischemic brain injury is associated with a high rate of mortality and disability with no effective therapeutic strategy. (hindawi.com)
  • The chief aim in this study was to investigate whether changing temperature during and after ischemia could minimize this damage by reducing the inflammatory injury. (banglajol.info)
  • We found remifentanil postconditioning markedly improved the spatial learning and memory as well as attenuated neuronal apoptosis in hippocampus caused by cerebral ischemia/reperfusion injury. (springer.com)
  • Zhou Y, Fathali N, Lekic T et al (2012) Remote limb ischemic postconditioning protects against neonatal hypoxic-ischemic brain injury in rat pups by the opioid receptor/Akt pathway. (springer.com)
  • Yuan Y, Guo Q, Ye Z et al (2011) Ischemic postconditioning protects brain from ischemia/reperfusion injury by attenuating endoplasmic reticulum stress-induced apoptosis through PI3K-Akt pathway. (springer.com)
  • Propofol improved the signs of injury in the cortical mitochondria that were exposed to reperfusion following 2 h of focal ischemia. (nih.gov)
  • Herein, we investigated the role of esketamine in propofol-induced brain injury. (degruyter.com)
  • A rat model of propofol-induced brain injury was established with or without the treatment of esketamine. (degruyter.com)
  • However, whether esketamine has an effect on propofol-induced brain injury has not been investigated. (degruyter.com)
  • Thus, MSCs were suggested as a promising candidate for ischemic brain injury patients[ 11 ]. (hindawi.com)
  • Ischemic hypoxic brain injury often causes irreversible brain damage. (biomedcentral.com)
  • Restoration of the antioxidant homeostasis in the brain after reperfusion may have helped the brain recover from ischemic injury. (biomedcentral.com)
  • The administration of Cordyceps sinensis extract significantly reduced focal cerebral ischemic/reperfusion injury. (biomedcentral.com)
  • The cascade of events leading to neuronal injury and death in ischemia includes the release of cytokines and free radicals, and induction of inflammation, apoptosis, and excitotoxicity [ 1 ]. (biomedcentral.com)
  • Zhu X, Cheng J, Yu J, Liu R, Ma H, Zhao Y. Nicotinamide mononucleotides alleviated neurological impairment via anti-neuroinflammation in traumatic brain injury. (medsci.org)
  • Traumatic brain injury (TBI) is one of the main factors of death and disability in adults with a high incidence worldwide. (medsci.org)
  • Taken together, our data showed that NMN alleviated neurological impairment via anti-neuroinflammation in traumatic brain injury and the mechanisms may involve TLR2/4-NF-κB signaling. (medsci.org)
  • Traumatic brain injury (TBI), as the most common cause of death in trauma centers, is also one of the major causes of death and disability in adults worldwide [ 1 , 2 ]. (medsci.org)
  • 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)
  • 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)
  • 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)
  • Cerebrovascular diseases (CVDs) have become a global public health problem and ischemia‑reperfusion injury, the major cause of neurological impairment exacerbation, is closely related to excitotoxicity. (spandidos-publications.com)
  • The present study aimed to investigate the effects of changes in heat shock protein (HSP)90β expression and verify whether HSP90β regulates EAAT2 expression in a cerebral ischemia‑reperfusion injury model. (spandidos-publications.com)
  • yet at the same time it can induce ischemia-reperfusion injury, which leads to brain damage both in the ischemic core and penumbra area. (spandidos-publications.com)
  • Cerebral perfusion was increased in progesterone-treated males at 4 h (p = 0.043) but not 24 h after injury. (duke.edu)
  • With a clinical background in neuroanesthesia and neurointensive care, I have a special interest in translational research in intracerebral hemorrhage and traumatic brain injury. (duke.edu)
  • Cerebral oedema is associated with significant neurological damage in patients with traumatic brain injury. (biomedcentral.com)
  • We evaluated the safety and effectiveness of the non-peptide bradykinin B2 receptor antagonist Anatibant in the treatment of patients with traumatic brain injury. (biomedcentral.com)
  • Adults with traumatic brain injury and a Glasgow Coma Scale score of 12 or less, who had a CT scan showing an intracranial abnormality consistent with trauma, and were within eight hours of their injury were randomly allocated to low, medium or high dose Anatibant or to placebo. (biomedcentral.com)
  • Cerebral oedema is associated with significant mortality and morbidity after traumatic brain injury (TBI). (biomedcentral.com)
  • A systematic review of controlled studies in animal brain injury models showed that BB2 antagonists reduce brain oedema and improve neurological outcome [ 6 ]. (biomedcentral.com)
  • It also regulates angiogenic factors and vascular permeability after focal cerebral ischemia-reperfusion, and regulates matrix metalloproteinase-9 activity after intracerebral hemorrhage. (wikipedia.org)
  • Vascular Integrin immunoreactivity is selectively lost on capillaries during rat focal cerebral ischemia and reperfusion. (mpg.de)
  • AQP4 is prevalently distributed in the central nervous system, and mainly regulates water flux in brain cells under normal and pathological conditions. (benthamscience.com)
  • Intravenous administraton of MEK inhibitor U0126 affords brain protection against forebrain ischemia and focal cerebral ischemia. (rndsystems.com)
  • The brain has been divided into 3 different areas: the hindbrain, the midbrain, and the forebrain. (medscape.com)
  • The forebrain is supported by the brain stem and buds out above it, drooping somewhat to fit inside the skull. (medscape.com)
  • moreover, Mdr-1 deactivation by pharmacological inhibition or genetic knockout preferably enhances the accumulation and efficacy of two neuroprotectants known as Mdr-1 substrates in the ischemic brain. (nature.com)
  • Neurotrophic factors, including brain-derived neurotrophic factor (BDNF), are indispensable regulators for the survival of glial cells and neurons in the central nervous system (CNS) [ 13 ]. (degruyter.com)
  • The billions of neurons in the brain are connected to neurons throughout the body by trillions of synapses. (medscape.com)
  • The brain contains more than 90% of the body's neurons. (medscape.com)
  • Figure 1: Mdr-1 is upregulated on capillary endothelium after focal cerebral ischemia. (nature.com)
  • The pathophysiology of cerebral hyperperfusion syndrome (CHS) may involve dysregulation. (biomedcentral.com)
  • As an intravenous anesthetic, propofol has been indicated to induce neurotoxicity in both animal and human brains. (degruyter.com)
  • 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)
  • The nervous system is organized into two parts: the central nervous system, which consists of the brain and the spinal cord, and the peripheral nervous system , which connects the central nervous system to the rest of the body. (medscape.com)
  • In the central nervous system, the brain and spinal cord are the main centers where correlation and integration of nervous information occur. (medscape.com)
  • The blood-brain barrier possesses active transporters carrying brain-permeable xenobiotics back into the blood against concentration gradients. (nature.com)
  • Excessive accumulation of brain water content causes a gradual expansion of brain parenchyma, decreased blood flow and increased intracranial pressure and, ultimately, cerebral herniation and death. (benthamscience.com)
  • rt-PA causes a dose-dependent increase in the extravasation of cellular and non-cellular blood elements after focal cerebral ischemia. (mpg.de)
  • Mast cells promote blood brain barrier breakdown and neutrophil infiltration in a mouse model of focal cerebral ischemia. (ukri.org)
  • A hydrogel model of the human blood-brain barrier using differentiated stem cells. (open.ac.uk)
  • An In Vitro Blood-Brain Barrier Model to Study Firm Shear Stress-Resistant Leukocyte Adhesion to Human Brain Endothelial Cells. (open.ac.uk)
  • The Blood-Brain Barrier: Methods and Protocols. (open.ac.uk)
  • These excitotoxic effects play important roles in neuronal and blood-brain barrier damage after cerebral ischemia ( 5 , 6 ). (spandidos-publications.com)
  • Bradykinin is an inflammatory mediator that may contribute to cerebral oedema by increasing the permeability of the blood-brain barrier. (biomedcentral.com)
  • An increase in the permeability of the blood-brain barrier (BBB) is believed to be responsible for oedema formation. (biomedcentral.com)
  • Hence, this review comprehensively addressed the alteration of miRNA expression across diverse sources such as peripheral blood, exosome, cerebrospinal fluid, and brain in AD patients. (bvsalud.org)
  • Both aim at removing the clot and restoring blood flow to the brain. (explorationpub.com)
  • It receives blood from a vein in the nasal cavity, runs backwards, and gradually increases in size as blood drains from veins of the brain and the DURA MATER. (bvsalud.org)
  • In this study, we observed the effects of propofol on multiple aspects of mitochondrial dysfunction by studying the mitochondria isolated from rat brains subjected to focal cerebral ischemia-reperfusion. (nih.gov)
  • Of brain computed tomography scans of 17 patients, 3 showed cerebral and/or cerebellar atrophy and 2 confirmed strokes. (cdc.gov)
  • The Mdr-1 inhibitor TQD preferably increases brain concentrations of FK506 and rifampicin in the ischemic brain. (nature.com)
  • We examined the effect of L-NAME, an inhibitor of NO synthase, on CSD-induced tolerance against transient focal cerebral ischemia. (elsevierpure.com)
  • Cortical spreading depression (CSD) has been documented to confer ischemic tolerance on brain. (elsevierpure.com)
  • We aim to provide the basis for establishing a future study to promote the clinical translation of stem cell therapy in ischemic brain diseases. (hindawi.com)
  • Recently, from the point of view of "self-medication" or "preventive medicine," several dietary supplements are used in the prevention of life-style related diseases including cerebral ischemia. (biomedcentral.com)
  • Although animal studies have yielded promising results on immunomodulatory therapies targeting poststroke leukocyte brain entry, these approaches have without exception failed in clinical trials [ 7 ]. (explorationpub.com)