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Brain IschemiaIschemiaMyocardial IschemiaReperfusionIschemic Attack, TransientReperfusion InjuryGerbillinaeBrainNeuroprotective AgentsInfarction, Middle Cerebral ArteryBrain ChemistryBrain InfarctionBrain InjuriesBrain EdemaRats, Sprague-DawleyIschemic PreconditioningDisease Models, AnimalCerebrovascular CirculationRats, WistarCerebral InfarctionCerebral CortexNeuronsTime FactorsBrain NeoplasmsHippocampusHypoxia-Ischemia, BrainMiddle Cerebral ArteryMenispermumBrain MappingHypoxia, BrainHypothermia, InducedCell DeathBlood-Brain BarrierMagnetic Resonance ImagingStrokeMyocardial Reperfusion InjuryMongoliaRecovery of FunctionWarm IschemiaArterial Occlusive DiseasesAstrocytesMice, Inbred C57BLPhenazocineGlutamic AcidCerebral ArteriesCerebrovascular DisordersOxygenImmunohistochemistryRats, Inbred StrainsBrain StemNerve Tissue ProteinsCorpus StriatumRats, Inbred SHRPhosphotungstic AcidAnalysis of VarianceCold IschemiaNecrosisThiocarbamatesCell HypoxiaNerve DegenerationGlial Fibrillary Acidic ProteinBody TemperatureThiopentalCells, CulturedBlotting, WesternSpinal Cord IschemiaMice, KnockoutMyocardiumNeurologic ExaminationSus scrofaGlucoseBlood PressureRNA, MessengerAnimals, NewbornAcute DiseaseEncephalitisApoptosisElectroencephalographyMicrogliaBehavior, AnimalLactatesIschemic Preconditioning, MyocardialCA1 Region, HippocampalDose-Response Relationship, DrugBrain AbscessIntracranial Embolism and ThrombosisReceptors, N-Methyl-D-AspartateRats, Long-EvansAcid Sensing Ion ChannelsIn Situ Nick-End LabelingRandom AllocationAntioxidantsNervous System DiseasesHeart ArrestMyocardial ReperfusionUltrasonography, Doppler, TranscranialIsofluraneCell SurvivalOxidative StressCell Count
ReperfusionOxygenProteinHypoxiaTraumatic brainAstrocytesResult in ischemiaReducing the production of reactiveStrokeAcuteCommon carotid artery oNatriuretic peptideMammalianInjuryMethodsFocalMitochondriaOxidative stressInflammationAstrogliosisGlutamateHemorrhageNeuronsNeuroprotectiveVasculitisHuman brainsVitroTissueExtracellularMetabolismNeurologicalHomeostasisTherapeuticIschemic brainMiddle cerebrInflammatoryBlood-cerebroAmyloid plaquesMildPathologicalMicePlasticityFindingsHeart attacksTissues
Reperfusion12
Oxygen19
  • Although reactive oxygen species (ROS) act as crucial factors in the onset and progression of a wide array of diseases, they are also involved in numerous signalling pathways related to cell metabolism, growth and survival. (nih.gov)
  • This leads to poor oxygen supply or cerebral hypoxia and thus leads to the death of brain tissue or cerebral infarction/ischemic stroke. (wikipedia.org)
  • The symptoms of brain ischemia reflect the anatomical region undergoing blood and oxygen deprivation. (wikipedia.org)
  • citation needed] Compression of blood vessels may also lead to brain ischemia, by blocking the arteries that carry oxygen to the brain. (wikipedia.org)
  • In the case of an acute stroke, inadequate blood flow to the brain leads to an interruption in the supply of oxygen and glucose to the neurons, resulting in massive cell death within the infarcted core [ 9 ]. (hindawi.com)
  • Neurodegenerative disorders and other CNS injuries share some common pathophysiological events with the metabolic injury cascade that follows TBI, such as the increased production of reactive oxygen species (ROS) and mitochondrial dysfunction. (nationalacademies.org)
  • Ischemia is the condition suffered by tissues & organs when deprived of blood flow -- mostly the effects of inadequate nutrient & oxygen. (benbest.com)
  • It plays important roles in cytokine and stress responses, as well as in reactive oxygen species (ROS)-mediated cellular responses. (umbc.edu)
  • 48], Superoxide is a reactive oxygen species that contributes to cellular oxidative stress and is linked to neuromuscular diseases and aging. (gowebamerica.com)
  • It is also a major contributor to cellular production of reactive oxygen species. (gowebamerica.com)
  • Somatosensory stimulation also evokes cerebral vasodilatation mediated by neurogenic NO. Oxygen and carbon dioxide alter cerebral blood flow and vascular tone mainly via constitutively formed NO. Endothelial dysfunction impairs cerebral hemodynamics by reducing the bioavailability of NO and increasing the production of reactive oxygen species (ROS). (aspetjournals.org)
  • Hypoxia and Ischemia are both diseases caused due to the insufficiency of oxygen supply in the body, but there is a difference between hypoxia and ischemia. (mcpcourse.com)
  • Ischemia is caused by problems with the circulatory system causing damage or dysfunction of oxygen sensitive tissues . (mcpcourse.com)
  • It causes a greater production of oxygen free radicals and reactive oxygen species that in turn damage cells and tissues. (mcpcourse.com)
  • Any organ of the body can get ischemia damage due to inadequate oxygen supply to meet the continuous demand for cellular metabolism. (mcpcourse.com)
  • Ischemia is damage or dysfunction of oxygen sensitive tissues due to reduction of blood supply. (mcpcourse.com)
  • However, oxygen sensitive tissues such as brain and heart may not recover unless the blood supply is restored rapidly. (mcpcourse.com)
  • February 04, 2016 Adityarup "Rup" Chakravorty, Waisman Communications Each year, thousands of newborn babies suffer complications during pregnancy or birth that deprive their brains of oxygen and nutrient-rich blood and result in brain injury. (wisc.edu)
  • The Ca 2+ -related activation of intracellular second messenger systems, the increase in reactive oxygen species formation, as well as hypoxia itself triggers the expression of a large number of pro-inflammatory genes following cerebral ischemia. (biomedcentral.com)
Protein10
  • 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)
  • The common cardiac biomarkers that are tested for CVD include troponin, creatine kinase-muscle/brain (CK-MB), B-type natriuretic peptide (BNP), high-sensitivity C-reactive protein (hs-CRP), and others. (alliedmarketresearch.com)
  • C-reactive protein (CRP) was mildly elevated at 1.3 mg/mL, and her vitamin D level and thyroid-stimulating hormone (TSH) were within normal limits. (aao.org)
  • 3 , 4 Inflammatory molecules including C-reactive protein and inerleukin-6 are elevated in blood years before dementia. (neurology.org)
  • Nalivaeva NN, Turner AJ (2013) The amyloid precursor protein: a biochemical enigma in brain development, function and disease. (springer.com)
  • Corrigan F, Thornton E, Roisman LC, Leonard AV, Vink R, Blumbergs PC (2014) The neuroprotective activity of the amyloid precursor protein against traumatic brain injury is mediated via the heparin binding site in residues 96-110. (springer.com)
  • Although there are many remaining uncertainties, this review highlights the idea that Best1 is a multifunctional protein, functioning as an anion channel with unique properties as well as a key regulator of various important brain functions. (en-journal.org)
  • Title: Up-regulation of NHE1 protein expression in reactive hippocampal astrocytes Legend: A.Expression of NHE1 protein in hippocampal astrocytes. (wisc.edu)
  • Thus, mediators of inflammation such as platelet-activating factor (PAF), tumor necrosis factor α (TNFα), interleukin 1β (IL-1β), chemokines (IL-8, monocyte chemoattractant protein-1) and other pro-inflammatory factors are produced by the ischemic brain tissue [ 3 ]. (biomedcentral.com)
  • Erythrocyte sedimentation rate and C-reactive protein are typically elevated. (msdmanuals.com)
Hypoxia20
  • Similar to cerebral hypoxia, severe or prolonged brain ischemia will result in unconsciousness, brain damage or death, mediated by the ischemic cascade. (wikipedia.org)
  • Hypoxia and ischemia of the brain are key pathophysiological mechanisms of ischemic stroke ( 5 , 6 ). (frontiersin.org)
  • Preterm Fetal Hypoxia-Ischemia Causes Hypertonia and Motor Deficits in the Neonatal Rabbit: A Model for Human Cerebral Palsy? (jneurosci.org)
  • Prenatal hypoxia-ischemia to the developing brain has been strongly implicated in the subsequent development of the hypertonic motor deficits of cerebral palsy (CP) in premature and full-term infants who present with neonatal encephalopathy. (jneurosci.org)
  • Antenatal hypoxia-ischemia at preterm gestation results in hypertonia and abnormalities in motor control. (jneurosci.org)
  • These findings provide a unique behavioral model to define mechanisms and sequelae of perinatal brain injury from antenatal hypoxia-ischemia. (jneurosci.org)
  • Hypoxia-ischemia (H-I) is also associated with subsequent cerebral injury in a disproportionately high percentage of the survivors of premature birth ( Volpe, 2001 ). (jneurosci.org)
  • Most previous studies have employed models of cerebral hypoxia-ischemia in postnatal animals. (jneurosci.org)
  • In the present study, a new neurobehavioral battery of tests was used to characterize the motor performance of newborn pups after sustained hypoxia-ischemia to the preterm rabbit fetus at 67-70% gestation. (jneurosci.org)
  • Cerebral ischemia was induced by two methods-transient bilateral common carotid artery occlusion (BCCAO) and permanent unilateral common carotid artery ligation with hypoxia (8% O2)-after which brains were treated (in the lateral ventricle or striatum) with doxycycline (DOX) in transgenic mice in which the four reprogramming factors were expressed by doxycycline. (yonsei.ac.kr)
  • 2009), but the ketogenic diet has been further shown to be neuroprotective in animal models of several central nervous system (CNS) disorders, including Alzheimer's disease (AD), Parkinson's disease, hypoxia, glutamate toxicity, ischemia, and traumatic brain injury (TBI) (see Prins, 2008, for a review). (nationalacademies.org)
  • They are consistent with our LPS-ischemia-hypoxia rat model that produces myelin aggregates that colocalize with Aβ and resemble amyloid-like plaques. (neurology.org)
  • N-acetylcysteine reduced the injury induced by hypoxia-ischemia in P3C-sensitized neonatal rats. (biomedcentral.com)
  • In the early stage of ischemia and hypoxia, cells will increase the energy supply to the ischemic area, especially the functional area of the ischemic penumbra, by regulating glycolysis. (ijpsonline.com)
  • Autophagy is a process that relies on lysosomal pathways for the degradation of cytoplasmic proteins and organelles and plays an important role in the pathology of brain injury such as hypoxia ischemia[ 3 ]. (ijpsonline.com)
  • Metabolomic analysis of carbohydrate and amino acid changes induced by hypoxia in naked mole-rat brain and liver Metabolites . (pamenterlab.ca)
  • Acute hypoxia alters extracellular vesicle signatures and the brain citrusllinome of naked mole-rats ( Heterocephalus glaber ). (pamenterlab.ca)
  • Astrogliosis following hypoxia-ischemia (HI) related brain injury plays a role in increased morbidity and mortality in neonates. (wisc.edu)
  • Title: Suppression of microglia activation after hypoxia-ischemia results in age-dependent improvements in neurologic injury. (wisc.edu)
  • Legend: P9 and P30 mice were exposed to unilateral hypoxia-ischemia and treated with minocycline or vehicle. (wisc.edu)
Traumatic brain10
  • Brain contusions commonly are identified in patients with traumatic brain injury (TBI) and represent regions of primary neuronal and vascular injury. (medscape.com)
  • Brain disease, especially ischemic stroke, epilepsy, and traumatic brain injury, triggers the dysregulation of ionic gradients and promotes the excessive release of neuro-transmitters and zinc. (bvsalud.org)
  • In this review, we summarize recent experimental research findings regarding how TRP channels (mainly TRPC and TRPM) and zinc are regulated in animal brain-disease models of global cerebral ischemia, epilepsy, and traumatic brain injury. (bvsalud.org)
  • Traumatic brain injury (TBI) causes transitory or permanent neurological and cognitive impairments, which can intensify over time due to secondary neuronal death. (bvsalud.org)
  • 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)
  • This implicates that tonic GABA release from reactive astrocyte via redistributed Best1 is a common phenomenon that occur in various pathological conditions with astrogliosis such as traumatic brain injury, neuroinflammation, neurodegeneration, and hypoxic and ischemic insults. (en-journal.org)
  • Adolescent traumatic brain injury (TBI) is a major public health concern, resulting in over 35,000 hospitalizations in the U.S. each year. (wisc.edu)
Astrocytes9
  • Reactive astrocytes prevent maladaptive plasticity after ischemic stroke. (gu.se)
  • Astrocytes, one of the most abundant cells in the brain, are activated by injury such as ischemia. (yonsei.ac.kr)
  • Reactive astrocytes, in particular, play a crucial role in recovery from brain injury. (yonsei.ac.kr)
  • That results showed that the astrocytes and neural progenitors were significantly proliferated, but not neurons or glial scar, and the condition of blood vessels in the injured brain was improved following in vivo reprogramming factor expression. (yonsei.ac.kr)
  • Taken together, newly generated astrocytes are essential for protecting neurons from damage following cerebral ischemia (BCCAO and HI mouse model) and for enhancing blood vessels. (yonsei.ac.kr)
  • These results show that a therapeutic potential of methods that aim to improve functional recovery by reducing reactive astrocytes (harmful A1 astrocytes) in BCCAO mouse models. (yonsei.ac.kr)
  • We found morphological change and change from astrocytes to reactive astroglia near the area of brain suffered from injury, infection, ischemia, and degenerative disease of neuron. (uni-leipzig.de)
  • Under pathological conditions such as neuroinflammation and neurodegeneration, reactive astrocytes phenotypically switch from GABA-negative to GABA-producing and redistribute Best1 from the perisynaptic microdomains to the soma and processes to tonically release GABA via Best1. (en-journal.org)
  • These properties of Best1, including the permeation and release of glutamate and GABA and its redistribution in reactive astrocytes, promise us exciting discoveries of novel brain functions to be uncovered in the future. (en-journal.org)
Result in ischemia2
  • citation needed] Blockage of arteries due to plaque buildup may also result in ischemia. (wikipedia.org)
  • Hemorrhage within the contusion can result in ischemia and edema, which can progress to tissue destruction, necrosis of neuronal structures, and cavitation with overlying reactive gliosis. (medscape.com)
Reducing the production of reactive1
  • This protective effect may be mediated by inhibiting the mitochondrial membrane permeability transition and reducing the production of reactive oxidative species in mitochondria. (nih.gov)
Stroke11
  • Other effects that may result from brain ischemia are stroke, cardiorespiratory arrest, and irreversible brain damage. (wikipedia.org)
  • citation needed] Other pathological events that may result in brain ischemia include cardiorespiratory arrest, stroke, and severe irreversible brain damage. (wikipedia.org)
  • Brain edema primarily occurs as a consequence of various cerebral injuries including ischemic stroke. (benthamscience.com)
  • Cerebral ischemia and stroke can lead incurable brain damage or death. (yonsei.ac.kr)
  • A hypoxic-ischemic (HI) model, a stroke model used in another experimental group, was used to compare efficacy of reprogrammed expression in two areas of the brain, the ventricle and striatum. (yonsei.ac.kr)
  • Excessive glutamate release resulting in excessive Ca +2 entry into cells is the excitotoxicity which initiates the brain ischemic damage seen in stroke and cardiac arrest. (benbest.com)
  • Recent studies on brain circulation provide quite useful information concerning the physiological roles of NO produced by constitutive isoforms of nitric-oxide synthase and how NO may promote cerebral pathogenesis under certain conditions, including cerebral ischemia/stroke, cerebral vasospasm after subarachnoid hemorrhage, and brain injury. (aspetjournals.org)
  • Astrocyte activation and reactive gliosis-A new target in stroke? (research.com)
  • His studies deal with areas such as Intermediate filament, Central nervous system, Stroke, Brain ischemia and Neuroplasticity as well as Homeostasis. (research.com)
  • Because prestroke blood glucose level, in contrast to post-stroke blood glucose level, did not have any predictive value concerning stroke outcome it is concluded that high fasting blood glucose values after stroke reflect a stress response to a more severe ischemic brain lesion. (docksci.com)
  • Thus, a crucial question concerning the association of post-stroke hyperglycemia and unfavourable prognosis is whether the high glucose values are the primary cause of more severe strokes or are they only a reflection, a stress response, of more severe strokes and brain lesions? (docksci.com)
Acute2
  • Although many authors use the term brain injury to mean acute traumatic damage to the central nervous system (CNS), others use the term head injury, which allows inclusion of skull injuries, fractures, or soft tissue damage to the face or head without any obvious neurologic consequences. (medscape.com)
  • These biomarkers act as a potential tool to detect various cardiovascular diseases (CVD) including cardiac ischemia, myocardial infarction, congestive heart failure, and acute coronary syndrome (ACS). (alliedmarketresearch.com)
Common carotid artery o1
  • 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)
Natriuretic peptide1
  • Cardiac biomarkers that are widely used as an integrated diagnostic approach for cardiovascular diseases (CVDs) include myocardial muscle creatine kinase (CK-MB), troponin I and T, myoglobin, brain natriuretic peptide (BNPs), ischemia modified albumin (IMA), and others. (alliedmarketresearch.com)
Mammalian2
  • In 1974, Hossmann and Zimmermann demonstrated that ischemia induced in mammalian brains for up to an hour can be at least partially recovered. (wikipedia.org)
  • However, it is now generally accepted that the mammalian brain may be more resistant to ischemia than previously thought. (biomedcentral.com)
Injury23
  • Several acquired lesions of the central nervous system (CNS) specifically affect infants born prematurely and result in long-term disability, including GM/IVH, periventricular white matter injury (eg, cystic periventricular leukomalacia [CPVL], periventricular hemorrhagic infarction [PVHI]), hemorrhage, and diffuse injury to the developing brain. (medscape.com)
  • Intraparenchymal hemorrhage is another type of brain injury that also occurs in this population and has similar risk factors and, possibly, pathophysiology to GM/IVH. (medscape.com)
  • Brain injury is often defined differently in published reports. (medscape.com)
  • Skull radiographs are notoriously unhelpful in predicting underlying brain injury. (medscape.com)
  • As such, the radiographic findings are usually associated with underlying brain contusions, although significant brain injury may occur without these findings. (medscape.com)
  • Hypoxic-ischemic brain injury results in cerebral palsy (CP), mental retardation, or learning disabilities in surviving children ( Robertson and Finer, 1985 ). (jneurosci.org)
  • In view of the major contribution of intrapartum risk factors and prematurity to subsequent neurological morbidity and mortality, studies are needed that address the underlying mechanisms of brain injury that occur in utero to the immature and near-term fetal CNS. (jneurosci.org)
  • Uterine ischemia in the dams resulted in a distinct neurobehavioral phenotype in the newborn pups, which was characterized by an increase in forelimb tone that was significantly correlated with histological evidence of persistent injury to subcortical motor pathways involving the basal ganglia and anterior thalamus. (jneurosci.org)
  • However, no therapy currently exists that can effectively treat brain injury following TBI. (bvsalud.org)
  • Numerous research efforts have sought to elucidate the function of trophic factors in neural development, maintenance of connections in the mature brain, and reparative processes after injury. (jneurosci.org)
  • 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)
  • Therefore, we speculate that purinergic receptors might play dualistic roles in response to EA effects treating inflammatory injury induced by ischemia. (biomedcentral.com)
  • Our previous studies have demonstrated that EA protects cerebral neural cells against inflammatory injury after cerebral ischemia, which appears at 24 h to 14 days after treatment. (biomedcentral.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)
  • 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)
  • 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)
  • 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)
  • Sun N, Wang H, Ma L, Lei P, Zhang Q (2016) Ghrelin attenuates brain injury in septic mice via PI3K/Akt signalling activation. (springer.com)
  • The use of antioxidant molecules have proved useful to protect the neonatal brain from injury. (biomedcentral.com)
  • Furthermore, Nrf2 activators were discovered to suppress HMGB1-induced inflammation and ROS-induced brain injury, as well as to minimise p38 MAPK overexpression, which can lower NF-kB expression. (digiwire.co.in)
  • Milos Pekny has included themes like Response to injury, Reactive Astrocyte and Disease in his Spinal cord pathology study. (research.com)
  • Recent clinical studies indicate that the severity of brain injury appears to be sex-dependent and that male neonates are more susceptible to the effects of HI resulting in worse neurological outcomes compared to females with comparable brain injuries. (wisc.edu)
  • Previous studies suggest that the cyclooxygenase-2 (COX-2) inhibitor nimesulide has a remarkable protective effect against different types of brain injury including ischemia. (biomedcentral.com)
Methods1
  • Methods: Remarkably, the expressions of GAP-43 and BDNF perfectly match in various neurons in the Human Brain Atlas database. (bvsalud.org)
Focal1
  • These data show that nimesulide protects against permanent focal cerebral ischemia, even with a 2 h post-treatment delay. (biomedcentral.com)
Mitochondria1
Oxidative stress1
  • Although adequate zinc is essential for regulating diverse physiological functions, the brain-disease-induced excessive release and translocation of zinc causes cell damage, including oxidative stress, apoptotic cascades, and disturbances in energy metabolism. (bvsalud.org)
Inflammation3
Astrogliosis1
Glutamate1
  • The most prominent feature of Best1 is its significant permeability to glutamate and GABA in addition to chloride ions because glutamate and GABA are important transmitters in the brain. (en-journal.org)
Hemorrhage2
  • The site of origin of germinal matrix/intraventricular hemorrhage (GM/IVH) is the subependymal germinal matrix, a region of the developing brain that regresses by term gestation. (medscape.com)
  • This molecule, formed by constitutive isomers of NO synthase, endothelial nitric-oxide synthase, and neuronal nitric-oxide synthase, plays pivotal roles in the regulation of cerebral blood flow and cell viability and in the protection of nerve cells or fibers against pathogenic factors associated with cerebral ischemia, trauma, and hemorrhage. (aspetjournals.org)
Neurons2
  • In the first minute after stoppage of blood flow to the brain, ATP in neurons is primarily regenerated from ADP by phosphate from PhosphoCreatine ( PCr ). (benbest.com)
  • Cerebral blood flow is increased and cerebral vascular resistance is decreased by NO derived from endothelial cells, autonomic nitrergic nerves, or brain neurons under resting and stimulated conditions. (aspetjournals.org)
Neuroprotective1
  • The blockade of zinc translocation via the inhibition of TRPC and TRPM channels using known channel antagonists, was shown to be neuroprotective in brain disease. (bvsalud.org)
Vasculitis1
  • Magnetic resonance imaging (MRI) of Ms. Culpepper's brain and orbits showed nonspecif-ic findings that possibly represented demyelinating disease, microvascular ischemia, or vasculitis. (aao.org)
Human brains1
  • We determined whether Gram-negative bacterial molecules are associated with Alzheimer disease (AD) neuropathology given that previous studies demonstrate Gram-negative Escherichia coli bacteria can form extracellular amyloid and Gram-negative bacteria have been reported as the predominant bacteria found in normal human brains. (neurology.org)
Vitro1
  • Area A will delineate the diagnostic potential of TSPO imaging by means of positron emission tomography (PET) in brain tumors in vivo and will enable the complementary characterization of brain tissue in vitro to delineate the neurobiological characteristics underlying TSPO PET labeling in the human brain. (uni-regensburg.de)
Tissue1
Extracellular1
  • Within two minutes of ischemia, extracellular pH can drop from about 7.3 to about 6.7. (benbest.com)
Metabolism2
  • Ischemia leads to alterations in brain metabolism, reduction in metabolic rates, and energy crisis. (wikipedia.org)
  • Among the several possibilities, e.g. micro- and macroangiopathy, hyperlipidemia and blood clotting disorders, the adverse effect of hyperglycemia on cerebral metabolism during ischemia have in the last decade been the focus of intensive research, both experimental Correspondence to: Karl Murros MD, Department of Neurology, Central Hospital of Central Finland, SF-40620 Jyviis~l[i, Finland. (docksci.com)
Neurological2
  • Here, we evaluate the therapeutic potential of irradiated engineered human mesenchymal stem cells over-expressing brain-derived neurotrophic factor (BDNF), which we denote by BDNF-eMSCs, in protecting the brain against neuronal death, neurological deficits, and cognitive impairment in TBI rats. (bvsalud.org)
  • 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)
Homeostasis1
  • Therefore, the regulation of zinc homeostasis following brain disease is critical for the prevention of brain damage. (bvsalud.org)
Therapeutic1
  • This raises the possibility of therapeutic intervention before brain damage has become irreversible. (biomedcentral.com)
Ischemic brain2
Middle cerebr1
Inflammatory1
  • We used multivariable linear regression to relate 10 log-transformed inflammatory biomarkers to brain MRI measures. (uthscsa.edu)
Blood-cerebro1
  • Because of its physical properties, honokiol can readily cross the blood brain barrier and the blood-cerebrospinal fluid barrier. (wikipedia.org)
Amyloid plaques2
  • Moreover, GAP-43 and BDNF are highly expressed in a healthy adults' hippocampus brain region and are inversely correlated with the amyloid beta (Aß), which is the pathological peptide of amyloid plaques found in the brains of patients with AD. (bvsalud.org)
  • LPS colocalized with Aβ 1-40/42 in amyloid plaques and with Aβ 1-40/42 around vessels in AD brains. (neurology.org)
Mild1
Pathological1
  • AQP4 is prevalently distributed in the central nervous system, and mainly regulates water flux in brain cells under normal and pathological conditions. (benthamscience.com)
Mice1
  • Tumor development was not observed in the lateral ventricle-targeted group, but the striatum-targeted group showed that abnormal cell proliferation in DOX-100 treated mice brain. (yonsei.ac.kr)
Plasticity1
  • Brain-derived neurotrophic factor (BDNF) is closely related to neurodegeneration and synaptic plasticity during the aging process. (bvsalud.org)
Findings2
  • [ 24 ] Imaging findings in brain contusions tend to vary because of the stages of evolution common to these lesions. (medscape.com)
  • Initially, CT findings can be normal or minimally abnormal because the partial volumes between the dense microhemorrhages and the hypodense edema can render contusions isoattenuating relative to the surrounding brain. (medscape.com)
Heart attacks2
Tissues2
  • Although TSPO is particularly abundant in steroid producing tissues it can be found substantially also in the brain, liver, heart and the immune system. (uni-regensburg.de)
  • Best1 is known to be expressed in a variety of tissues including the brain, and is thought to be involved in many physiological processes. (en-journal.org)