Localized reduction of blood flow to brain tissue due to arterial obstruction or systemic hypoperfusion. This frequently occurs in conjunction with brain hypoxia (HYPOXIA, BRAIN). Prolonged ischemia is associated with BRAIN INFARCTION.
A hypoperfusion of the BLOOD through an organ or tissue caused by a PATHOLOGIC CONSTRICTION or obstruction of its BLOOD VESSELS, or an absence of BLOOD CIRCULATION.
A disorder of cardiac function caused by insufficient blood flow to the muscle tissue of the heart. The decreased blood flow may be due to narrowing of the coronary arteries (CORONARY ARTERY DISEASE), to obstruction by a thrombus (CORONARY THROMBOSIS), or less commonly, to diffuse narrowing of arterioles and other small vessels within the heart. Severe interruption of the blood supply to the myocardial tissue may result in necrosis of cardiac muscle (MYOCARDIAL INFARCTION).
Restoration of blood supply to tissue which is ischemic due to decrease in normal blood supply. The decrease may result from any source including atherosclerotic obstruction, narrowing of the artery, or surgical clamping. It is primarily a procedure for treating infarction or other ischemia, by enabling viable ischemic tissue to recover, thus limiting further necrosis. However, it is thought that reperfusion can itself further damage the ischemic tissue, causing REPERFUSION INJURY.
Brief reversible episodes of focal, nonconvulsive ischemic dysfunction of the brain having a duration of less than 24 hours, and usually less than one hour, caused by transient thrombotic or embolic blood vessel occlusion or stenosis. Events may be classified by arterial distribution, temporal pattern, or etiology (e.g., embolic vs. thrombotic). (From Adams et al., Principles of Neurology, 6th ed, pp814-6)
Adverse functional, metabolic, or structural changes in ischemic tissues resulting from the restoration of blood flow to the tissue (REPERFUSION), including swelling; HEMORRHAGE; NECROSIS; and damage from FREE RADICALS. The most common instance is MYOCARDIAL REPERFUSION INJURY.
A subfamily of the Muridae consisting of several genera including Gerbillus, Rhombomys, Tatera, Meriones, and Psammomys.
The part of CENTRAL NERVOUS SYSTEM that is contained within the skull (CRANIUM). Arising from the NEURAL TUBE, the embryonic brain is comprised of three major parts including PROSENCEPHALON (the forebrain); MESENCEPHALON (the midbrain); and RHOMBENCEPHALON (the hindbrain). The developed brain consists of CEREBRUM; CEREBELLUM; and other structures in the BRAIN STEM.
Drugs intended to prevent damage to the brain or spinal cord from ischemia, stroke, convulsions, or trauma. Some must be administered before the event, but others may be effective for some time after. They act by a variety of mechanisms, but often directly or indirectly minimize the damage produced by endogenous excitatory amino acids.
NECROSIS occurring in the MIDDLE CEREBRAL ARTERY distribution system which brings blood to the entire lateral aspects of each CEREBRAL HEMISPHERE. Clinical signs include impaired cognition; APHASIA; AGRAPHIA; weak and numbness in the face and arms, contralaterally or bilaterally depending on the infarction.
Changes in the amounts of various chemicals (neurotransmitters, receptors, enzymes, and other metabolites) specific to the area of the central nervous system contained within the head. These are monitored over time, during sensory stimulation, or under different disease states.
Tissue NECROSIS in any area of the brain, including the CEREBRAL HEMISPHERES, the CEREBELLUM, and the BRAIN STEM. Brain infarction is the result of a cascade of events initiated by inadequate blood flow through the brain that is followed by HYPOXIA and HYPOGLYCEMIA in brain tissue. Damage may be temporary, permanent, selective or pan-necrosis.
Acute and chronic (see also BRAIN INJURIES, CHRONIC) injuries to the brain, including the cerebral hemispheres, CEREBELLUM, and BRAIN STEM. Clinical manifestations depend on the nature of injury. Diffuse trauma to the brain is frequently associated with DIFFUSE AXONAL INJURY or COMA, POST-TRAUMATIC. Localized injuries may be associated with NEUROBEHAVIORAL MANIFESTATIONS; HEMIPARESIS, or other focal neurologic deficits.
Increased intracellular or extracellular fluid in brain tissue. Cytotoxic brain edema (swelling due to increased intracellular fluid) is indicative of a disturbance in cell metabolism, and is commonly associated with hypoxic or ischemic injuries (see HYPOXIA, BRAIN). An increase in extracellular fluid may be caused by increased brain capillary permeability (vasogenic edema), an osmotic gradient, local blockages in interstitial fluid pathways, or by obstruction of CSF flow (e.g., obstructive HYDROCEPHALUS). (From Childs Nerv Syst 1992 Sep; 8(6):301-6)
A strain of albino rat used widely for experimental purposes because of its calmness and ease of handling. It was developed by the Sprague-Dawley Animal Company.
A technique in which tissue is rendered resistant to the deleterious effects of prolonged ISCHEMIA and REPERFUSION by prior exposure to brief, repeated periods of vascular occlusion. (Am J Physiol 1995 May;268(5 Pt 2):H2063-7, Abstract)
Naturally occurring or experimentally induced animal diseases with pathological processes sufficiently similar to those of human diseases. They are used as study models for human diseases.
The circulation of blood through the BLOOD VESSELS of the BRAIN.
A strain of albino rat developed at the Wistar Institute that has spread widely at other institutions. This has markedly diluted the original strain.
The formation of an area of NECROSIS in the CEREBRUM caused by an insufficiency of arterial or venous blood flow. Infarcts of the cerebrum are generally classified by hemisphere (i.e., left vs. right), lobe (e.g., frontal lobe infarction), arterial distribution (e.g., INFARCTION, ANTERIOR CEREBRAL ARTERY), and etiology (e.g., embolic infarction).
The thin layer of GRAY MATTER on the surface of the CEREBRAL HEMISPHERES that develops from the TELENCEPHALON and folds into gyri and sulchi. It reaches its highest development in humans and is responsible for intellectual faculties and higher mental functions.
The basic cellular units of nervous tissue. Each neuron consists of a body, an axon, and dendrites. Their purpose is to receive, conduct, and transmit impulses in the NERVOUS SYSTEM.
Elements of limited time intervals, contributing to particular results or situations.
Neoplasms of the intracranial components of the central nervous system, including the cerebral hemispheres, basal ganglia, hypothalamus, thalamus, brain stem, and cerebellum. Brain neoplasms are subdivided into primary (originating from brain tissue) and secondary (i.e., metastatic) forms. Primary neoplasms are subdivided into benign and malignant forms. In general, brain tumors may also be classified by age of onset, histologic type, or presenting location in the brain.
A curved elevation of GRAY MATTER extending the entire length of the floor of the TEMPORAL HORN of the LATERAL VENTRICLE (see also TEMPORAL LOBE). The hippocampus proper, subiculum, and DENTATE GYRUS constitute the hippocampal formation. Sometimes authors include the ENTORHINAL CORTEX in the hippocampal formation.
A disorder characterized by a reduction of oxygen in the blood combined with reduced blood flow (ISCHEMIA) to the brain from a localized obstruction of a cerebral artery or from systemic hypoperfusion. Prolonged hypoxia-ischemia is associated with ISCHEMIC ATTACK, TRANSIENT; BRAIN INFARCTION; BRAIN EDEMA; COMA; and other conditions.
The largest of the cerebral arteries. It trifurcates into temporal, frontal, and parietal branches supplying blood to most of the parenchyma of these lobes in the CEREBRAL CORTEX. These are the areas involved in motor, sensory, and speech activities.
A plant genus of the family MENISPERMACEAE. Members contain dauricine and other ALKALOIDS.
Imaging techniques used to colocalize sites of brain functions or physiological activity with brain structures.
A reduction in brain oxygen supply due to ANOXEMIA (a reduced amount of oxygen being carried in the blood by HEMOGLOBIN), or to a restriction of the blood supply to the brain, or both. Severe hypoxia is referred to as anoxia, and is a relatively common cause of injury to the central nervous system. Prolonged brain anoxia may lead to BRAIN DEATH or a PERSISTENT VEGETATIVE STATE. Histologically, this condition is characterized by neuronal loss which is most prominent in the HIPPOCAMPUS; GLOBUS PALLIDUS; CEREBELLUM; and inferior olives.
Abnormally low BODY TEMPERATURE that is intentionally induced in warm-blooded animals by artificial means. In humans, mild or moderate hypothermia has been used to reduce tissue damages, particularly after cardiac or spinal cord injuries and during subsequent surgeries.
The termination of the cell's ability to carry out vital functions such as metabolism, growth, reproduction, responsiveness, and adaptability.
Specialized non-fenestrated tightly-joined ENDOTHELIAL CELLS with TIGHT JUNCTIONS that form a transport barrier for certain substances between the cerebral capillaries and the BRAIN tissue.
Non-invasive method of demonstrating internal anatomy based on the principle that atomic nuclei in a strong magnetic field absorb pulses of radiofrequency energy and emit them as radiowaves which can be reconstructed into computerized images. The concept includes proton spin tomographic techniques.
A group of pathological conditions characterized by sudden, non-convulsive loss of neurological function due to BRAIN ISCHEMIA or INTRACRANIAL HEMORRHAGES. Stroke is classified by the type of tissue NECROSIS, such as the anatomic location, vasculature involved, etiology, age of the affected individual, and hemorrhagic vs. non-hemorrhagic nature. (From Adams et al., Principles of Neurology, 6th ed, pp777-810)
Damage to the MYOCARDIUM resulting from MYOCARDIAL REPERFUSION (restoration of blood flow to ischemic areas of the HEART.) Reperfusion takes place when there is spontaneous thrombolysis, THROMBOLYTIC THERAPY, collateral flow from other coronary vascular beds, or reversal of vasospasm.
The country is bordered by RUSSIA on the north and CHINA on the west, south, and east. The capita is Ulaanbaatar.
A partial or complete return to the normal or proper physiologic activity of an organ or part following disease or trauma.
A tissue or organ remaining at physiological temperature during decreased BLOOD perfusion or in the absence of blood supply. During ORGAN TRANSPLANTATION it begins when the organ reaches physiological temperature before the completion of SURGICAL ANASTOMOSIS and ends with reestablishment of the BLOOD CIRCULATION through the tissue.
Pathological processes which result in the partial or complete obstruction of ARTERIES. They are characterized by greatly reduced or absence of blood flow through these vessels. They are also known as arterial insufficiency.
A class of large neuroglial (macroglial) cells in the central nervous system - the largest and most numerous neuroglial cells in the brain and spinal cord. Astrocytes (from "star" cells) are irregularly shaped with many long processes, including those with "end feet" which form the glial (limiting) membrane and directly and indirectly contribute to the BLOOD-BRAIN BARRIER. They regulate the extracellular ionic and chemical environment, and "reactive astrocytes" (along with MICROGLIA) respond to injury.
An opioid analgesic with actions and uses similar to MORPHINE. (From Martindale, The Extra Pharmacopoeia, 30th ed, p1095)
A non-essential amino acid naturally occurring in the L-form. Glutamic acid is the most common excitatory neurotransmitter in the CENTRAL NERVOUS SYSTEM.
The arterial blood vessels supplying the CEREBRUM.
A spectrum of pathological conditions of impaired blood flow in the brain. They can involve vessels (ARTERIES or VEINS) in the CEREBRUM, the CEREBELLUM, and the BRAIN STEM. Major categories include INTRACRANIAL ARTERIOVENOUS MALFORMATIONS; BRAIN ISCHEMIA; CEREBRAL HEMORRHAGE; and others.
An element with atomic symbol O, atomic number 8, and atomic weight [15.99903; 15.99977]. It is the most abundant element on earth and essential for respiration.
Histochemical localization of immunoreactive substances using labeled antibodies as reagents.
Genetically identical individuals developed from brother and sister matings which have been carried out for twenty or more generations or by parent x offspring matings carried out with certain restrictions. This also includes animals with a long history of closed colony breeding.
The part of the brain that connects the CEREBRAL HEMISPHERES with the SPINAL CORD. It consists of the MESENCEPHALON; PONS; and MEDULLA OBLONGATA.
Striped GRAY MATTER and WHITE MATTER consisting of the NEOSTRIATUM and paleostriatum (GLOBUS PALLIDUS). It is located in front of and lateral to the THALAMUS in each cerebral hemisphere. The gray substance is made up of the CAUDATE NUCLEUS and the lentiform nucleus (the latter consisting of the GLOBUS PALLIDUS and PUTAMEN). The WHITE MATTER is the INTERNAL CAPSULE.
A strain of Rattus norvegicus with elevated blood pressure used as a model for studying hypertension and stroke.
Tungsten hydroxide oxide phosphate. A white or slightly yellowish-green, slightly efflorescent crystal or crystalline powder. It is used as a reagent for alkaloids and many other nitrogen bases, for phenols, albumin, peptone, amino acids, uric acid, urea, blood, and carbohydrates. (From Merck Index, 11th ed)
A statistical technique that isolates and assesses the contributions of categorical independent variables to variation in the mean of a continuous dependent variable.
The chilling of a tissue or organ during decreased BLOOD perfusion or in the absence of blood supply. Cold ischemia time during ORGAN TRANSPLANTATION begins when the organ is cooled with a cold perfusion solution after ORGAN PROCUREMENT surgery, and ends after the tissue reaches physiological temperature during implantation procedures.
The pathological process occurring in cells that are dying from irreparable injuries. It is caused by the progressive, uncontrolled action of degradative ENZYMES, leading to MITOCHONDRIAL SWELLING, nuclear flocculation, and cell lysis. It is distinct it from APOPTOSIS, which is a normal, regulated cellular process.
Carbamates in which the -CO- group has been replaced by a -CS- group.
A condition of decreased oxygen content at the cellular level.
Loss of functional activity and trophic degeneration of nerve axons and their terminal arborizations following the destruction of their cells of origin or interruption of their continuity with these cells. The pathology is characteristic of neurodegenerative diseases. Often the process of nerve degeneration is studied in research on neuroanatomical localization and correlation of the neurophysiology of neural pathways.
An intermediate filament protein found only in glial cells or cells of glial origin. MW 51,000.
The measure of the level of heat of a human or animal.
A barbiturate that is administered intravenously for the induction of general anesthesia or for the production of complete anesthesia of short duration.
Cells propagated in vitro in special media conducive to their growth. Cultured cells are used to study developmental, morphologic, metabolic, physiologic, and genetic processes, among others.
Identification of proteins or peptides that have been electrophoretically separated by blot transferring from the electrophoresis gel to strips of nitrocellulose paper, followed by labeling with antibody probes.
Reduced blood flow to the spinal cord which is supplied by the anterior spinal artery and the paired posterior spinal arteries. This condition may be associated with ARTERIOSCLEROSIS, trauma, emboli, diseases of the aorta, and other disorders. Prolonged ischemia may lead to INFARCTION of spinal cord tissue.
Strains of mice in which certain GENES of their GENOMES have been disrupted, or "knocked-out". To produce knockouts, using RECOMBINANT DNA technology, the normal DNA sequence of the gene being studied is altered to prevent synthesis of a normal gene product. Cloned cells in which this DNA alteration is successful are then injected into mouse EMBRYOS to produce chimeric mice. The chimeric mice are then bred to yield a strain in which all the cells of the mouse contain the disrupted gene. Knockout mice are used as EXPERIMENTAL ANIMAL MODELS for diseases (DISEASE MODELS, ANIMAL) and to clarify the functions of the genes.
The muscle tissue of the HEART. It is composed of striated, involuntary muscle cells (MYOCYTES, CARDIAC) connected to form the contractile pump to generate blood flow.
Assessment of sensory and motor responses and reflexes that is used to determine impairment of the nervous system.
A species of SWINE, in the family Suidae, comprising a number of subspecies including the domestic pig Sus scrofa domestica.
A primary source of energy for living organisms. It is naturally occurring and is found in fruits and other parts of plants in its free state. It is used therapeutically in fluid and nutrient replacement.
RNA sequences that serve as templates for protein synthesis. Bacterial mRNAs are generally primary transcripts in that they do not require post-transcriptional processing. Eukaryotic mRNA is synthesized in the nucleus and must be exported to the cytoplasm for translation. Most eukaryotic mRNAs have a sequence of polyadenylic acid at the 3' end, referred to as the poly(A) tail. The function of this tail is not known for certain, but it may play a role in the export of mature mRNA from the nucleus as well as in helping stabilize some mRNA molecules by retarding their degradation in the cytoplasm.
Refers to animals in the period of time just after birth.
Disease having a short and relatively severe course.
Inflammation of the BRAIN due to infection, autoimmune processes, toxins, and other conditions. Viral infections (see ENCEPHALITIS, VIRAL) are a relatively frequent cause of this condition.
One of the mechanisms by which CELL DEATH occurs (compare with NECROSIS and AUTOPHAGOCYTOSIS). Apoptosis is the mechanism responsible for the physiological deletion of cells and appears to be intrinsically programmed. It is characterized by distinctive morphologic changes in the nucleus and cytoplasm, chromatin cleavage at regularly spaced sites, and the endonucleolytic cleavage of genomic DNA; (DNA FRAGMENTATION); at internucleosomal sites. This mode of cell death serves as a balance to mitosis in regulating the size of animal tissues and in mediating pathologic processes associated with tumor growth.
Recording of electric currents developed in the brain by means of electrodes applied to the scalp, to the surface of the brain, or placed within the substance of the brain.
The third type of glial cell, along with astrocytes and oligodendrocytes (which together form the macroglia). Microglia vary in appearance depending on developmental stage, functional state, and anatomical location; subtype terms include ramified, perivascular, ameboid, resting, and activated. Microglia clearly are capable of phagocytosis and play an important role in a wide spectrum of neuropathologies. They have also been suggested to act in several other roles including in secretion (e.g., of cytokines and neural growth factors), in immunological processing (e.g., antigen presentation), and in central nervous system development and remodeling.
The observable response an animal makes to any situation.
Salts or esters of LACTIC ACID containing the general formula CH3CHOHCOOR.
Exposure of myocardial tissue to brief, repeated periods of vascular occlusion in order to render the myocardium resistant to the deleterious effects of ISCHEMIA or REPERFUSION. The period of pre-exposure and the number of times the tissue is exposed to ischemia and reperfusion vary, the average being 3 to 5 minutes.
One of four subsections of the hippocampus described by Lorente de No, located furthest from the DENTATE GYRUS.
The relationship between the dose of an administered drug and the response of the organism to the drug.
A circumscribed collection of purulent exudate in the brain, due to bacterial and other infections. The majority are caused by spread of infected material from a focus of suppuration elsewhere in the body, notably the PARANASAL SINUSES, middle ear (see EAR, MIDDLE); HEART (see also ENDOCARDITIS, BACTERIAL), and LUNG. Penetrating CRANIOCEREBRAL TRAUMA and NEUROSURGICAL PROCEDURES may also be associated with this condition. Clinical manifestations include HEADACHE; SEIZURES; focal neurologic deficits; and alterations of consciousness. (Adams et al., Principles of Neurology, 6th ed, pp712-6)
Embolism or thrombosis involving blood vessels which supply intracranial structures. Emboli may originate from extracranial or intracranial sources. Thrombosis may occur in arterial or venous structures.
A class of ionotropic glutamate receptors characterized by affinity for N-methyl-D-aspartate. NMDA receptors have an allosteric binding site for glycine which must be occupied for the channel to open efficiently and a site within the channel itself to which magnesium ions bind in a voltage-dependent manner. The positive voltage dependence of channel conductance and the high permeability of the conducting channel to calcium ions (as well as to monovalent cations) are important in excitotoxicity and neuronal plasticity.
An outbred strain of rats developed in 1915 by crossing several Wistar Institute white females with a wild gray male. Inbred strains have been derived from this original outbred strain, including Long-Evans cinnamon rats (RATS, INBRED LEC) and Otsuka-Long-Evans-Tokushima Fatty rats (RATS, INBRED OLETF), which are models for Wilson's disease and non-insulin dependent diabetes mellitus, respectively.
A family of proton-gated sodium channels that are primarily expressed in neuronal tissue. They are AMILORIDE-sensitive and are implicated in the signaling of a variety of neurological stimuli, most notably that of pain in response to acidic conditions.
An in situ method for detecting areas of DNA which are nicked during APOPTOSIS. Terminal deoxynucleotidyl transferase is used to add labeled dUTP, in a template-independent manner, to the 3 prime OH ends of either single- or double-stranded DNA. The terminal deoxynucleotidyl transferase nick end labeling, or TUNEL, assay labels apoptosis on a single-cell level, making it more sensitive than agarose gel electrophoresis for analysis of DNA FRAGMENTATION.
A process involving chance used in therapeutic trials or other research endeavor for allocating experimental subjects, human or animal, between treatment and control groups, or among treatment groups. It may also apply to experiments on inanimate objects.
Naturally occurring or synthetic substances that inhibit or retard the oxidation of a substance to which it is added. They counteract the harmful and damaging effects of oxidation in animal tissues.
Diseases of the central and peripheral nervous system. This includes disorders of the brain, spinal cord, cranial nerves, peripheral nerves, nerve roots, autonomic nervous system, neuromuscular junction, and muscle.
Cessation of heart beat or MYOCARDIAL CONTRACTION. If it is treated within a few minutes, heart arrest can be reversed in most cases to normal cardiac rhythm and effective circulation.
Generally, restoration of blood supply to heart tissue which is ischemic due to decrease in normal blood supply. The decrease may result from any source including atherosclerotic obstruction, narrowing of the artery, or surgical clamping. Reperfusion can be induced to treat ischemia. Methods include chemical dissolution of an occluding thrombus, administration of vasodilator drugs, angioplasty, catheterization, and artery bypass graft surgery. However, it is thought that reperfusion can itself further damage the ischemic tissue, causing MYOCARDIAL REPERFUSION INJURY.
A non-invasive technique using ultrasound for the measurement of cerebrovascular hemodynamics, particularly cerebral blood flow velocity and cerebral collateral flow. With a high-intensity, low-frequency pulse probe, the intracranial arteries may be studied transtemporally, transorbitally, or from below the foramen magnum.
A stable, non-explosive inhalation anesthetic, relatively free from significant side effects.
The span of viability of a cell characterized by the capacity to perform certain functions such as metabolism, growth, reproduction, some form of responsiveness, and adaptability.
A disturbance in the prooxidant-antioxidant balance in favor of the former, leading to potential damage. Indicators of oxidative stress include damaged DNA bases, protein oxidation products, and lipid peroxidation products (Sies, Oxidative Stress, 1991, pxv-xvi).
The number of CELLS of a specific kind, usually measured per unit volume or area of sample.
Blocking of a blood vessel in the SKULL by an EMBOLUS which can be a blood clot (THROMBUS) or other undissolved material in the blood stream. Most emboli are of cardiac origin and are associated with HEART DISEASES. Other non-cardiac sources of emboli are usually associated with VASCULAR DISEASES.
A diagnostic technique that incorporates the measurement of molecular diffusion (such as water or metabolites) for tissue assessment by MRI. The degree of molecular movement can be measured by changes of apparent diffusion coefficient (ADC) with time, as reflected by tissue microstructure. Diffusion MRI has been used to study BRAIN ISCHEMIA and tumor response to treatment.
Any of the processes by which nuclear, cytoplasmic, or intercellular factors influence the differential control (induction or repression) of gene action at the level of transcription or translation.
A proteolytic enzyme in the serine protease family found in many tissues which converts PLASMINOGEN to FIBRINOLYSIN. It has fibrin-binding activity and is immunologically different from UROKINASE-TYPE PLASMINOGEN ACTIVATOR. The primary sequence, composed of 527 amino acids, is identical in both the naturally occurring and synthetic proteases.
A condition characterized by long-standing brain dysfunction or damage, usually of three months duration or longer. Potential etiologies include BRAIN INFARCTION; certain NEURODEGENERATIVE DISORDERS; CRANIOCEREBRAL TRAUMA; ANOXIA, BRAIN; ENCEPHALITIS; certain NEUROTOXICITY SYNDROMES; metabolic disorders (see BRAIN DISEASES, METABOLIC); and other conditions.
A basic element found in nearly all organized tissues. It is a member of the alkaline earth family of metals with the atomic symbol Ca, atomic number 20, and atomic weight 40. Calcium is the most abundant mineral in the body and combines with phosphorus to form calcium phosphate in the bones and teeth. It is essential for the normal functioning of nerves and muscles and plays a role in blood coagulation (as factor IV) and in many enzymatic processes.
The rate at which oxygen is used by a tissue; microliters of oxygen STPD used per milligram of tissue per hour; the rate at which oxygen enters the blood from alveolar gas, equal in the steady state to the consumption of oxygen by tissue metabolism throughout the body. (Stedman, 25th ed, p346)
Clinical or subclinical disturbances of cortical function due to a sudden, abnormal, excessive, and disorganized discharge of brain cells. Clinical manifestations include abnormal motor, sensory and psychic phenomena. Recurrent seizures are usually referred to as EPILEPSY or "seizure disorder."
A galectin found abundantly in smooth muscle (MUSCLE, SMOOTH) and SKELETAL MUSCLE and many other tissues. It occurs as a homodimer with two 14-kDa subunits.
Laboratory mice that have been produced from a genetically manipulated EGG or EMBRYO, MAMMALIAN.
The circulation of blood through the CORONARY VESSELS of the HEART.
A positive regulatory effect on physiological processes at the molecular, cellular, or systemic level. At the molecular level, the major regulatory sites include membrane receptors, genes (GENE EXPRESSION REGULATION), mRNAs (RNA, MESSENGER), and proteins.
Semiautonomous, self-reproducing organelles that occur in the cytoplasm of all cells of most, but not all, eukaryotes. Each mitochondrion is surrounded by a double limiting membrane. The inner membrane is highly invaginated, and its projections are called cristae. Mitochondria are the sites of the reactions of oxidative phosphorylation, which result in the formation of ATP. They contain distinctive RIBOSOMES, transfer RNAs (RNA, TRANSFER); AMINO ACYL T RNA SYNTHETASES; and elongation and termination factors. Mitochondria depend upon genes within the nucleus of the cells in which they reside for many essential messenger RNAs (RNA, MESSENGER). Mitochondria are believed to have arisen from aerobic bacteria that established a symbiotic relationship with primitive protoeukaryotes. (King & Stansfield, A Dictionary of Genetics, 4th ed)
Either of two extremities of four-footed non-primate land animals. It usually consists of a FEMUR; TIBIA; and FIBULA; tarsals; METATARSALS; and TOES. (From Storer et al., General Zoology, 6th ed, p73)
The intracellular transfer of information (biological activation/inhibition) through a signal pathway. In each signal transduction system, an activation/inhibition signal from a biologically active molecule (hormone, neurotransmitter) is mediated via the coupling of a receptor/enzyme to a second messenger system or to an ion channel. Signal transduction plays an important role in activating cellular functions, cell differentiation, and cell proliferation. Examples of signal transduction systems are the GAMMA-AMINOBUTYRIC ACID-postsynaptic receptor-calcium ion channel system, the receptor-mediated T-cell activation pathway, and the receptor-mediated activation of phospholipases. Those coupled to membrane depolarization or intracellular release of calcium include the receptor-mediated activation of cytotoxic functions in granulocytes and the synaptic potentiation of protein kinase activation. Some signal transduction pathways may be part of larger signal transduction pathways; for example, protein kinase activation is part of the platelet activation signal pathway.
Fibrinolysin or agents that convert plasminogen to FIBRINOLYSIN.
The hollow, muscular organ that maintains the circulation of the blood.
The phenotypic manifestation of a gene or genes by the processes of GENETIC TRANSCRIPTION and GENETIC TRANSLATION.
Treatment process involving the injection of fluid into an organ or tissue.
Use of infusions of FIBRINOLYTIC AGENTS to destroy or dissolve thrombi in blood vessels or bypass grafts.
The introduction of a phosphoryl group into a compound through the formation of an ester bond between the compound and a phosphorus moiety.
The domestic dog, Canis familiaris, comprising about 400 breeds, of the carnivore family CANIDAE. They are worldwide in distribution and live in association with people. (Walker's Mammals of the World, 5th ed, p1065)
Either of the two principal arteries on both sides of the neck that supply blood to the head and neck; each divides into two branches, the internal carotid artery and the external carotid artery.
Abnormally high BLOOD GLUCOSE level.
Projection neurons in the CEREBRAL CORTEX and the HIPPOCAMPUS. Pyramidal cells have a pyramid-shaped soma with the apex and an apical dendrite pointed toward the pial surface and other dendrites and an axon emerging from the base. The axons may have local collaterals but also project outside their cortical region.
The movement and the forces involved in the movement of the blood through the CARDIOVASCULAR SYSTEM.
The anterior of the three primitive cerebral vesicles of the embryonic brain arising from the NEURAL TUBE. It subdivides to form DIENCEPHALON and TELENCEPHALON. (Stedmans Medical Dictionary, 27th ed)
NECROSIS of the MYOCARDIUM caused by an obstruction of the blood supply to the heart (CORONARY CIRCULATION).
The normality of a solution with respect to HYDROGEN ions; H+. It is related to acidity measurements in most cases by pH = log 1/2[1/(H+)], where (H+) is the hydrogen ion concentration in gram equivalents per liter of solution. (McGraw-Hill Dictionary of Scientific and Technical Terms, 6th ed)
A pathological process characterized by injury or destruction of tissues caused by a variety of cytologic and chemical reactions. It is usually manifested by typical signs of pain, heat, redness, swelling, and loss of function.
The physical activity of a human or an animal as a behavioral phenomenon.
An imbalance between myocardial functional requirements and the capacity of the CORONARY VESSELS to supply sufficient blood flow. It is a form of MYOCARDIAL ISCHEMIA (insufficient blood supply to the heart muscle) caused by a decreased capacity of the coronary vessels.
A technique of inputting two-dimensional images into a computer and then enhancing or analyzing the imagery into a form that is more useful to the human observer.
The act of constricting.
Components of a cell produced by various separation techniques which, though they disrupt the delicate anatomy of a cell, preserve the structure and physiology of its functioning constituents for biochemical and ultrastructural analysis. (From Alberts et al., Molecular Biology of the Cell, 2d ed, p163)
Agents that have a strengthening effect on the heart or that can increase cardiac output. They may be CARDIAC GLYCOSIDES; SYMPATHOMIMETICS; or other drugs. They are used after MYOCARDIAL INFARCT; CARDIAC SURGICAL PROCEDURES; in SHOCK; or in congestive heart failure (HEART FAILURE).
The species Oryctolagus cuniculus, in the family Leporidae, order LAGOMORPHA. Rabbits are born in burrows, furless, and with eyes and ears closed. In contrast with HARES, rabbits have 22 chromosome pairs.
The flow of BLOOD through or around an organ or region of the body.
Obstruction of the flow in the SPLANCHNIC CIRCULATION by ATHEROSCLEROSIS; EMBOLISM; THROMBOSIS; STENOSIS; TRAUMA; and compression or intrinsic pressure from adjacent tumors. Rare causes are drugs, intestinal parasites, and vascular immunoinflammatory diseases such as PERIARTERITIS NODOSA and THROMBOANGIITIS OBLITERANS. (From Juergens et al., Peripheral Vascular Diseases, 5th ed, pp295-6)
Accumulation of a drug or chemical substance in various organs (including those not relevant to its pharmacologic or therapeutic action). This distribution depends on the blood flow or perfusion rate of the organ, the ability of the drug to penetrate organ membranes, tissue specificity, protein binding. The distribution is usually expressed as tissue to plasma ratios.
Conversion of an inactive form of an enzyme to one possessing metabolic activity. It includes 1, activation by ions (activators); 2, activation by cofactors (coenzymes); and 3, conversion of an enzyme precursor (proenzyme or zymogen) to an active enzyme.
Recording of the moment-to-moment electromotive forces of the HEART as projected onto various sites on the body's surface, delineated as a scalar function of time. The recording is monitored by a tracing on slow moving chart paper or by observing it on a cardioscope, which is a CATHODE RAY TUBE DISPLAY.
Contractile activity of the MYOCARDIUM.
Therapy for MOVEMENT DISORDERS, especially PARKINSON DISEASE, that applies electricity via stereotactic implantation of ELECTRODES in specific areas of the BRAIN such as the THALAMUS. The electrodes are attached to a neurostimulator placed subcutaneously.
The inferior part of the lower extremity between the KNEE and the ANKLE.
Evaluation undertaken to assess the results or consequences of management and procedures used in combating disease in order to determine the efficacy, effectiveness, safety, and practicability of these interventions in individual cases or series.
Controlled physical activity which is performed in order to allow assessment of physiological functions, particularly cardiovascular and pulmonary, but also aerobic capacity. Maximal (most intense) exercise is usually required but submaximal exercise is also used.
The region of the lower limb in animals, extending from the gluteal region to the FOOT, and including the BUTTOCKS; HIP; and LEG.
A normal intermediate in the fermentation (oxidation, metabolism) of sugar. The concentrated form is used internally to prevent gastrointestinal fermentation. (From Stedman, 26th ed)
An endogenous substance found mainly in skeletal muscle of vertebrates. It has been tried in the treatment of cardiac disorders and has been added to cardioplegic solutions. (Reynolds JEF(Ed): Martindale: The Extra Pharmacopoeia (electronic version). Micromedex, Inc, Englewood, CO, 1996)
The application of repeated, brief periods of vascular occlusion at the onset of REPERFUSION to reduce REPERFUSION INJURY that follows a prolonged ischemic event. The techniques are similar to ISCHEMIC PRECONDITIONING but the time of application is after the ischemic event instead of before.
The circulation of the BLOOD through the MICROVASCULAR NETWORK.
Proteins prepared by recombinant DNA technology.
An adenine nucleotide containing three phosphate groups esterified to the sugar moiety. In addition to its crucial roles in metabolism adenosine triphosphate is a neurotransmitter.
A nucleoside that is composed of ADENINE and D-RIBOSE. Adenosine or adenosine derivatives play many important biological roles in addition to being components of DNA and RNA. Adenosine itself is a neurotransmitter.
A method of non-invasive, continuous measurement of MICROCIRCULATION. The technique is based on the values of the DOPPLER EFFECT of low-power laser light scattered randomly by static structures and moving tissue particulates.
Prolonged dysfunction of the myocardium after a brief episode of severe ischemia, with gradual return of contractile activity.
Any of various animals that constitute the family Suidae and comprise stout-bodied, short-legged omnivorous mammals with thick skin, usually covered with coarse bristles, a rather long mobile snout, and small tail. Included are the genera Babyrousa, Phacochoerus (wart hogs), and Sus, the latter containing the domestic pig (see SUS SCROFA).
Body organ that filters blood for the secretion of URINE and that regulates ion concentrations.
A method of computed tomography that uses radionuclides which emit a single photon of a given energy. The camera is rotated 180 or 360 degrees around the patient to capture images at multiple positions along the arc. The computer is then used to reconstruct the transaxial, sagittal, and coronal images from the 3-dimensional distribution of radionuclides in the organ. The advantages of SPECT are that it can be used to observe biochemical and physiological processes as well as size and volume of the organ. The disadvantage is that, unlike positron-emission tomography where the positron-electron annihilation results in the emission of 2 photons at 180 degrees from each other, SPECT requires physical collimation to line up the photons, which results in the loss of many available photons and hence degrades the image.
The gradual irreversible changes in structure and function of an organism that occur as a result of the passage of time.
The removal of a limb or other appendage or outgrowth of the body. (Dorland, 28th ed)
A transferase that catalyzes formation of PHOSPHOCREATINE from ATP + CREATINE. The reaction stores ATP energy as phosphocreatine. Three cytoplasmic ISOENZYMES have been identified in human tissues: the MM type from SKELETAL MUSCLE, the MB type from myocardial tissue and the BB type from nervous tissue as well as a mitochondrial isoenzyme. Macro-creatine kinase refers to creatine kinase complexed with other serum proteins.
The development of new BLOOD VESSELS during the restoration of BLOOD CIRCULATION during the healing process.
Relatively complete absence of oxygen in one or more tissues.
The mitochondria of the myocardium.
The part of brain that lies behind the BRAIN STEM in the posterior base of skull (CRANIAL FOSSA, POSTERIOR). It is also known as the "little brain" with convolutions similar to those of CEREBRAL CORTEX, inner white matter, and deep cerebellar nuclei. Its function is to coordinate voluntary movements, maintain balance, and learn motor skills.
The number of times the HEART VENTRICLES contract per unit of time, usually per minute.
Compounds or agents that combine with an enzyme in such a manner as to prevent the normal substrate-enzyme combination and the catalytic reaction.
A degenerative disease of the BRAIN characterized by the insidious onset of DEMENTIA. Impairment of MEMORY, judgment, attention span, and problem solving skills are followed by severe APRAXIAS and a global loss of cognitive abilities. The condition primarily occurs after age 60, and is marked pathologically by severe cortical atrophy and the triad of SENILE PLAQUES; NEUROFIBRILLARY TANGLES; and NEUROPIL THREADS. (From Adams et al., Principles of Neurology, 6th ed, pp1049-57)
The making of a radiograph of an object or tissue by recording on a photographic plate the radiation emitted by radioactive material within the object. (Dorland, 27th ed)
The symptom of paroxysmal pain consequent to MYOCARDIAL ISCHEMIA usually of distinctive character, location and radiation. It is thought to be provoked by a transient stressful situation during which the oxygen requirements of the MYOCARDIUM exceed that supplied by the CORONARY CIRCULATION.
Spectroscopic method of measuring the magnetic moment of elementary particles such as atomic nuclei, protons or electrons. It is employed in clinical applications such as NMR Tomography (MAGNETIC RESONANCE IMAGING).
Non-human animals, selected because of specific characteristics, for use in experimental research, teaching, or testing.
Conditions characterized by persistent brain damage or dysfunction as sequelae of cranial trauma. This disorder may result from DIFFUSE AXONAL INJURY; INTRACRANIAL HEMORRHAGES; BRAIN EDEMA; and other conditions. Clinical features may include DEMENTIA; focal neurologic deficits; PERSISTENT VEGETATIVE STATE; AKINETIC MUTISM; or COMA.
A tetrameric enzyme that, along with the coenzyme NAD+, catalyzes the interconversion of LACTATE and PYRUVATE. In vertebrates, genes for three different subunits (LDH-A, LDH-B and LDH-C) exist.
Wave-like oscillations of electric potential between parts of the brain recorded by EEG.
The chemical reactions involved in the production and utilization of various forms of energy in cells.
A hemeprotein from leukocytes. Deficiency of this enzyme leads to a hereditary disorder coupled with disseminated moniliasis. It catalyzes the conversion of a donor and peroxide to an oxidized donor and water. EC
Maintenance of blood flow to an organ despite obstruction of a principal vessel. Blood flow is maintained through small vessels.
The non-neuronal cells of the nervous system. They not only provide physical support, but also respond to injury, regulate the ionic and chemical composition of the extracellular milieu, participate in the BLOOD-BRAIN BARRIER and BLOOD-RETINAL BARRIER, form the myelin insulation of nervous pathways, guide neuronal migration during development, and exchange metabolites with neurons. Neuroglia have high-affinity transmitter uptake systems, voltage-dependent and transmitter-gated ion channels, and can release transmitters, but their role in signaling (as in many other functions) is unclear.
A large lobed glandular organ in the abdomen of vertebrates that is responsible for detoxification, metabolism, synthesis and storage of various substances.
Measurable and quantifiable biological parameters (e.g., specific enzyme concentration, specific hormone concentration, specific gene phenotype distribution in a population, presence of biological substances) which serve as indices for health- and physiology-related assessments, such as disease risk, psychiatric disorders, environmental exposure and its effects, disease diagnosis, metabolic processes, substance abuse, pregnancy, cell line development, epidemiologic studies, etc.
Descriptions of specific amino acid, carbohydrate, or nucleotide sequences which have appeared in the published literature and/or are deposited in and maintained by databanks such as GENBANK, European Molecular Biology Laboratory (EMBL), National Biomedical Research Foundation (NBRF), or other sequence repositories.
A technique for measuring extracellular concentrations of substances in tissues, usually in vivo, by means of a small probe equipped with a semipermeable membrane. Substances may also be introduced into the extracellular space through the membrane.
A free radical gas produced endogenously by a variety of mammalian cells, synthesized from ARGININE by NITRIC OXIDE SYNTHASE. Nitric oxide is one of the ENDOTHELIUM-DEPENDENT RELAXING FACTORS released by the vascular endothelium and mediates VASODILATION. It also inhibits platelet aggregation, induces disaggregation of aggregated platelets, and inhibits platelet adhesion to the vascular endothelium. Nitric oxide activates cytosolic GUANYLATE CYCLASE and thus elevates intracellular levels of CYCLIC GMP.
Any disturbances of the normal rhythmic beating of the heart or MYOCARDIAL CONTRACTION. Cardiac arrhythmias can be classified by the abnormalities in HEART RATE, disorders of electrical impulse generation, or impulse conduction.
The veins and arteries of the HEART.
The domestic cat, Felis catus, of the carnivore family FELIDAE, comprising over 30 different breeds. The domestic cat is descended primarily from the wild cat of Africa and extreme southwestern Asia. Though probably present in towns in Palestine as long ago as 7000 years, actual domestication occurred in Egypt about 4000 years ago. (From Walker's Mammals of the World, 6th ed, p801)
The hemodynamic and electrophysiological action of the left HEART VENTRICLE. Its measurement is an important aspect of the clinical evaluation of patients with heart disease to determine the effects of the disease on cardiac performance.
Observation of a population for a sufficient number of persons over a sufficient number of years to generate incidence or mortality rates subsequent to the selection of the study group.
The process by which chemical compounds provide protection to cells against harmful agents.
Tomography using x-ray transmission and a computer algorithm to reconstruct the image.
Neural tracts connecting one part of the nervous system with another.
An alternative to amputation in patients with neoplasms, ischemia, fractures, and other limb-threatening conditions. Generally, sophisticated surgical procedures such as vascular surgery and reconstruction are used to salvage diseased limbs.
Method in which prolonged electrocardiographic recordings are made on a portable tape recorder (Holter-type system) or solid-state device ("real-time" system), while the patient undergoes normal daily activities. It is useful in the diagnosis and management of intermittent cardiac arrhythmias and transient myocardial ischemia.
Application of a ligature to tie a vessel or strangulate a part.
Striated muscle cells found in the heart. They are derived from cardiac myoblasts (MYOBLASTS, CARDIAC).
Behavioral manifestations of cerebral dominance in which there is preferential use and superior functioning of either the left or the right side, as in the preferred use of the right hand or right foot.
A large vessel supplying the whole length of the small intestine except the superior part of the duodenum. It also supplies the cecum and the ascending part of the colon and about half the transverse part of the colon. It arises from the anterior surface of the aorta below the celiac artery at the level of the first lumbar vertebra.
Characteristic restricted to a particular organ of the body, such as a cell type, metabolic response or expression of a particular protein or antigen.
Decrease in the size of a cell, tissue, organ, or multiple organs, associated with a variety of pathological conditions such as abnormal cellular changes, ischemia, malnutrition, or hormonal changes.

Genetic and gender influences on sensitivity to focal cerebral ischemia in the stroke-prone spontaneously hypertensive rat. (1/7625)

We have investigated genetic transmission of increased sensitivity to focal cerebral ischemia and the influence of gender in the stroke-prone spontaneously hypertensive rat (SHRSP). Halothane-anesthetized, 3- to 5-month-old male and female Wistar-Kyoto rats (WKY), SHRSP, and the first filial generation rats (F1 crosses 1 and 2) underwent distal (2 mm) permanent middle cerebral artery occlusion (MCAO) by electrocoagulation. Infarct volume was measured by using hematoxylin-eosin-stained sections and image analysis 24 hours after ischemia and expressed as a percentage of the volume of the ipsilateral hemisphere. Infarct volume in males and females grouped together were significantly larger in SHRSP, F1 cross 1 (SHRSP father), and F1 cross 2 (WKY father), at 36.6+/-2.3% (mean+/-SEM, P<0.001, n=15), 25.4+/-2.4% (P<0.01, n=14), and 33. 9+/-1.6% (P<0.001, n=18), respectively, compared with WKY (14+/-2%, n=17). Male F1 cross 1 (18.9+/-2.4%, n=6) developed significantly smaller infarcts than male F1 cross 2 (32.8+/-2%, n=8, P<0.005). Females, which underwent ischemia during metestrus, developed larger infarcts than respective males. A group of females in which the cycle was not controlled for developed significantly smaller infarcts than females in metestrus. Thus, the increased sensitivity to MCAO in SHRSP is retained in both F1 cross 1 and cross 2 hybrids, suggesting a dominant or codominant trait; response to cerebral ischemia appears to be affected by gender and stage in the estrous cycle. In addition, the male progenitor of the cross (ie, SHRSP versus WKY) influences stroke sensitivity in male F1 cohorts.  (+info)

Ischemic tolerance in murine cortical cell culture: critical role for NMDA receptors. (2/7625)

Murine cortical cultures containing both neurons and glia (days in vitro 13-15) were exposed to periods of oxygen-glucose deprivation (5-30 min) too brief to induce neuronal death. Cultures "preconditioned" by sublethal oxygen-glucose deprivation exhibited 30-50% less neuronal death than controls when exposed to a 45-55 min period of oxygen-glucose deprivation 24 hr later. This preconditioning-induced neuroprotection was specific in that neuronal death induced by exposure to excitotoxins or to staurosporine was not attenuated. Neuroprotection was lost if the time between the preconditioning and severe insult were decreased to 7 hr or increased to 72 hr and was blocked if the NMDA antagonist 100 microM 3-((D)-2-carboxypiperazin-4-yl)-propyl-1-phosphonic acid was applied during the preconditioning insult. This was true even if the duration of preconditioning was increased as far as possible (while still remaining sublethal). A similar preconditioning effect was also produced by sublethal exposure to high K+, glutamate, or NMDA but not to kainate or trans-1-aminocyclopentane-1, 3-dicarboxylic acid.  (+info)

Disease pattern in cranial and large-vessel giant cell arteritis. (3/7625)

OBJECTIVE: To identify variables that distinguish large-vessel giant cell arteritis (GCA) with subclavian/axillary/brachial artery involvement from cranial GCA. METHODS: Seventy-four case patients with subclavian/axillary GCA diagnosed by angiography and 74 control patients with temporal artery biopsy-proven GCA without large vessel involvement matched for the date of first diagnosis were identified. Pertinent initial symptoms, time delay until diagnosis, and clinical symptoms, as well as clinical and laboratory findings at the time of diagnosis, were recorded by retrospective chart review. Expression of cytokine messenger RNA in temporal artery tissue from patients with large-vessel and cranial GCA was determined by semiquantitative polymerase chain reaction analysis. Distribution of disease-associated HLA-DRB1 alleles in patients with aortic arch syndrome and cranial GCA was assessed. RESULTS: The clinical presentation distinguished patients with large-vessel GCA from those with classic cranial GCA. Upper extremity vascular insufficiency dominated the clinical presentation of patients with large-vessel GCA, whereas symptoms related to impaired cranial blood flow were infrequent. Temporal artery biopsy findings were negative in 42% of patients with large-vessel GCA. Polymyalgia rheumatica occurred with similar frequency in both patient groups. Large-vessel GCA was associated with higher concentrations of interleukin-2 gene transcripts in arterial tissue and overrepresentation of the HLA-DRB1*0404 allele, indicating differences in pathogenetic mechanisms. CONCLUSION: GCA is not a single entity but includes several variants of disease. Large-vessel GCA produces a distinct spectrum of clinical manifestations and often occurs without involvement of the cranial arteries. Large-vessel GCA requires a different approach to the diagnosis and probably also to treatment.  (+info)

N-Acetylaspartate distribution in rat brain striatum during acute brain ischemia. (4/7625)

Brain N-acetylaspartate (NAA) can be quantified by in vivo proton magnetic resonance spectroscopy (1H-MRS) and is used in clinical settings as a marker of neuronal density. It is, however, uncertain whether the change in brain NAA content in acute stroke is reliably measured by 1H-MRS and how NAA is distributed within the ischemic area. Rats were exposed to middle cerebral artery occlusion. Preischemic values of [NAA] in striatum were 11 mmol/L by 1H-MRS and 8 mmol/kg by HPLC. The methods showed a comparable reduction during the 8 hours of ischemia. The interstitial level of [NAA] ([NAA]e) was determined by microdialysis using [3H]NAA to assess in vivo recovery. After induction of ischemia, [NAA]e increased linearly from 70 micromol/L to a peak level of 2 mmol/L after 2 to 3 hours before declining to 0.7 mmol/L at 7 hours. For comparison, [NAA]e was measured in striatum during global ischemia, revealing that [NAA]e increased linearly to 4 mmol/L after 3 hours and this level was maintained for the next 4 h. From the change in in vivo recovery of the interstitial space volume marker [14C]mannitol, the relative amount of NAA distributed in the interstitial space was calculated to be 0.2% of the total brain NAA during normal conditions and only 2 to 6% during ischemia. It was concluded that the majority of brain NAA is intracellularly located during ischemia despite large increases of interstitial [NAA]. Thus, MR quantification of NAA during acute ischemia reflects primarily changes in intracellular levels of NAA.  (+info)

Delayed increase in infarct volume after cerebral ischemia: correlations with thrombolytic treatment and clinical outcome. (5/7625)

BACKGROUND AND PURPOSE: Growing experimental evidence indicates that the development of cerebral ischemic damage is slower than previously believed. The aims of this work were (1) to study the evolution of CT hypoattenuation between 24 to 36 hours and 7 days in ischemic stroke patients; (2) to evaluate whether thrombolytic treatment given within 6 hours of stroke affects delayed infarction evolution; and (3) to investigate possible correlations between lesion volume changes over time and clinical outcome. METHODS: Of 620 patients included in the European Cooperative Acute Stroke Study 1 (ECASS1), we selected 450 patients whose control CT scans at day 1 (CT1) and day 7 (CT7) were available. They had been randomly divided into 2 groups: 206 patients had been treated with rtPA and 244 with placebo. CT1 and CT7 were classified according to the location of the infarct. The volume of CT hypoattenuation was measured using the formula AxBxC/2 for irregular volumes. The 95% confidence interval of inter- and intrarater variability was used to determine whether significant changes in lesion volume had occurred between CT1 and CT7. Clinical severity was evaluated by means of the Scandinavian Stroke Scale (SSS) at entry (SSS0) and at day 30 (SSS30). RESULTS: Mean lesion volumes were significantly (P<0.0001) higher at day 7 than at day 1 in all the subgroups of patients and particularly in patients with a subcortical lesion. Of the 450 patients studied, 287 (64%) did not show any significant change in lesion volume between CT1 and CT7, 143 (32%) showed a significant increase and the remaining 20 (4%) a significant decrease. No significant correlation was observed between treatment and lesion evolution between CT1 and CT7. Both clinical scores (SSS0 and SSS30) and degree of neurological recovery were significantly (P<0.05) lower in the subgroup of patients with a significant lesion volume increase than in the other 2 groups. CONCLUSIONS: In approximately two thirds of patients, infarct size is established 24 to 36 hours after stroke onset, whereas in the remaining one third, changes in lesion volume may occur later than the first 24 to 36 hours. Many factors may be responsible for delayed infarct enlargement and for a lower degree of clinical recovery, both of which may occur despite early recombinant tissue plasminogen activator treatment.  (+info)

Dose escalation study of the NMDA glycine-site antagonist licostinel in acute ischemic stroke. (6/7625)

BACKGROUND AND PURPOSE: Licostinel (ACEA 1021; 5-nitro-6, 7-dichloro-2,3-quinoxalinedione), a competitive antagonist of glycine at the N-methyl-D-aspartate (NMDA) receptor, is an effective neuroprotective agent in animal models of cerebral ischemia. The purpose of this study was to assess the safety, tolerability, and pharmacokinetics of licostinel in patients with acute stroke. METHODS: In this 5-center dose escalation trial, patients were enrolled within 48 hours of an ischemic stroke and treated with ascending doses of a short infusion of licostinel or a placebo. Adverse effects were assessed with clinical and laboratory measurements, and patient outcome was determined with the National Institutes of Health Stroke Scale. RESULTS: Sixty-four patients (44 treated with escalating doses of licostinel and 20 who received placebo) were treated. Lower doses of licostinel (0.03 to 0.60 mg/kg) were not associated with any significant adverse effects. Higher doses of licostinel (1.2 to 3.0 mg/kg) were associated with a variety of mild-to-moderate adverse effects including neurological and gastrointestinal complaints. No major psychotomimetic effects or significant safety concerns occurred. At the higher dose levels, peak plasma concentrations of licostinel were substantially higher than those required for neuroprotection in animal stroke models. A similar improvement in National Institutes of Health Stroke Scale scores over time was seen in both the placebo group and the licostinel-treated patients. CONCLUSIONS: A short infusion of licostinel in doses up to 3.0 mg/kg is safe and tolerable in acute stroke patients. Licostinel may be a safer and better tolerated neuroprotective agent than many of the previously evaluated NMDA antagonists.  (+info)

Anger expression and incident stroke: prospective evidence from the Kuopio ischemic heart disease study. (7/7625)

BACKGROUND AND PURPOSE: High levels of anger are associated with an increased risk of coronary heart disease and hypertension, but little is known about the role of anger in stroke risk. METHODS: Anger expression style and risk of incident stroke were examined in 2074 men (mean age, 53.0+/-5.2 years) from a population-based, longitudinal study of risk factors for ischemic heart disease and related outcomes in eastern Finland. Self-reported style of anger expression was assessed by questionnaire at baseline. Linkage to the FINMONICA stroke and national hospital discharge registers identified 64 first strokes (50 ischemic) through 1996. Average follow-up time was 8.3+/-0.9 (mean+/-SD) years. RESULTS: Men who reported the highest level of expressed anger were at twice the risk of stroke (relative hazard, 2.03; 95% CI, 1.05 to 3.94) of men who reported the lowest level of anger, after adjustments for age, resting blood pressure, smoking, alcohol consumption, body mass index, low-density and high-density lipoprotein cholesterol, fibrinogen, socioeconomic status, history of diabetes, and use of antihypertensive medications. Additional analysis showed that these associations were evident only in men with a history of ischemic heart disease (n=481), among whom high levels of outwardly expressed anger (high anger-out) predicted >6-fold increased risk of stroke after risk factor adjustment (relative hazard, 6.87; 95% CI, 1.50 to 31.4). Suppressed anger (anger-in) and controlled anger (anger-control) were not consistently related to stroke risk. CONCLUSIONS: This is the first population-based study to show a significant relationship between high levels of expressed anger and incident stroke. Additional research is necessary to explore the mechanisms that underlie this association.  (+info)

Increased platelet activation in the chronic phase after cerebral ischemia and intracerebral hemorrhage. (8/7625)

BACKGROUND AND PURPOSE: Enhanced thromboxane (TX) biosynthesis has previously been reported in the acute phase after ischemic stroke. We investigated whether enhanced urinary excretion of 11-dehydro-TXB2, a noninvasive index of platelet activation, was present in the chronic phase after a transient ischemic attack (TIA) or stroke, including intracerebral hemorrhage. METHODS: We obtained a single urinary sample from 92 patients between 3 and 9 months after onset of stroke or TIA. The urinary excretion of the major enzymatic metabolite of TXA2, 11-dehydro-TXB2, was measured by a previously validated radioimmunoassay. The excretion rates were compared with those of 20 control patients with nonvascular neurological diseases. RESULTS: Urinary 11-dehydro-TXB2 averaged 294+/-139, 413+/-419, and 557+/-432 pmol/mmol creatinine for patients with TIA, ischemic stroke, and intracerebral hemorrhage, respectively; the values were higher in all subgroups (P<0.01) than that in control patients (119+/-66 pmol/mmol). Increased 11-dehydro-TXB2 excretion was present in 59% of all patients, in 60% (P<0.001) of patients with TIA, in 56% (P<0.001) of patients with ischemic stroke, and in 73% (P<0.001) of patients with intracerebral hemorrhage. Atrial fibrillation, no aspirin use, and severity of symptoms at follow-up contributed independently to the level of 11-dehydro-TXB2 excretion in a multiple linear regression analysis. CONCLUSIONS: Platelet activation is often present in patients in the chronic phase after stroke, including those with intracerebral hemorrhage. Persistent platelet activation, which is associated with atrial fibrillation and poor stroke outcome, can be substantially suppressed by aspirin treatment.  (+info)

We investigated the effects of the angiotensin-converting enzyme inhibitor captopril on neurologic outcome in a rat model of incomplete cerebral ischemia. Twenty male Sprague-Dawley rats were anesthetized with 70% nitrous oxide in oxygen and fentanyl (10 micrograms x kg-1 i.v. bolus, 25 micrograms x kg-1 x hr-1 i.v. continuous infusion). Animals in group 1 (n = 10) received no angiotensin-converting enzyme inhibitor while animals in group 2 (n = 10) were given 10 mg x kg-1 i.v. captopril 30 minutes prior to the ischemic period. Ischemia was produced by unilateral carotid artery ligation and hemorrhagic hypotension to 35 mm Hg for 30 minutes. Body temperature, arterial blood gases, and arterial pH were maintained constant. Neurologic outcome was evaluated every 24 hours for 3 days using a graded deficit score (0, normal; 18, stroke-related death). On the third day after ischemia, captopril significantly improved neurologic outcome (median deficit score = 4) compared with controls (median deficit ...
TY - JOUR. T1 - Treatment of acute focal cerebral ischemia with dimethyl sulfoxide. AU - Little, J. R.. AU - Cook, A.. AU - Lesser, Ronald P. PY - 1981. Y1 - 1981. N2 - The object of this investigation was to study the effects of dimethyl sulfoxide (DMSO) upon the evolution of cerebral infarction. Twenty adult cats anesthetized lightly with ketamine hydrochloride underwent right middle cerebral artery occlusion for 6 hours. Ten cats were not treated and 10 cats received DMSO (2.5 g/kg i.v.) immediately after occlusion. Regional cerebral blood flow (rCBF) changes in the right sylvian region were similar in the untreated and treated groups. The mean rCBF before occlusion was 46 ± 10 ml/100 g/minute in the untreated group and 45 ± 10 ml/100 g/minute in the treated group. Eight cats in both groups had rCBF measurements consistently below 18 ml/100 g/minute during the 6-hour period after occlusion. An index of erythrocyte flow was determined by measuring the transit of technetium-99 (99Tc)-labeled ...
The effects of isosmolar loads of glucose and saline after onset of focal cerebral ischaemia (middle cerebral artery occlusion) were compared in cats. In cats given saline cerebral blood flow (CBF) fell and then rose slightly on the marginal gyrus (infarct penumbra). There was a sustained fall in CBF on the suprasylvian and ectosylvian gyri (infarct core). Reperfusion restored blood flow to preocclusion levels with no overall postischaemic hypoperfusion. Below ischaemic flows of 14 ml/100 g/min brain specific gravity was reduced in a smaller proportion of gyri by contrast with non reperfused cortex, suggesting that in some gyri resolution of cerebral oedema had taken place. GABA uptake was normal in the infarct core, but was reduced within the ischaemic penumbra. In animals given glucose after occlusion, CBF fell on the marginal gyrus during reperfusion. The degree of resolution of cerebral oedema was less than in saline infused cats. GABA uptake showed a pattern of abnormality similar to that ...
Interleukin-1 (IL-1) is a key regulator of inflammation and ischaemic brain injury, but the contribution of central and peripheral sources of IL-1 to brain injury is not well understood. Here we show that haematopoietic-derived IL-1 is a key driver of ischaemic brain injury. Wild type (WT) mice transplanted with IL-1αβ-deficient bone marrow displayed a significant (40%) reduction in brain injury induced by focal cerebral ischaemia compared to WT mice transplanted with WT bone marrow. This was paralleled by improved neurological outcome and the almost complete absence of splenic-derived, but not liver-derived, IL-1α after stroke in WT mice lacking haematopoietic-derived IL-1. IL-1αβ knockout (KO) mice transplanted with IL-1αβ-deficient bone marrow showed a 60% reduction in brain injury compared to WT mice receiving WT bone marrow. Transplantation of WT bone marrow in IL-1αβ KO mice resulted in a similar level of blood-brain-barrier injury to that observed in WT mice receiving ...
OBJECTIVES: Prolonged global cerebral ischaemia leads to irreversible injury, often with lethal outcome. Brain injuries are partly caused by the uncontrolled reperfusion that occurs once the circulation is re-established. Recent animal experiments suggest that controlled reperfusion following lengthy ischaemia might prevent severe brain injury. This study aimed at further exploring cerebral alterations and outcome following prolonged global cerebral ischaemia and mechanically manipulated reperfusion.. METHODS: Three groups of pigs were included; one sham operated (n = 3) and two that underwent 30-min global cerebral ischaemia. All vessels that supply the brain were isolated intrathoracically, after which they were occluded for 30 min in the ischaemic groups. In one of the ischaemic groups uncontrolled reperfusion was applied (URep, n = 6), i.e. normal circulation was restored 30 min after arrested cerebral circulation. The second ischaemic group received mechanical reperfusion (MRep, n = 6) with ...
TY - JOUR. T1 - Serial diffusion tensor MRI after transient and permanent cerebral ischemia in nonhuman primates. AU - Liu, Yutong. AU - DArceuil, Helen E.. AU - Westmoreland, Susan. AU - He, Julian. AU - Duggan, Michael. AU - Gonzalez, R. Gilberto. AU - Pryor, Johnny. AU - De Crespigny, Alex J.. N1 - Copyright: Copyright 2008 Elsevier B.V., All rights reserved.. PY - 2007/1. Y1 - 2007/1. N2 - BACKGROUND AND PURPOSE - We measured the temporal evolution of the T2 and diffusion tensor imaging parameters after transient and permanent cerebral middle cerebral artery occlusion (MCAo) in macaques, and compared it to standard histological analysis at the study end point. METHODS - Stroke was created in adult male macaques by occluding a middle cerebral artery branch for 3 hours (transient MCAo, n=4 or permanent occlusion, n=3). Conventional MRI and diffusion tensor imaging scans were performed 0 (acute day), 1, 3, 7, 10, 17, and 30 days after MCAo. Animals were euthanized after the final scan and the ...
TY - JOUR. T1 - Intraluminal suture occlusion of the middle cerebral artery in spontaneously hypertensive rats. AU - Doǧan, Aclan. AU - Başkaya, Mustafa K.. AU - Rao, V. L.Raghavendra. AU - Rao, A. Muralikrishna. AU - Dempsey, Robert J.. PY - 1998/4. Y1 - 1998/4. N2 - In models of middle cerebral artery occlusion using intraluminal suture, the size and the distribution of ischemic injury vary considerably among laboratories. In transcranial models of cerebral ischemia, a more consistent cerebral ischemic lesion is seen in Spontaneously Hypertensive rats (SHR). In the present study, we performed intraluminal suture occlusion of the MCA in SHR and compared its reproducibility with those in Sprague-Dawley (SD) rats. Male SHR and SD rats were anesthetized with halothane and subjected to 2 h of temporary middle cerebral artery occlusion by an intraluminal suture. Comparisons of regional cerebral blood flow figures taken throughout the experiment and lesion volume figures taken at 24 h after ...
Hypoxic-ischaemic brain injury at birth is associated with 1-3/1000 cases of moderate to severe encephalopathy. Previously, we have shown that connexin 43 hemichannel blockade, with a specific mimetic peptide, reduced the occurrence of seizures, improved recovery of EEG power and sleep state cycling, and improved cell survival following global cerebral ischaemia. In the present study, we examined the dose response for intracerebroventricular mimetic peptide infusion (50 µmol/kg/h for 1 h, followed by 50 µmol/kg/24 h (low dose) or 50 µmol/kg/h for 25 h (high dose) or vehicle only (control group), starting 90 min after the end of ischaemia), following global cerebral ischaemia, induced by 30 min bilateral carotid artery occlusion, in near-term fetal sheep (128 ± 1 days gestation). Both peptide infusion groups were associated with a transient significant increase in EEG power between 2-12 h after ischaemia. The ischaemia-low dose group showed a significant recovery of EEG power from day five compared
Modern functional brain imaging techniques rely on the constancy of the neurovascular coupling process, measured by its hemodynamic response function (HRF). Nevertheless, brain pathology may alter the HRF confounding the interpretation of imaging studies. We have recently proposed a method to investigate HRF by taking advantage of the discontinuous burst-suppression (BS) EEG pattern induced by chloral-hydrate anesthesia. BS also occurs during reperfusion following global ischemia (GCI). The aim of this study was to investigate in rats whether the HRF is altered during early reperfusion after a minimally injuring GCI. In 6 male Wistar rats (control), BS patterns were induced by an overdose of chloral-hydrate. In other 5 rats, BS was induced by a 5-minute GCI using a variation of the 4-vessel occlusion model. Simultaneous electroencephalo-graphic (EEG) activity and Laser Doppler (LD) signal were recorded from the left hemisphere. During recovery following GCI, with decreasing bursting frequency ...
The present study shows that PC-SOD, the lecithinized form of SOD, decreased infarct volume and improved neurological outcomes at different time points after focal cerebral ischemic injury. PC-SOD decreased oxidative stress and provided neuronal protection through antiapoptotic mechanisms.. Previous studies have highlighted that unmodified SOD plays an important role in attenuating different forms of brain injury, including cerebral ischemia.1,2,3 However, its short in vivo half-life and low tissue affinity have hampered the practical use of unmodified SOD formulations.4 The enzymatic activity of PC-SOD is comparable to that of unmodified SOD. The in vitro activity of unmodified SOD by the xanthine-xanthine oxidase method was 3467 U/mg, whereas that of PC-SOD was 2876 U/mg. Therefore, the activity of PC-SOD was equivalent to 83% of unmodified SOD.15 PC-SOD, however, has many advantages, such as longer in vivo half-life, greater tissue affinity, and better drug delivery, resulting in ...
Brain ischemia (a.k.a. cerebral ischemia, cerebrovascular ischemia) is a condition in which there is insufficient blood flow to the brain to meet metabolic demand. This leads to poor oxygen supply or cerebral hypoxia and thus to the death of brain tissue or cerebral infarction / ischemic stroke. It is a sub-type of stroke along with subarachnoid hemorrhage and intracerebral hemorrhage. Ischemia leads to alterations in brain metabolism, reduction in metabolic rates, and energy crisis. There are two types of ischemia: focal ischemia, which is confined to a specific region of the brain; and global ischemia, which encompasses wide areas of brain tissue. The main symptoms involve impairments in vision, body movement, and speaking. The causes of brain ischemia vary from sickle cell anemia to congenital heart defects. Symptoms of brain ischemia can include unconsciousness, blindness, problems with coordination, and weakness in the body. Other effects that may result from brain ischemia are stroke, ...
TY - JOUR. T1 - Postischemic gene transfer of midkine, a neurotrophic factor, protects against focal brain ischemia. AU - Takada, J.. AU - Ooboshi, H.. AU - Ago, T.. AU - Kitazono, T.. AU - Yao, H.. AU - Kadomatsu, K.. AU - Muramatsu, T.. AU - Ibayashi, S.. AU - Iida, M.. PY - 2005/3/1. Y1 - 2005/3/1. N2 - Gene therapy may be a promising approach for treatment of brain ischemia. In this study, we examined the effect of postischemic gene transfer of midkine, a heparin-binding neurotrophic factor, using a focal brain ischemia model with the photothrombotic occlusion method. At 90 min after induction of brain ischemia in spontaneously hypertensive rats, a replication-deficient recombinant adenovirus encoding mouse midkine (AdMK, n = 7) or a control vector encoding β-galactosidase (Adβgal, n = 7) was injected into the lateral ventricle ipsilateral to ischemia. At 2 days after ischemia, we determined infarct volume by 2,3,5-triphenyltetrazolium chloride staining. There were no significant ...
Introduction: The aim of the study was to evaluate the endothelioprotective activity of 4-hydroxy-3,5-di-tret-butylcinnamic acid in conditions of experimental cerebral ischemia. Materials and methods: The brain ischemia was reproduced by the method of irreversible right-sided thermocoagulation of the middle cerebral artery. As comparative drugs, mexidol (30 mg/kg) and sulodexide (30 U/kg) were used. The vasodilating function of the vascular endothelium was assessed by the change in the rate of cerebral blood flow when the synthesis of nitric oxide was modified. Antithrombotic function was assessed by changes in the concentration of thromboxane A2, fibrinogen, von Willebrand factor activity and platelet aggregation activity. Serum concentration of C-reactive protein served as a marker of the state of anti-inflammatory endothelial function. To determine the potential mechanism of endothelioprotective activity of 4-4-hydroxy-3,5-di-tret-butylcinnamic acid, the anti-radical activity of
אינדוקציה כירורגי של נזק מוחי איסכמי בחולדה הוא מודל בשימוש נרחב עבור מחקר שבץ. כאן אנו מדגימים את האינדוקציה של איסכמיה מוחית המוקד על ...
Aging is a risk factor for stroke. Animal models of stroke have been widely used to study the pathophysiology of ischemic stroke, which in turn helped to develop numerous therapeutic strategies. Despite the considerable success of therapeutic strategies in animal models of ischemic stroke, almost all of them have been proved to be unsuccessful in the clinical trials. One of explanation is that data obtained from young animals may not fully resemble the effects of ischemic stroke in aged animals or elder patients, causing the discrepancy between animal experiments and clinical trials. To investigate these differences with regard to age, pathway specific gene arrays were used to identify and isolate differentially expressed genes in periinfarct following focal cerebral ischemia. The results from this study showed a persistent up-regulation of pro-apoptotic and inflammatory-related genes up to 14 days post stroke, a 50% reduction in the number of transcriptionally active stem cell-related genes and ...
Aging is a risk factor for stroke. Animal models of stroke have been widely used to study the pathophysiology of ischemic stroke, which in turn helped to develop numerous therapeutic strategies. Despite the considerable success of therapeutic strategies in animal models of ischemic stroke, almost all of them have been proved to be unsuccessful in the clinical trials. One of explanation is that data obtained from young animals may not fully resemble the effects of ischemic stroke in aged animals or elder patients, causing the discrepancy between animal experiments and clinical trials. To investigate these differences with regard to age, pathway specific gene arrays were used to identify and isolate differentially expressed genes in periinfarct following focal cerebral ischemia. The results from this study showed a persistent up-regulation of pro-apoptotic and inflammatory-related genes up to 14 days post stroke, a 50% reduction in the number of transcriptionally active stem cell-related genes and ...
TY - JOUR. T1 - Bone morphogenetic protein-6 reduces ischemia-induced brain damage in rats. AU - Wang, Yun. AU - Chang, Chen Fu. AU - Morales, Marisela. AU - Chou, Jenny. AU - Chen, Hui Ling. AU - Chiang, Yung Hsiao. AU - Lin, Shinn Zong. AU - Cadet, Jean Lud. AU - Deng, Xiaolin. AU - Wang, Jia Yi. AU - Chen, Su Yu. AU - Kaplan, Paul L.. AU - Hoffer, Barry J.. PY - 2001. Y1 - 2001. N2 - Background and Purpose - Bone morphogenetic protein-6 (BMP6) and its receptors are expressed in adult and fetal brain. Receptors for BMP6 are upregulated in adult brain after injury, leading to the suggestion that BMP6 is involved in the physiological response to neuronal injury. The purpose of this study was to determine whether there was a neuroprotective effect of BMP6 in vivo and in vitro. Methods - Lactate dehydrogenase and microtubule-associated protein-2 (MAP-2) activities were used to determine the protective effect of BMP6 against H2O2 in primary cortical cultures. The neuroprotective effects of BMP6 ...
TY - JOUR. T1 - Ablation of Neurogenesis Attenuates Recovery of Motor Function after Focal Cerebral Ischemia in Middle-Aged Mice. AU - Sun, Fen. AU - Wang, Xiaomei. AU - Mao, Xiao Ou. AU - Xie, Lin. AU - Jin, Kunlin. PY - 2012/10/26. Y1 - 2012/10/26. N2 - Depletion of neurogenesis worsens functional outcome in young-adult mice after focal cerebral ischemia, but whether a similar effect occurs in older mice is unknown. Using middle-aged (12-month-old) transgenic (DCX-TK(+)) mice that express herpes simplex virus thymidine kinase (HSV-TK) under control of the doublecortin (DCX) promoter, we conditionally depleted DCX-positive cells in the subventricular zone (SVZ) and hippocampus by treatment with ganciclovir (GCV) for 14 days. Focal cerebral ischemia was induced by permanent occlusion of the middle cerebral artery (MCAO) or occlusion of the distal segment of middle cerebral artery (dMCAO) on day 14 of vehicle or GCV treatment and mice were killed 24 hr or 12 weeks later. Increased infarct volume ...
ABSTRACT MECHANISMS OF PERSISTENT TRANSLATION ARREST FOLLOWING GLOBAL BRAIN ISCHEMIA and REPERFUSION by JILL T. JAMISON December 2011 Advisor: Donald J. DeGracia, Ph.D. Major: Physiology Degree: Doctor of Philosophy The information presented here studies the mechanisms that underlie persistent translation arrest (TA) following global brain ischemia and reperfusion (I/R). To summarize the main findings I have discovered a new mechanism for prolonged post-ischemic TA that correlated exactly with in vivo translation rates and correlated precisely with cell outcome. Through the extensive colocalization studies, my results indicate that the mRNA granules are ribonomic structures involved with mRNA regulation. This finding is significant because it shifts the focus onto mRNA metabolism and away from ribosomal molecular biology. I have identified new pathways to investigate for understanding why there is selective delayed death in post-ischemic neurons, however my work also gives insight into why resistant
It is crucial to establish an MCAO/R animal model according to the clinical characteristics of a human cerebral natural infarct. The model characteristics are as follows: i) single damage mechanism that is easy to study; ii) simple method, small wound, easy to control condition, stable infarct site, and distinct symptomatic reaction and high achievement ratio; iii) uniformity of cerebral infarction and good reproducibility; and iv) necrotic brain tissue following injury, with a similar pathophysiological process to clinical cerebral ischemia. In this study, a rat cerebral ischemia-reperfusion injury model was established according to the Zea-Longa method (4). Following cerebral ischemia for 1 h, the rats developed severe nervous and behavioral functional impairment symptoms, indicating the establishment of a successful model.. The Bederson (5) score method was employed for qualitative and semiquantitative evaluation, with particular emphasis on motor function evaluation. The balance beam walking ...
1. Li PA, He Q. Mechanisms of hyperglycemia-enhanced ischemic brain damage. Transl Med Res. 2013;3:1-11 2. Capes SE, Hunt D, Malmberg K, Pathak P, Gerstein HC. Stress hyperglycemia and prognosis of stroke in nondiabetic and diabetic patients: a systematic overview. Stroke. 2001;32:2426-2432 3. Rajesh G, Ajay C, Frederick M, Paresh D. Hyperglycemia, insulin, and acute ischemic stroke: A mechanistic justification for a trial of insulin infusion therapy. Stroke. 2006;37:267-273 4. Balan IS, Fiskum G, Hazelton J, Cotto-Cumba C, Rosenthal RE. Oximetry-guided reoxygenation improves neurological outcome after experimental cardiac arrest. Stroke. 2006;37:3008-3013 5. Cipolla MJ, Godfrey JA. Effect of hyperglycemia on brain penetrating arterioles and cerebral blood flow before and after ischemia/reperfusion. Transl Stroke Res. 2010;1:127-134 6. Stead LG, Gilmore RM, Bellolio MF, Mishra S, Bhagra A, Vaidyanathan L, Decker WW, Brown RD Jr. Hyperglycemia as an independent predictor of worse outcome in ...
Increasing evidence suggests that toll-like receptors (TLRs) play an important role in cerebral ischemia-reperfusion injury. The endogenous ligands released from ischemic neurons activate the TLR signaling pathway, resulting in the production of a large number of inflammatory cytokines, thereby causing secondary inflammation damage following cerebral ischemia. However, the preconditioning for minor cerebral ischemia or the preconditioning with TLR ligands can reduce cerebral ischemic injury by regulating the TLR signaling pathway following ischemia in brain tissue (mainly, the inhibition of the TLR4/NF-κB signaling pathway and the enhancement of the interferon regulatory factor-dependent signaling), resulting in TLR ischemic tolerance. Additionally, recent studies found that postconditioning with TLR ligands after cerebral ischemia can also reduce ischemic damage through the regulation of the TLR signaling pathway, showing a significant therapeutic effect against cerebral ischemia. These studies
Cerebral ischemia is a life-threatening condition associated with a substantial morbidity and mortality. Hyperglycemia, a common coexisting phenomenon in both stroke and cardiac arrest (CA), may further aggravate ischemic brain injury. To date, the therapeutic possibilities are lim-ited and the search for new treatment modalities is warranted. One aspect of such a research could be to better understand the cerebral pathogenesis induced by hyperglycemic ischemia-reperfusion.. We investigated the combination of ischemia and hyperglycemia in two experimental models of stroke and CA. The aims were to test the neuroprotective potential of the sulfonated nitrone 2-sulfophenyl-N-tert-butylnitrone (S-PBN) in focal hyperglycemic cerebral ischemia (1), to outline the short-terms effects of hyperglycemia in prolonged (2) and short CA (3) and to performed a global transcriptome analysis of brain from hyperglycemic and normoglycemic CA (4).. In a stroke model rats were made hyperglycemic prior to transient ...
To determine whether the Tat-K13 following systemic application can prevent the ischemic nuclear PTEN translocation and hence reduce the ischemic neuronal injuries, we first tested whether Tat-K13, following systemic application, could enter neurons in the ischemic penumbra using a fluorophore-tagged peptide Tat-K13-carboryfluorescein. As shown in Figure 3B, this fluorescent Tat-K13 (10 mg/kg, i.v.) administered 6 h after stroke onset not only effectively entered the brain, but was enriched in neurons in the infarct area within 1 h following application (Fig. 3B). This apparent enrichment in the infarct brain area is likely due to a transient increase in blood-brain-Barrier leakage following ischemic insults (Belayev et al., 1996; Fernandez-Lopez et al., 2012) These results indicate that post-stroke systemic administration could effectively deliver this peptide into neurons in the ischemic/infarct regions of the brain.. Having proved the effective delivery of the peptide into ischemic regions, ...
DrLinOng. Chan SJ, Esposito E, Hayakawa K, Mandaville E, Smith RAA, Guo S, Niu W, Wong PT-H, Cool SM, Lo EH, Nurcombe V. Vascular Endothelial Growth Factor 165-Binding Heparan Sulfate Promotes Functional Recovery From Cerebral Ischemia. Stroke. 2020;51:2844-2853.. Angiogenesis and neurogenesis are crucial processes for brain recovery after stroke. While the brain has the capacity to form new cerebral blood vessels and to generate new neurons from neural stem cells after stroke, these self-repair mechanisms are limited. Therefore, strategies to promote brain restorative processes beyond the endogenous recovery are highly desirable. In this study, Chan and colleagues demonstrated that an exogenously applied heparan sulfate with increased affinity for vascular endothelial growth factor was able to enhance angiogenesis and neurogenesis within the peri-infarct regions, as well as to promote neurological recovery after experimental stroke.. The team first purified heparan sulfate variant 7, a ...
phdthesis{e6a24cb9-3a1a-4b11-91f1-3152114bb8fb, abstract = {Enriched environment (EE) housing significantly ameliorates neurological deficits induced by cortical brain ischemia without changing infarction size, suggesting that EE-related functional benefits are associated with neuronal plasticity events in the remaining tissue. Brain-derived neurotrophic factor (BDNF), nerve growth factor-induced gene A (NGFI-A) and corticosteroid receptors (mineralocorticoid receptor, MR; glucocorticoid receptor, GR) have been demonstrated to be involved in brain plasticity. The purpose of this thesis was to determine if post-ischemic housing conditions had a significant effect on transcription and/or translation of BDNF, NGFI-A and corticosteroid receptors. We found that BDNF gene was down regulated in EE-housed rats when compared to the rats housed in standard cages at 2~12 days after cortical brain ischemia in peri-infarct cortex, contralateral cortex and bilateral hippocampus. The protein level of BDNF in ...
Female gender, which is abolished following ovariectomy and reproductive senescence, is associated with improved outcome following cerebral stroke. Estrogen replacement partially restores this benefit of the female gender but the effect of progesterone in hormone-deficient animals is currently unknown. We evaluated various outcomes following middle cerebral artery occlusion (MCAO) in ovariectomised female mice, with a physiologically relevant restoration of progesterone levels. Ovariectomised female mice had significantly elevated plasma (P=,0.05) and brain progesterone levels (P=,0.01) following implantation of a 21-day release pellet (50mg) compared with mice that received placebo implants 7 days prior to undergoing 60 min MCAO. Assessment of well-being (body weight recovery) and neurological score at 24h and 48h post-MCAO indicated that MCAO significantly worsened outcome compared with sham-operated mice but progesterone had no effect. MCAO resulted in a substantial lesion formation and a ...
Bilateral carotid occlusion coupled with systemic hypotension produces global brain ischemia in the rat, resulting in damage to the...
Dysregulated microRNAs (miRNAs) are crucial regulators of cerebrovascular conditions, including ischemic stroke. Circulating miR-125a-5p is associated with ischemic stroke and may have clinical utility as an early diagnostic biomarker. This study conducted a series of experiments that were...
Older research outputs will score higher simply because theyve had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 222,049 tracked outputs that were published within six weeks on either side of this one in any source. This one is in the 1st percentile - i.e., 1% of its contemporaries scored the same or lower than it ...
Reversible protein phosphorylation is under the control of opposing activities of protein kinases and protein phosphatases, and has a crucial role in the regulation of cellular signal transduction in a plethora of neural cell functions, including neurogenesis, differentiation, gene transcription and cell death signalling (Klumpp & Krieglstein, 2002b). During the symposium, expert reviews of research on reversible protein phosphorylation, examples from screening approaches for kinase functions in neurons and studies on particular signalling pathways highlighted the importance of this fast‐emerging topic for the understanding of neuronal cell death, and the development of novel neuroprotective strategies.. Protein kinases have been established as key regulators in many important cellular processes, such as proliferation, maintenance of cell shape, survival signalling and apoptosis. Approximately 500 genes encode members of the kinase family in the human genome, and the predicted human kinome ...
Diabetes is a major risk factor for ischemic stroke and is associated with increased mortality. Additionally, hyperglycemia, a common complication in acute stroke, is associated with poor outcome.In order to identify the correlation between blood glucose and early mortality, multiple logistic regression analyses were used and odds ratios calculated in a retrospective study of 447 stroke patients. Eighty-one patients (18%) had diabetes. The odds ratios for 30-day case-fatality and blood glucose were 1.9 and 1.6 in diabetic and non-diabetic patients respectively. Optimal blood glucose concentrations in respective group were 10.3 and 6.3 mmol/L, as determined by receiver operator characteristic (ROC) curves.Cerebral ischemia triggers different signaling pathways including mitogen-activated protein kinases (MAPK) which regulate fundamental cell functions. In an experimental rat model of combined hyperglycemia and transient middle cerebral artery occlusion (MCAO), the activation pattern of one such ...
Several experimental studies have indicated that nicotinamide adenine dinucleotide phosphate (NADPH) oxidases (Nox) exert detrimental effects on ischemic brain tissue; Nox-knockout mice generally exhibit resistance to damage due to experimental stroke following middle cerebral artery occlusion (MCAO). Furthermore, our previous MCAO study indicated that infarct size and blood-brain barrier breakdown are enhanced in mice with pericyte-specific overexpression of Nox4, relative to levels observed in controls. However, it remains unclear whether Nox affects the stroke outcome directly by increasing oxidative stress at the site of ischemia, or indirectly by modifying physiological variables such as blood pressure or cerebral blood flow (CBF ...
Cerebral Resuscitation After Global Brain Ischemia: Linking Research to Practice | Richmond, Therese S. | download | BookSC. Download books for free. Find books
The initial ASPECTS-CTP lesion was significantly larger than the final infarct determined by ASPECTS in case of recanalization. Initial perfusion lesion, including CBV, is reversible in case of reperfusion, especially in early reperfusion.
Cerebral hyperperfusion, or reperfusion syndrome, is a rare, but serious, complication following revascularization. Hyperperfusion is defined as a major increase in ipsilateral cerebral blood flow (CBF) that is well above the metabolic demands of the brain tissue.
TY - CHAP. T1 - Histopathology of Cerebral Ischemia and Stroke. AU - Dalton Dietrich, W.. PY - 2017/3/7. Y1 - 2017/3/7. N2 - Ischemic stroke is a serious neurological problem and one of the leading causes of death and disability worldwide. The histopathological consequences of stroke are complex and may result in a variety of deficits including severe motor and cognitive disturbances. The histopathological consequences of severe focal ischemia are well described with characteristic structural changes occurring in both gray and white brain regions depending on the severity, location, and duration of the ischemic insult. Following focal ischemic injury, neuronal, astrocytic, vascular endothelial, and inflammatory cell changes occur. In white mater tracts, axonal injury with oligodendrocyte damage and subsequent demyelination are also commonly observed. In contrast, less severe or more transient ischemic insults can lead to patterns of selective neuronal injury whereby vulnerable neuronal ...
In our previous study, β-hydroxybutyrate (BHB) was found to prolong survival time and to inhibit cerebral edema by improving energy metabolism in the hypoxia, anoxia and global cerebral ischemia models. In this study, the cerebroprotective effect of BHB was examined in rats with permanent (p)-occlusion and transient (t)-occlusion of middle cerebral artery (MCA). BHB (30 mg · kg,sup,−,/sup,,sup,1,/sup, · h,sup,−,/sup,,sup,1,/sup,) was continuously administered through the femoral vein. In rats with p-MCA occlusion, BHB significantly reduced infarct area at 24 h after the occlusion, but not at 72 h after the occlusion. In rats with 2-h t-MCA occlusion followed by 22-h reperfusion, BHB significantly reduced cerebral infarct area, edema formation, lipid peroxidation and neurological deficits. Moreover, in the t-MCA occlusion model, delayed administration of BHB started at 1 h after the initiation of the MCA occlusion also significantly reduced cerebral infarct area. Taking together the ...
1. Stub D, Bernard S, Duffy SJ, Kaye DM. Post cardiac arrest syndrome: a review of therapeutic strategies. Circulation. 2011;123:1428-35 2. Harukuni I, Bhardwaj A. Mechanisms of brain injury after global cerebral ischemia. Neurol Clin. 2006;24:1-21 3. Bernard SA, Gray TW, Buist MD, Jones BM, Silvester W, Gutteridge G. et al. Treatment of comatose survivors of out-of-hospital cardiac arrest with induced hypothermia. N Engl J Med. 2002;346:557-63 4. Camara AK, Bienengraeber M, Stowe DF. Mitochondrial approaches to protect against cardiac ischemia and reperfusion injury. Front Physiol. 2011;2:13 5. Honda HM, Korge P, Weiss JN. Mitochondria and ischemia/reperfusion injury. Ann N Y Acad Sci. 2005;1047:248-58 6. Perez-Pinzon MA, Stetler RA, Fiskum G. Novel mitochondrial targets for neuroprotection. J Cereb Blood Flow Metab. 2012;32:1362-76 7. Cour M, Loufouat J, Paillard M, Augeul L, Goudable J, Ovize M. et al. Inhibition of mitochondrial permeability transition to prevent the post-cardiac arrest ...
If the entire ischemic region supplied by the occluded artery evolved into infarction within minutes or even 1 to 2 hours after onset, there would be little if any opportunity to successfully intervene to improve functional and neurologic outcome. Abundant experimental data suggest that brain injury, secondary to an arterial occlusion, is a dynamic process involving varying degrees of early ischemic injury related primarily to the severity of local cerebral blood flow (CBF) impairment. Ischemic regions with very low CBF (,10 mL/100 g/min) rapidly become irreversibly damaged and are referred to as the ischemic core. [14] In stroke models, surrounding or intermixed zones of less severely impaired CBF (approximately 15 to 40 mL/100 g/min) occur and likely also exist in many ischemic stroke patients. This zone of mild to moderately reduced CBF relates to the concept of the ischemic penumbra originally suggested by Astrup et al. [15] As initially defined, the ischemic penumbra encompasses that ...
The present study aimed to investigate the anti-inflammatory effect of 4-methylcyclopentadecanone (4-MCPC) in rats suffering from a cerebral ischemia/ reperfusion (I/R) injury. In this study, the focal cerebral ischemia in rats was induced by middle cerebral artery occlusion (MCAO) for 2 h, and the rats were treated with 4-MCPC (8 mg/kg) just 0.5 h before reperfusion. The ischemic infarct volume was recorded 24 h after the MCAO. In addition, myeloperoxidase (MPO) activity and TNF-α and IL-1β levels in the ischemic cerebral cortex were determined by ELISA, while nuclear translocation of NF-κB p65 subunit and expression of p-IκBα were investigated by western blotting ...
This article examines the pathophysiology of lesions caused by focal cerebral ischemia. Ischemia due to middle cerebral artery occlusion encompasses a densely ischemic focus and a less densely ischemic penumbral zone. Cells in the focus are usually doomed unless reperfusion is quickly instituted. In …
The animal model of stroke that is most frequently used is a rat model of focal brain ischemia caused by middle cerebral artery occlusion (MCAO). Several studies have reported a link between levels of cell-free DNA (CFD) and neurologic outcome in human stroke. The purpose of this study was to assess brain injury and measure CFD levels in 2 models of MCAO in rats, and to determine whether brain injury correlates with CFD. A total of 60 rats were used for this study. Twenty rats underwent a sham procedure, 20 rats had MCAO using a monofilament, and 20 rats had MCAO with a silicon-coated filament. Groups were further divided into 2 subgroups. In 1 subgroup of 10 rats, neurologic performance [measured as a neurologic severity score, (NSS)] was measured at 1 and 24 hours after the procedure, and brain edema and infarct volume were determined at 24 hours. In the second subgroup of 10 rats, CFD was measured at 0, 1, 2, 4, 8, 12, and 24 hours and at 2, 3, 4, and 5 days. Neurologic performance (measured ...
The histologic description of cerebral ischemia is complex, and within most lesions there are regional variations in degrees of neuronal cell injury, edema, and neuropil disruption. These parameters of tissue injury were analyzed histopathologically in transient and permanent experimental cerebral ischemia in 15 rabbits and the results were spatially correlated with MR images of pre- and postmortem (formalin-fixed) brains. MR was performed at 1.5 T (eight animals) and at 0.38 T (seven animals). Areas of high signal on T2-weighted MR images were closely correlated with histologic signs of cytotoxic glial edema and with disruption of the neuropil (widening of the interstitial spaces in the background matrix of glial and neuronal cellular processes), but MR tended to underestimate the extent of ischemic neuronal injury, especially low-grade histologic changes (mild neuronal shrinkage and nuclear basophilia). Low-grade ischemic neuronal changes were often found in the penumbra zone of ischemic ...
TY - JOUR. T1 - Isovolemic hemodilution in experimental focal cerebral ischemia. Part 1. T2 - Effects on hemodynamics, hemorheology, and intracranial pressure. AU - Tu, Y. K.. AU - Heros, R. C.. AU - Candia, G.. AU - Hyodo, A.. AU - Lagree, K.. AU - Callahan, R.. AU - Zervas, N. T.. AU - Karacostas, D.. PY - 1988/1/1. Y1 - 1988/1/1. N2 - A total of 76 splenectomized dogs were entered in a study of the value and effects of isovolemic hemodilution. Of these, seven were not included in the analysis because of technical errors. Of the remaining 69 dogs, 35 were treated with hemodilution; 28 were subjected to a 6-hour period of temporary occlusion of the distal internal carotid artery and the proximal middle cerebral artery, and seven underwent a sham operation only, with arterial manipulation but no occlusion. The other 34 dogs were not subjected to hemodilution; 26 of these underwent temporary arterial occlusion and eight had a sham operation only. In each group the animals were about equally ...
In this experimental study, the neuroprotective effect of the xanthine oxidase inhibitor allopurinol on focal cerebral ischaemia created by permanent middle cerebral artery occlusion (MCAO) was investigated. Using high performance liquid chromatography (HPLC), we measured hypoxanthine, xanthine, and uric acid (UA) levels in rabbit brains following focal cerebral ischaemia. Rabbits were randomly and blindly assigned into four groups of eight animals each. The control groups received 2% carboxymethylcellulose solution, while 10% allopurinol 150 mg/kg was given to the treatment group 1 h before ischaemia. Each group was subdivided into two groups which were sacrificed 4 h or 24 h after ischaemia, respectively. UA and xanthine values of the rabbits in the control groups were quite high at both times and highest after 24 h, particularly in the centre of the ischaemia. A significant decrease in UA and xanthine values was observed in rabbits that were given allopurinol ( ...
Experimental focal cerebral ischemia was produced in monkeys (Macaca radiata) by occlusion of the right middle cerebral artery (MCA). The release of the lysosomal glycosidases, β-D-hexosaminidase, α-L-fucosidase and α-D-mannosidase into the soluble fraction in the right basal ganglia of the experimental animals was measured at different periods from 30 min to 12 hr after occlusion and compared with the corresponding sham operated control animals. There was a significant increase in the released lysosomal enzymes in the MCA occluded animals at all periods and particularly at 4 hr after occlusion. The CSF from the experimental animals also showed elevated levels of hexosaminidase and fucosidase. The free fatty acids (FFA) measured in the basal ganglia at 30 min and 2 hr after occlusion showed a 100 fold increase in the experimental animals. The predominant fatty acid released was linoleic acid (18:2) followed by arachidonic acid (20:4). Lipid peroxidation in the basal ganglia measured by the ...
Der ischämische Schlaganfall ist ein ernstzunehmendes Ereignis, welches rascher Rekanalisationstherapie bedarf. Hierfür stehen mehrere Therapieansätze zur Verfügung. Bildgebungsgestützte Patientenselektion zur individuell geeigneten Therapie kann das abschließende klinische Behandlungsergebnis des einzelnen Patienten maßgeblich verbessern. Der Alberta Stroke Program Early CT Score (ASPECTS), eine einfach und schnell anwendbare 10-Punkte-Skala zur Auswertung von Schädel-CT-Untersuchungen, wurde bereits als hilfreicher Prädiktor für das klinische Behandlungsergebnis nach erfolgreicher thrombolytischer Therapie identifiziert. Ein Nachteil der nativen Schädel-CT ist, dass der Infarktkern erst mit mehreren Stunden Verzögerung erkennbar wird. Das aktuelle Ausmaß des Infarktkerns kann durch Bestimmung des zerebralen Blutvolumens (CBV) anhand von Perfusions-CT-Untersuchungen schneller ermittelt werden. Diese Studie analysiert retrospektiv multimodale CT-Bildgebung einer Patientenkohorte von ...
TY - JOUR. T1 - Characteristics of Transient Cerebral Ischemia-Induced Deficits on Various Learning and Memory Tasks in Male Mongolian Gerbils. AU - Amano, Manabu. AU - Hasegawa, Masaya. AU - Hasegawa, Takaaki. AU - Nabeshima, Toshitaka. PY - 1993/1/1. Y1 - 1993/1/1. N2 - We examined the characteristics of 5-min cerebral ischemia-induced behavioral deficits in spontaneous locomotor activity and their effects on the performance of habituation (HAB), passive avoidance (PA) and 8-arm radial maze (RM) tasks in Mongolian gerbils. Performances in HAB, PA and RM were impaired within 2 days after occlusion, and gerbils showed hyperlocomotion during this period. Ten days after ischemia, the hyperlocomotion disappeared and performance in the HAB and PA was the same as that in the sham-operated group. Retention in the RM was impaired at that period, but this impairment was overcome, and retention recovered easily to the sham-operated level with a few additional trials. When the acquisition trial in the RM ...
Introduction: The detection and interpretation of early ischemic changes and salvageable brain parenchyma in acute ischemic stroke is critical in determining appropriate treatment. The Alberta Stroke Program Early CT Score (ASPECTS) was devised as a semi-quantitative method to accurately and reliably determine early ischemic changes in non-contrast CT (NCCT) and CT-perfusion (CTP) imaging. Our objective was to determine the inter-observer variability In assigning ASPECTS to admission NCCT, CTP, and follow-up imaging. Methods: A retrospective study was performed of imaging and clinical data obtained for ischemic stroke patients admitted to the MUSC stroke center between October 1, 2008 - September 30, 2009. Patients were included in the study if they: received a good quality CT and CTP at admission and follow-up NCCT and/or MRI within 7 days, had a National Institute of Health Stroke Scale (NIHSS) score ~ 8 at admission, and were ~ 45 years old. Patients were excluded if they: received a primary ...
In the setting of stroke, ischemia-related blood-brain barrier (BBB) dysfunction aggravates the cerebral edema, which critically impacts on the clinical outcome. Further, an impaired vascular integrity is associated with the risk of intracranial bleeding, especially after therapeutic recanalization. Therefore, the present study was aimed to investigate early vascular alterations from 30 min to 4 h after experimental middle cerebral artery occlusion (MCAO) in mice. Here, an extravasation of the permeability marker FITC-albumin was detectable in animals 2 and 4 h after MCAO. Thereby, BBB breakdown correlated with alterations of the endothelial surface, indicated by a discontinuous isolectin-B4 staining, while tight junction strands remained detectable using electron and immunofluorescence microscopy. Noteworthy, already 30 min after MCAO, up to 60% of the ischemia-affected vessels showed an endothelial edema, paralleled by edematous astrocytic endfeet, clearly preceding FITC-albumin extravasation. With
TY - JOUR. T1 - Activation of protein kinase c delta following cerebral ischemia leads to release of cytochrome c from the mitochondria via bad pathway. AU - Dave, Kunjan R.. AU - Bhattacharya, Sanjoy K.. AU - Saul, Isabel. AU - DeFazio, R. Anthony. AU - Dezfulian, Cameron. AU - Lin, Hung Wen. AU - Raval, Ami P.. AU - Perez-Pinzon, Miguel A.. PY - 2011/7/19. Y1 - 2011/7/19. N2 - Background: The release of cytochrome c from the mitochondria following cerebral ischemia is a key event leading to cell death. The goal of the present study was to determine the mechanisms involved in post-ischemic activation of protein kinase c delta (δPKC) that lead to cytochrome c release. Methods/Findings: We used a rat model of cardiac arrest as an in vivo model, and an in vitro analog, oxygen glucose deprivation (OGD) in rat hippocampal synaptosomes. Cardiac arrest triggered translocation of δPKC to the mitochondrial fraction at 1 h reperfusion. In synaptosomes, the peptide inhibitor of δPKC blocked OGD-induced ...
Platelet-Oriented Inhibition in New TIA and minor ischemic stroke (POINT) Trial, is a prospective, randomized, double-blind, multicenter trial with the primary null hypothesis that, in patients with TIA or minor ischemic stroke treated with aspirin 50-325 mg/day, there is no difference in the event-free survival at 90 days in those treated with clopidogrel (600 mg loading dose then 75 mg/day) compared to placebo when subjects are randomized within 12 hours of time last known free of new ischemic symptoms.. Its primary objective is to determine whether clopidogrel 75 mg/day by mouth after a loading dose of 600 mg of clopidogrel is effective in preventing major ischemic vascular events (ischemic stroke, myocardial infarction, and ischemic vascular death) at 90 days when initiated within 12 hours of TIA or minor ischemic stroke onset in patients receiving aspirin 50-325 mg/day (with a dose of 150-200 mg daily for 5 days followed by 75-100 mg daily strongly recommended).. Patients over 18 years of ...
Platelet-Oriented Inhibition in New TIA and minor ischemic stroke (POINT) Trial, is a prospective, randomized, double-blind, multicenter trial with the primary null hypothesis that, in patients with TIA or minor ischemic stroke treated with aspirin 50-325 mg/day, there is no difference in the event-free survival at 90 days in those treated with clopidogrel (600 mg loading dose then 75 mg/day) compared to placebo when subjects are randomized within 12 hours of time last known free of new ischemic symptoms.. Its primary objective is to determine whether clopidogrel 75 mg/day by mouth after a loading dose of 600 mg of clopidogrel is effective in preventing major ischemic vascular events (ischemic stroke, myocardial infarction, and ischemic vascular death) at 90 days when initiated within 12 hours of TIA or minor ischemic stroke onset in patients receiving aspirin 50-325 mg/day (with a dose of 150-200 mg daily for 5 days followed by 75-100 mg daily strongly recommended).. Patients over 18 years of ...
Sekhon, Ainslie and Griesdale identify Cerebral Oedema as one of the factors relevant to secondary brain injury after Hypoxic Ischaemic Brain Injury (HIBI). The authors note that Cerebral Oedema leads to intracranial hypertension which leads to Decreasing Cerebral Perfusion Pressure which leads to Decreasing Cerebral Blood Flow which leads to Reduced regional oxygen saturation…
Background: Given the limited time window available for treatment with tPA in acute ischemic stroke patients, guidelines recommend door-to-imaging time within 25 minutes of hospital arrival and a door-to-needle time (DTN) within 60 minutes. Despite temporal improvements in door-to-image and DTN, tPA treatment times remain suboptimal.. Objectives: To examine the contributions of door-to-image and imaging-to-needle times to delays in timely delivery of tPA to ischemic stroke patients, and to examine between-hospital variation in DTN.. Methods: A cohort analysis of 1,193 ischemic stroke patients treated with intravenous tPA from 2009-2012 at 25 Michigan hospitals participating in the Paul Coverdell National Acute Stroke Registry. The primary outcome was DTN (time in minutes from emergency department arrival to tPA delivery). Multi-level linear regression models included hospital-specific random effects.. Results: Mean patient age was 68 years, median NIHSS score was 11 (IQR 6-17), 51% were female, ...
Ischemic stroke causes neuronal cell death and triggers a cascade of inflammatory signals that contribute to secondary brain damage. Microglia, the brain-resident macrophages that remove dead neurons, play a critical role in the brains response to ischemic injury. Our previous studies showed that IRF2BP2 regulates peripheral macrophage polarization, limits their inflammatory response and reduces susceptibility to atherosclerosis. Here, we show that loss of IRF2BP2 in microglia leads to increased inflammatory cytokine expression in response to lipopolysaccharide challenge and impaired activation of anti-inflammatory markers in response to interleukin-4 (IL4) stimulation. Focal ischemic brain injury of the sensorimotor cortex induced by photothrombosis caused more severe functional deficits in mice with IRF2BP2 ablated in macrophages/microglia, associated with elevated expression of inflammatory cytokines in the brain. These mutant mice had larger infarctions 4 days after stroke associated with fewer
The effect of the free radical spin-trap alpha-phenyl-butyl-tert-nitrone (alpha-PBN) in permanent focal cerebral ischemia in rats was examined in two series of experiments. In the first, rats were subjected to permanent occlusion of the middle cerebral artery (MCAO) and treated 1 h after occlusion with a single dose of alpha-PBN (100 mg/kg) or saline. Body temperature was measured and controlled for the first 24 h to obtain identical temperature curves in the two groups. Cortical infarct volumes were determined on histological sections 7 days later. alpha-PBN did not significantly reduce infarct volume (control: 28.3+/-16.3 mm3 vs. alpha-PBN 23.7+/-7.4 mm3). In the second series of experiments, periinfarct depolarizations (PIDs) were recorded with an extracellular DC electrode at two locations in the ischemic penumbra for the initial 3 h following MCAO. alpha-PBN (100 mg/kg, single dose in conjunction with occlusion) significantly reduced the total number (median value of 3 PIDs in the control ...
article{3f0ddea8-dd33-4fdd-a777-97a29bef9f47, abstract = {Stroke outcome is determined by a complex interplay, where age and stroke severity are predominant predictors. Studies on hemorrhagic stroke indicate that APOE genotype is a predictor of poststroke outcomes,1,2 but results from studies on ischemic stroke are more conflicting.1,3 There is 1 study suggesting an influence of APOE genotype on age at ischemic stroke onset,4 and sex-specific effects on outcome have been reported.5 Taken together, there is a need for larger studies on APOE and ischemic stroke outcomes with integrated information on age, severity, and sex.,br/,,br/,The 3 common APOE alleles ε2, ε3, and ε4 can be separated by a combination of 2 single nucleotide polymorphisms (SNPs), rs429358 and rs7412. Thus, associations with APOE alleles are not directly captured in a regular genome-wide association study (GWAS), where each SNP is investigated separately. We derived the 3 common APOE alleles and investigated the interplay ...
Background: Nationwide data on the clinical profile and outcomes of ischemic stroke in younger adults are still scarce. Our aim was to analyze clinical characteristics and outcomes of young patients with first-ever ischemic stroke compared to older patients.Methods: The National Acute Stroke ISraeli (NASIS) registry is a nationwide prospective hospital-based study performed triennially. Younger adults, aged 50 years and younger, were compared with patients, aged 51-84 years regarding risk factors, clinical presentation, stroke severity, stroke etiology and outcomes. A logistic model for stroke outcome was fitted for each age group. Results: 336 first-ever ischemic strokes were identified among patients aged 50 years and younger and 3,243 among patients 51-84 years. Younger adults had lower rates of traditional vascular risk factors, but 82.7% had at least one of these risk factors. Younger adults were more likely to be male (62.8%), current smokers (47.3%), and to have a family history of stroke (7.4%).
Antiplatelet therapy for acute ischaemic stroke.. Cochrane Database Syst Rev. 2008;(3):CD000029. Authors: Sandercock PA, Counsell C, Gubitz GJ, Tseng MC. BACKGROUND: In patients with acute ischaemic stroke, platelets become activated. Antiplatelet therapy might reduce the volume of brain damaged by ischaemia and reduce the risk of early recurrent ischaemic stroke. This might reduce the risk of early death and improve long-term outcome in survivors. However, antiplatelet therapy might also increase the risk of fatal or disabling intracranial haemorrhage. OBJECTIVES: To assess the efficacy and safety of antiplatelet therapy in acute ischaemic stroke. SEARCH STRATEGY: We searched the Cochrane Stroke Group Trials Register (last searched June 2007), the Cochrane Central Register of Controlled Trials (CENTRAL) (The Cochrane Library Issue 2, 2007), MEDLINE (June 1998 to May 2007), and EMBASE (June 1998 to May 2007). In 1998, for a previous version of this review, we searched the register of the ...
Object. A critical review of the literature indicates that the effects of nitric oxide synthase (NOS) inhibitors on focal cerebral ischemia are contradictory. In this experiment the authors methodically examined the dose-dependent effects of two NOS inhibitors and two NO donors on cortical infarction volume in an animal model of temporary focal cerebral ischemia simulating potential ischemia during neurovascular interventions.. Methods. Ninety-two Wistar rats underwent 3 hours of combined left middle cerebral artery and bilateral common carotid artery occlusion after having been anesthetized with 1% halothane. A nonselective NOS inhibitor, NG-nitro-l-arginine-methyl-ester (l-NAME), and two NO donors, 3-morpholinosydnonimine hydrochloride and NOC-18, DETA/NO, (Z)-1-[2(2-aminoethyl)-N-(2-ammonioethyl)amino]diazen-1-ium-1,2-diolate, were administered intravenously 30 minutes before ischemia was induced. A selective neuronal NOS inhibitor, 7-nitroindazole (7-NI), was administered intraperitoneally ...
Evidence suggests that brain infiltration of lymphocytes contributes to acute neural injury after cerebral ischemia. However, the spatio-temporal dynamics of brain-infiltrating lymphocytes during the late stage after cerebral ischemia remains unclear. C57BL/6 (B6) mice were subjected to sham, photothrombosis, or 60-min transient middle cerebral artery occlusion (MCAO) procedures. Infarct volume, neurodeficits, production of reactive oxygen species (ROS) and inflammatory factors, brain-infiltrating lymphocytes, and their activation as well as pro-inflammatory cytokine IFN-γ production were assessed. Brain-infiltrating lymphocytes were also measured in tissue sections from post-mortem patients after ischemic stroke by immunostaining. In mice subjected to transient MCAO or photothrombotic stroke, we found that lymphocyte infiltration persists in the ischemic brain until at least day 14 after surgery, during which brain infarct volume significantly diminished. These brain-infiltrating lymphocytes express
BACKGROUND AND PURPOSE: The purpose of this study was to determine whether neuroprotection is feasible without cerebral blood flow augmentation in experimental permanent middle cerebral artery occlusion. METHODS: Rats were subjected to permanent middle cerebral artery occlusion by the suture occlusion method and were treated 1 hour thereafter with a single 5-minute intravenous infusion of the postsynaptic density-95 protein inhibitor Tat-NR2B9c (7.5 mg/kg) or saline (n=8/group). Arterial spin-labeled perfusion-weighted MRI and diffusion weighted MRI were obtained with a 4.7-T Bruker system at 30, 45, 70, 90, 120, 150, and 180 minutes postmiddle cerebral artery occlusion to determine cerebral blood flow and apparent diffusion coefficient maps, respectively. At 24 hours, animals were neurologically scored (0 to 5), euthanized, and the brains stained with 2-3-5-triphenyl tetrazolium chloride to ascertain infarct volumes corrected for edema. Additionally, the effects of Tat-NR2B9c on adenosine 5
BRAIN ischemia stroke is a devastating disease, with more than 10% stroke patients either severely disabled or dead. Although rodent fil- ament middle cerebral artery occlusion (MCAO) model can mimic human brain ischemic stroke well, its wide use was
Ischemic stroke, a major cause of mortality, is frequently accompanied by life-threatening cerebral edema. Aquaporin-4 (Aqp4), an astrocytic transmembrane water channel, is an important molecular contributor to cerebral edema formation. Past studies of Aqp4 expression and localization after ischemia examined grey matter exclusively. However, as white matter astrocytes differ developmentally, physiologically, and molecularly from grey matter astrocytes, we hypothesized that functionally important regional heterogeneity exists in Aqp4 expression and subcellular localization following cerebral ischemia. Subcellular localization of Aqp4 was compared between cortical and white matter astrocytes in postmortem specimens of patients with focal ischemic stroke versus controls. Subcellular localization and expression of Aqp4 was examined in rats subjected to experimental stroke. Volumetric analysis was performed on the cortex and white matter of rats subjected to experimental stroke. Following cerebral ischemia,
MECHANISMS OF TRANSLATION ARREST FOLLOWING FOCAL BRAIN ISCHEMIA by MONIQUE K. LEWIS August 2011 Advisor: Dr. Donald DeGracia Major: Physiology Degree: Doctor of Philosophy The loss of blood flow to the brain is termed ischemia and the subsequent resumption of blood flow is termed reperfusion. Brain ischemia and reperfusion (I/R) occurs primarily following resuscitation from cardiac arrest and stroke and presents one of the most significant clinical challenges. At present, there are no clinically effective pharmacologic interventions to halt brain damage following I/R. The major Aim of this dissertation will be to investigate possible mechanisms involved in neuron death following brain I/R, which may potentially lead to the development of effective therapies. A second major facet of this dissertation will be to address the issue of stroke and diabetes. It is very well established clinically that stroke outcome in diabetic patients is significantly worse than in non-diabetic patients. Diabetes has
33 New Zealand white rabbits were taken and randomly divided into a control group, a hyperbaric air group, and a hyperbaric oxyengation (HBO) group. All were reirrigated types following the creation of acute, incomplete cerebral ischemia. Respective measurements were taken of the overall carotid artery and interior jugular vein blood gases as well as cortical brain tissue homogenate amounts of 6-Keto-PGF1 and TXB2 contained. In conjunction with this, pathological investigations were made. The results were that: the amounts of 6-Keto-PGF1 contained for the HBO group were clearly greatly increased (P< 0.01). TXB2 clearly dropped (P< 0.05). Blood P02 in the HB0 group clearly went up (P < 0.0l). Pathological investigations showed that the HBO groups brain tissue damage was relatively light. Conclusion: there were clear effects on PGI2 and TXA2 with HBO when there was reirrigation after acute cerebral ischemia in the domestic rabbits. This is possibly one mechanism of HBO
Although post-ischemic inflammation induced by the innate immune response is considered an essential step in the progression of cerebral ischemia injury, the role of triggering receptor expressed on myeloid cells 2 (TREM2) in the pathogenesis of ischemic stroke remains to be elucidated. Here, we found that the transcriptional and post-transcriptional levels of TREM2 were increased in cultured primary microglia after oxygen-glucose deprivation and reoxygenation and in the ischemic penumbra of the cerebral cortex after middle cerebral artery occlusion (MCAO) and reperfusion in mice. TREM2 was mainly expressed in microglia, but not in astrocytes, neurons, or oligodendrocytes in mice subjected to MCAO. Manipulating TREM2 expression levels in vitro and in vivo significantly regulated the production of pro- and anti-inflammatory mediators after ischemic stroke. TREM2 overexpression markedly suppressed the inflammatory response and neuronal apoptosis. By contrast, TREM2 gene silencing intensified the ...
BACKGROUND AND PURPOSE: Alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor inhibition has been hypothesized to provide neuroprotective efficacy after cerebral ischemia on the basis of the activity in experimental ischemia models of a variety of compounds with varying selectivity for AMPA over other glutamate receptor subtypes. CP-465,022 is a new, potent, and selective noncompetitive AMPA receptor antagonist. The present study investigated the ability of this compound to reduce neuronal loss after experimental cerebral ischemia to probe the neuroprotective potential of AMPA receptor inhibition. METHODS: To demonstrate that CP-465,022 gains access to the brain, the effects of systemic administration of CP-465,022 were investigated on AMPA receptor-mediated electrophysiological responses in hippocampus and on chemically induced seizures in rats. The compound was then investigated for neuroprotective efficacy in rat global and focal ischemia models at doses demonstrated to be
Background: Cerebral ischemia-reperfusion injury (CIRI) can cause brain tissue inflammation, neuronal degeneration, and apoptosis. There is increasing evidence that microRNAs (miRNA) exert neuroprotective effects by regulating the inflammatory process during cerebral ischemia-reperfusion injury. Additionally, it is increasingly acknowledged that neuroinflammation is regulated by Toll-like receptor 4 (TLR4). However, it is unclear whether miRNA can exert its neuroprotective effects by regulating TLR4-mediated inflammation. Methods: The effects of BMSCs over-expressing miR-202-3p on CIRI, angiogenesis in midbrain tissue, and the release of inflammatory factors (IFs) in the serum were measured using in vivo rat models. We also used SH-SY5Y cells to establish an ischemia-reperfusion in vitro cell model. The interaction between miR-202-3p and TLR4 was analyzed by overexpressing miR-202-3p and knocking down TLR4. Knockdown of TLR4 was performed using siRNA. Results:
TY - JOUR. T1 - Flow cytometric analysis of inflammatory cells in ischemic rat brain. AU - Campanella, Marilena. AU - Sciorati, Clara. AU - Tarozzo, Glauco. AU - Beltramo, Massimiliano. PY - 2002. Y1 - 2002. N2 - Background and Purpose - Inflammation plays a key role in cerebral ischemia through activation of microglia and infiltration by leukocytes. Flow cytometry is a well-established method for quantitative and qualitative analysis of inflammatory cells. However, this technique has not been applied to the study of cerebral ischemia inflammation. The aim of this study was to establish a flow cytometric method to measure inflammatory cells in ischemic brain. Methods - To perform flow cytometry on brain tissue, we developed 2 cell-isolation methods based on different mechanical dissociation and Percoll gradient separation techniques. The methods were tested on a rat model of permanent middle cerebral artery occlusion. Morphological and immunophenotypic analyses, with the use of anti-CD11b, ...
TY - JOUR. T1 - Post-ischaemic thyroid hormone treatment in a rat model of acute stroke. AU - Genovese, Tiziana. AU - Impellizzeri, Daniela. AU - Ahmad, Akbar. AU - Cornelius, Carolin. AU - Campolo, Michela. AU - Cuzzocrea, Salvatore. AU - Esposito, Emanuela. PY - 2013/6/4. Y1 - 2013/6/4. N2 - Stroke is a devastating brain injury that is a leading cause of adult disability with limited treatment options. We examined the effects of prohormone thyroxine (T4) and the underlying mechanisms in the post-ischaemic rat brain after transient focal cerebral ischemia-induced brain injury. Ischaemic injury was induced for 2 h by middle cerebral artery occlusion (MCAo) followed by 24-h reperfusion. T4 (1.1 μg/100 g BW) was administered by intraperitoneally injection twice, at 1 after the onset of ischemia and 6 h after reperfusion. Cerebral infarct area and infarct volume were measured 24 h after MCAo. Furthermore, the mechanism of neuroprotective effect of T4 was investigated with a focus on inflammatory ...
Antagonism of the adenosine A2A receptor (A2AR) has been shown to elicit substantial neuroprotective properties when given immediately after cerebral ischemia. We asked whether the continuous application of a selective A2AR antagonist within a clinically relevant time window will be a feasible and effective approach to treat focal cerebral ischemia. To answer this question, we subjected 20 male spontaneously hypertensive rats to permanent middle cerebral artery occlusion and randomized them equally to a verum and a control group. Two hours after stroke onset, the animals received a subcutaneous implantation of an osmotic minipump filled with 5 mg kg−1 day−1 8-(3-chlorostyryl) caffeine (CSC) or vehicle solution. The serum level of CSC was measured twice a day for three consecutive days. The infarct volume was determined at days 1 and 3 using magnetic resonance imaging. We found the serum level of CSC showing a bell-shaped curve with its maximum at 36 h. The infarct volume was not affected by ...
Lipoic acid (LA) is a naturally occurring compound and dietary supplement with powerful antioxidant properties. Although LA is neuroprotective in models of stroke, little is known about the cellular mechanisms by which it confers protection during the early stages of ischemia. Here, using a rat model of permanent middle cerebral artery occlusion (MCAO), we demonstrated that administration of LA 30 min prior to stroke, reduces infarct volume in a dose dependent manner. Whole-cell patch clamp Show moreLipoic acid (LA) is a naturally occurring compound and dietary supplement with powerful antioxidant properties. Although LA is neuroprotective in models of stroke, little is known about the cellular mechanisms by which it confers protection during the early stages of ischemia. Here, using a rat model of permanent middle cerebral artery occlusion (MCAO), we demonstrated that administration of LA 30 min prior to stroke, reduces infarct volume in a dose dependent manner. Whole-cell patch clamp ...
Protection against focal ischemic injury Special edition Journal of Neurosurgery podcast. Manuscript editor Anne Stanford speaks with Dr. Kevin Lee of the University of Virginia in Charlottesville. They discuss trans-sodium crocetinate and its neuroprotective effects as demonstrated in an animal model of cerebral ischemia and about brain ischemic injury in general.
Our results for diabetes duration are consistent with prior research conducted within a general population of patients, which found an increased rate of ischemic stroke as duration increased compared with nondiabetic patients (9,10). However, our results for HbA1c in diabetic patients with AF are not consistent with prior research conducted in diabetic patients in general. In our study, increased HbA1c did not have a substantial effect on the rate of ischemic stroke, whereas elevated HbA1c was significantly associated with ischemic stroke in predominantly non-AF populations (11-13). A possible reason for HbA1c having no association with ischemic stroke in diabetic patients with AF is the difference in the primary mechanism for stroke in diabetic patients with and without AF. Among patients with diabetes without AF, stroke is often due to underlying atherosclerosis (22,23). This mechanism may not be as important among diabetic patients with AF, because the primary mechanism for ischemic stroke is ...
Recurrent strokes make up almost 25% of the nearly 800,000 strokes that occur annually in the United States. Risk factors for ischemic stroke include hypertension, diabetes mellitus, hyperlipidemia, sleep apnea, and obesity. Lifestyle modifications, including tobacco cessation, decreased alcohol use, and increased physical activity, are also important in the management of patients with a history of stroke or transient ischemic attack. Antiplatelet therapy is recommended to reduce the risk of recurrent ischemic stroke. The selection of antiplatelet therapy should be based on timing, safety, effectiveness, cost, patient characteristics, and patient preference. Aspirin is recommended as initial treatment to prevent recurrent ischemic stroke. Clopidogrel is recommended as an alternative monotherapy and in patients allergic to aspirin. The combination of clopidogrel and aspirin is not recommended for long-term use (more than two to three years) because of increased bleeding risk. Aspirin/dipyridamole is at
Oxidative stress induced cell injury is reported to contribute to the pathogenesis of cerebral ischemia. Reactive oxygen species such as hydrogen peroxide (H2O2) and superoxide radical along with nitric oxide and peroxynitrite generated during ischemia-reperfusion injury, causes the overactivation of poly (ADP-ribose) polymerase (PARP) leading to neuronal cell death. In the present study we have evaluated the effects of PARP inhibitor, 8-hydroxy-2 methyl-quinazolin-4-[3H]one (NU1025) in H2O2 and 3-morphilinosyndonimine (SIN-1) induced cytotoxicity in PC12 cells as well as in middle cerebral artery occlusion (MCAO) induced focal cerebral ischemia in rats. Exposure of PC12 cells to H2O2 (0.4 mM) and SIN-1 (0.8 mM) resulted in a significant decrease in cell viability after 6 h. Pretreatment with NU1025 (0.2 mM) restored cell viability to approximately 73 and 82% in H2O2 and SIN-1 injured cells, respectively. In MCAO studies, NU1025 was administered at different time points (1 h before reperfusion, ...
Carbamylerythropoietin (CEPO) does not bind to the classical erythropoietin (EPO) receptor. Nevertheless, similarly to EPO, CEPO promotes neuroprotection on the histologic level in short-term stroke models. In the present study, we investigated whether CEPO and other nonerythropoietic EPO analogs could enhance functional recovery and promote long-term histologic protection after experimental focal cerebral ischemia. Rats were treated with the compounds after focal cerebral ischemia. Animals survived 1, 7, or 60 days and underwent behavioral testing (sensorimotor and foot-fault tests). Brain sections were stained and analyzed for Iba-1, myeloperoxidase, Tau-1, CD68 (ED1), glial fibrillary acidic protein (GFAP), Fluoro-Jade B staining, and overall infarct volumes. Treatment with CEPO reduced perifocal microglial activation (P, 0.05), polymorphomonuclear cell infiltration (P, 0.05), and white matter damage (P , 0.01) at 1 day after occlusion. Carbamylerythropoietin- treated rats showed better ...
Nitroxyl (HNO) donor compounds function as potent vasorelaxants, improve myocardial contractility and reduce ischemia-reperfusion injury in the cardiovascular system. With respect to the nervous system, HNO donors have been shown to attenuate NMDA receptor activity and neuronal injury, suggesting that its production may be protective against cerebral ischemic damage. Hence, we studied the effect of the classical HNO-donor, Angelis salt (AS), on a cerebral ischemia/reperfusion injury in a mouse model of experimental stroke and on related in vitro paradigms of neurotoxicity. I.p. injection of AS (40 mumol/kg) in mice prior to middle cerebral artery occlusion exacerbated cortical infarct size and worsened the persistent neurological deficit. AS not only decreased systolic blood pressure, but also induced systemic oxidative stress in vivo indicated by increased isoprostane levels in urine and serum. In vitro, neuronal damage induced by oxygen-glucose-deprivation of mature neuronal cultures was exacerbated
TY - JOUR. T1 - Delayed transplantation of human neural precursor cells improves outcome from focal cerebral ischemia in aged rats. AU - Jin, Kunlin. AU - Mao, Xiao Ou. AU - Xie, Lin. AU - Greenberg, Rose B.. AU - Peng, Botao. AU - Moore, Alexander. AU - Greenberg, Maeve B.. AU - Greenberg, David A.. PY - 2010/12. Y1 - 2010/12. N2 - Neural precursor cell (NPC) transplantation may have a role in restoring brain function after stroke, but how aging might affect the brains receptivity to such transplants is unknown. We reported previously that transplantation of human embryonic stem cell (hESC)-derived NPCs together with biomaterial (Matrigel) scaffolding into the brains of young adult Sprague-Dawley rats 3-weeks after distal middle cerebral artery occlusion (MCAO) reduced infarct volume and improved neurobehavioral performance. In this study, we compared the effect of NPC and Matrigel transplants in young adult (3-month-old) and aged (24-month-old) Fisher 344 rats from the National Institute on ...
Nonthrombolytic approach to acute brain ischemia". Critical Care Clinics. 15 (4): 755-776. doi:10.1016/s0749-0704(05)70086-5. ... In the early 1990s he coined the phrase Time is Brain!, as an argument for the need to expedite the treatment of stroke victims ... He has published extensively and is credited with having coined the phrase Time is Brain! to denote the urgency required in the ... 1-9. ISBN 9780521876391., additional History Gomez CR: Time is Brain! J Stroke and Cerebrovasc Dis 3:1-2. 1993, additional Time ...
... brain, and lung injury; injury due to ischemia in the heart, brain, kidney, and gut; and stress-induced central nervous system ... Based on these and other studies, the overproduction of cyclopentenone prostaglandins by the brain has been suggested to ... 14-PGJ2 appears to cause the dilation of coronary arteries and thereby protect against cardiac ischemia and heart attack in a ...
Richmond, T. S. (May 1997). "Cerebral Resuscitation after Global Brain Ischemia", AACN Clinical Issues 8 (2). Retrieved on 2007 ... In some cases coma can give the brain an opportunity to heal and regenerate, but, in general, the longer a coma, the greater ... The deoxygenated blood then passes through the systemic circulation to the vital organs, including the brain, and rapidly ... Free full text Archived September 27, 2007, at the Wayback Machine Phillips, Helen (2006-07-03). "'Rewired brain' revives ...
... brain ischemia). Cell death and irreversible brain damage occurs after 3-6 minutes with no oxygen, due to excitotoxicity. Some ... Cited in Shanna Freeman (17 September 2008). "Top 10 Myths About the Brain". How Stuff Works. p. 5: Your Brain Stays Active ... Such an injury is invariably fatal to humans and most other animals, since it deprives the brain of oxygenated blood, while all ... Other studies indicate that electrical activity in the brain has been demonstrated to persist for 13 to 14 seconds following ...
... d-Deprenyl attenuates apoptosis in experimental brain ischaemia". European Journal of Pharmacology. 430 (2-3): 235-241. doi: ... Molecular Brain Research. 49 (1-2): 127-136. doi:10.1016/S0169-328X(97)00135-6. PMID 9387872. Srinivasan ThyagaRajan; Kelley S ...
On 7 October 2017, Mele died, aged 60, of a brain ischemia. "Morto l'ex parlamentare Udc Cosimo Mele". La Stampa (in Italian). ...
AEP is activated during brain ischemia or brain acidosis and epilepsia seizure. It digests SET protein, which is an inhibitor ... Since stroke elicits acidity in the brain AEP become active due to low pH level. Then it cleaves SET which causes death of ... Increased activity of AEP in brain is also observed in patients with Alzheimer's disease and Parkinson's disease (PD). AEP ... brain, testis tissue and heart and the protein is mostly localised to lysosomes and endosomes. It is also interesting that AEP ...
"Matrix Metalloproteinases in Ischemia - Reperfusion Injury in Brain: Anti-oxidants as Rescuer". Role of Proteases in Cellular ... "Matrix Metalloproteinases in Ischemia - Reperfusion Injury in Brain: Anti-oxidants as Rescuer". Role of Proteases in Cellular ... brain, oral, breast, pancreatic, blood and cervical cancers. She led a team of scientists who worked on the therapeutic ...
"Behaviorally-induced ultrastructural plasticity in the hippocampal region after cerebral ischemia". Brain Research. 997 (2): ... BDNF, brain-derived neurotrophic factor, ANON2, BULN2, Brain-derived neurotrophic factor, brain derived neurotrophic factor. ... Neurotrophic factors are found in the brain and the periphery. BDNF was first isolated from pig brain in 1982 by Yves-Alain ... Brain-derived neurotrophic factor (BDNF), or abrineurin,[5] is a protein[6] that, in humans, is encoded by the BDNF gene.[7][8] ...
"Neuroprotective role of a brain-enriched tyrosine phosphatase, STEP, in focal cerebral ischemia". The Journal of Neuroscience. ... a subfamily of brain-enriched protein tyrosine phosphatases". Brain Research. Molecular Brain Research. 32 (1): 87-93. doi: ... Thus, STEP levels or activity is decreased in Huntington's disease, cerebral ischemia, alcohol abuse, and stress disorders. The ... was the first brain-specific PTP discovered. The human STEP locus maps to chromosome 11p15.2-p15.1 and the murine STEP gene to ...
This causes reduced cardiac output and hypotension, which may result in brain ischemia. A delayed return of symptoms have been ... which can lead to edema and necrosis within the brain. This brain damage occurs mainly during the recovery period. This may ... Brain damage is confirmed following MRI or CAT scans. Extensive follow up and supportive treatment is often required for ... In the brain this causes further mitochondrial dysfunction, capillary leakage, leukocyte sequestration, and apoptosis. The ...
Lei, B; Popp, S; Cottrell, JE; Kass, IS (2009). "Effects of Midazolam on Brain Injury After Transient Focal Cerebral Ischemia ... A Symposium: Acute Blood Pressure and the Brain". American Journal of Cardiology. 63 (6): 43C-47C. doi:10.1016/0002-9149(89) ... Brain and Behavior. 6 (9): e00514. doi:10.1002/brb3.514. PMC 5036436. PMID 27688943. Wang, J; Meng, F; Cottrell, JE; Sacktor, ... Brain Research. 844 (1-2): 143-149. doi:10.1016/s0006-8993(99)01944-7. PMID 10536270. S2CID 45268119. Wang, T; Susman, K; Wang ...
These symptoms can be indicative of insufficient blood flow to the brain (ischemia) as well as compression of arterioles. In ... Compression then results in diminished blood supply to the brain, a condition known as cerebral ischemia. During the increase ... 2005). "Value of Cushing Reflex as warning sign for brain ischemia during neuroendoscopy". Br J Anaesth. 94 (6): 791-9. ... As a result, the Cushing reflex is a last-ditch effort by the body to maintain homeostasis in the brain. It is widely accepted ...
... "miR-497 regulates neuronal death in mouse brain after transient focal cerebral ischemia". Neurobiology of Disease. 38 (1): 17- ... "MicroRNAs show mutually exclusive expression patterns in the brain of adult male rats". PLOS ONE. 4 (10): e7225. doi:10.1371/ ...
Shimizu K, Rajapakse N, Horiguchi T, Payne M, Busija D (2003). "Neuroprotection against hypoxia-ischemia in neonatal rat brain ... M40401 was also found to protect against hypoxic-ischemic brain injury. Mn (III) Salen complexes are found to be more stable ... causing a one hundredfold increase in catalytic activity in treatment of ischemia-reperfusion injuries. ...
... causes an altered mental status due to ischemia in the brain. The normal partial pressure reference values ... brain stem lesion, extreme obesity) A decrease in the area of the lung available for gas exchange (such as in chronic ...
In particular, bEnd.3 cells can serve as blood-brain barrier models for ischemia. Yuen, D; et al. (4 June 2014). "Novel ... bEnd.3 is a mouse brain cell line derived from BALB/c mice. The cell line is commonly used in vascular research and studies of ...
This is especially important after an ischemia, when arachidonic acid levels are elevated. The brain preferentially uses ... "Does CDP-choline modulate phospholipase activities after transient forebrain ischemia?". Brain Research. 893 (1-2): 268-72. doi ... "Neuroprotection afforded by prior citicoline administration in experimental brain ischemia: effects on glutamate transport". ... Once these cross the blood-brain barrier it is reformed into citicoline by the rate-limiting enzyme in phosphatidylcholine ...
January 2019). "Hippo/YAP signaling pathway mitigates blood-brain barrier disruption after cerebral ischemia/reperfusion injury ... signaling pathway may exert neuroprotective effects through mitigating blood-brain barrier disruption after cerebral ischemia/ ... ". Behavioural Brain Research. 356: 8-17. doi:10.1016/j.bbr.2018.08.003. PMC 6193462. PMID 30092249.. ...
The most common application of conventional DWI (without DTI) is in acute brain ischemia. DWI directly visualizes the ischemic ... Applications in the brain: Tract-specific localization of white matter lesions such as trauma and in defining the severity of ... This is often true, but it can be estimated that in more than 30% of the voxels in a standard resolution brain image, there are ... Applications in brain research include the investigation of neural networks in vivo, as well as in connectomics. Applications ...
"Hippo/YAP signaling pathway mitigates blood-brain barrier disruption after cerebral ischemia/reperfusion injury". Behavioural ... Brain Research. 356: 8-17. doi:10.1016/j.bbr.2018.08.003. PMC 6193462. PMID 30092249. Valentina Rausch, Carsten G. Hansen (2020 ...
The release of glutamate during brain anoxia or ischaemia triggers the death of neurons, causing mental or physical handicap. ... Rossi, David J.; Oshima, Takeo; Attwell, David (20 January 2000). "Glutamate release in severe brain ischaemia is mainly by ... "Welcome to Molecular Brain". Molecular Brain. 1 (1): 1-2. doi:10.1186/1756-6606-1-1. PMC 2491439. PMID 18803854. "Editorial ... General Secretary of Korean Society for Brain and Neural Sciences 2015: Secretariat of Korean Society for Brain and Neural ...
"Blood-brain barrier taurine transport during osmotic stress and in focal cerebral ischemia". Journal of Cerebral Blood Flow and ... Taurine crosses the blood-brain barrier[27][28][29] and has been implicated in a wide array of physiological phenomena ... Urquhart N, Perry TL, Hansen S, Kennedy J (May 1974). "Passage of taurine into adult mammalian brain". Journal of ... Tsuji A, Tamai I (1996). "Sodium- and chloride-dependent transport of taurine at the blood-brain barrier". Taurine 2. Advances ...
"Endocannabinoids mediate neuroprotection after transient focal cerebral ischemia". Brain Research. 1240: 213-20. doi:10.1016/j. ... Proposed role in the diseased brain". Experimental Neurology. 224 (1): 48-55. doi:10.1016/j.expneurol.2010.03.022. PMID ... October 2012). "Palmitoylethanolamide reduces early renal dysfunction and injury caused by experimental ischemia and ... Brain, Behavior, and Immunity. 25 (6): 1099-112. doi:10.1016/j.bbi.2011.02.006. PMID 21354467. S2CID 11062539. Scuderi C, ...
Functional changes include evidence of ischemia in vessels of the brain (ICA, ACA, MCA, specifically). It is important to also ... The arteries are either sewn directly into the brain circulation, or placed on the surface of the brain to reestablish new ... brain reaching out to grasp and develop new and more efficient means of bringing blood to the brain and bypassing the areas of ... The artery is then sutured to a branch of the middle cerebral artery on the surface of the brain and the bone is replaced. In ...
"Lubeluzole protects hippocampal neurons from excitotoxicity in vitro and reduces brain damage caused by ischemia". European ... Brain Research. 745 (1-2): 210-21. doi:10.1016/s0006-8993(96)01094-3. PMID 9037412. S2CID 27971291. Maiese K, TenBroeke M, Kue ...
Bobu died in 2014 in a Bucharest hospital, as the result of a brain ischemia. He married Maria Cristian in 1957; she served as ...
... in a primate model of transient focal brain ischemia". Molecular and Chemical Neuropathology. 29 (2-3): 193-210. doi:10.1007/ ... The brain regions where Olney's lesions occur show hypermetabolism [R]ats have rates of brain metabolism that are almost twice ... After 4 years of addiction lesions spread throughout the brain and damage is evident in the pons and other deeper brain ... In 2013 a study using magnetic resonance imaging showed brain lesions in ketamine addicts (using from 0.2g twice a week up to ...
Elevated MMP9 levels can be found in the cases of rheumatoid arthritis and focal brain ischemia. One of MMP9's most widely ... activities in human brain after focal ischemia". Neuroscience Letters. 238 (1-2): 53-6. doi:10.1016/s0304-3940(97)00859-8. PMID ... Brain. 128 (Pt 7): 1622-33. doi:10.1093/brain/awh489. PMID 15800021. Vandooren J, Van den Steen PE, Opdenakker G (2013). " ... "Time course of upregulation of inflammatory mediators in the hemorrhagic brain in rats: correlation with brain edema". ...
November 2008). "Antioxidant, antiinflammatory and antiapoptotic effects of dapsone in a model of brain ischemia/reperfusion in ...
... an endogenous clonidine-displacing substance in the brain. Science. 1994 Feb 18;263(5149):966-9. PMID 7906055 ... Neuroprotective effect of agmatine in rats with transient cerebral ischemia using MR imaging and histopathologic evaluation. ...
If this is not done fast enough, the tissue or organ with ischemia may be too badly hurt, and it might not be able to be saved ... If the blocked artery brought blood to the brain, people can have a stroke. If the blocked artery is to the kidneys, it can ... For all of these types of ischemia or infarction, doctors can try to reopen the blocked artery. This may be done by surgery or ... People with atherosclerosis must also be watched by doctors to make sure they do not get ischemia or infarction. Since they are ...
... also has neuroprotective properties in its demonstrated anti-hypoxia or anti-ischemia effects; there is a ... Moclobemide increases levels of extracellular monoamines and decreases levels of their metabolites in rat brains; tolerance to ... Moclobemide has good penetration across the blood brain barrier with peak plasma levels within the central nervous system ...
a b Richmond, T. S. (May 1997). "Cerebral Resuscitation after Global Brain Ischemia", AACN Clinical Issues 8 (2). Retrieved on ... TIA is now defined as a transient episode of neurologic dysfunction caused by focal brain, spinal cord, or retinal ischemia, ... Global cerebral ischemia - A complete stoppage of blood flow to the brain. ... The brain requires approximately 3.3 ml of oxygen per 100 g of brain tissue per minute. Initially the body responds to lowered ...
Schematic representation of the circle of Willis, arteries of the brain and brain stem. Blood flows up to the brain through the ... blood flow from the other blood vessels can often preserve the cerebral perfusion well enough to avoid the symptoms of ischemia ... Based on a study of 1413 brains, the classic anatomy of the circle is only seen in 34.5% of cases.[3] In one common variation ... The arteries of the base of the brain. Basilar artery labeled below center. The temporal pole of the cerebrum and the ...
"Application of autologous bone marrow mononuclear cells in six patients with advanced chronic critical limb ischemia as a ... ISRAEL21c: Israeli scientists reverse brain birth defects using stem cells December 25, 2008. (Researchers from the Hebrew ...
... or mesenteric ischemia, are observed.[5][9] The use of plasmapheresis in those with GPA and acute kidney failure (renal ... Heart, gastrointestinal tract, brain, other organs: rarely affected.. CausesEdit. The cause of GPA is unknown, although ...
It may lead to brain tumors such as astrocytomas.[95] In some of the late-onset neurodegenerative diseases that share ... "The ubiquitin proteasome system and myocardial ischemia". American Journal of Physiology. Heart and Circulatory Physiology ...
Brain function[edit]. A 2017 systematic review found lower vitamin C concentrations in people with cognitive impairment, ... "Liposomal-encapsulated Ascorbic Acid: Influence on Vitamin C Bioavailability and Capacity to Protect Against Ischemia- ...
Taste messages are sent via these cranial nerves to the brain. The brain can distinguish between the chemical qualities of the ... This can cause mesenteric ischemia if severe enough. A common disorder of the bowel is diverticulitis. Diverticula are small ... The brain has to decide very quickly whether the food should be eaten or not. It was the findings in 1991, describing the first ...
... brain tumours, infection, poisoning, hypoxia, ischemia, encephalopathy or substance abuse).[1] ABI does not include damage to ... See also: Brain injury. Acquired brain injury (ABI) is brain damage caused by events after birth, rather than as part of a ... United Kingdom Acquired Brain Injury Forum. *The Brain Injury Hub - information and practical advice to parents and family ... Ontario Brain Injury Association. "What is Acquired Brain Injury". Retrieved 5 March 2011.. .mw-parser-output cite.citation{ ...
... gene knock-out on the proteolysis of blood-brain barrier and white matter components after cerebral ischemia". Neuroprotection ... "Calgary Stroke Program (E.E.S.), Hotchkiss Brain Institute, University of Calgary, Canada; Duke Clinical Research Institute (L. ... Empat jenis FABP terdapat di sistem saraf, dua diantaranya hanya ditemukan di sistem saraf pusat orang dewasa, yaitu brain-type ... "Gelatinase B modulates selective opening of the blood-brain barrier during inflammation". Department of Neurology, University ...
"Behaviorally-induced ultrastructural plasticity in the hippocampal region after cerebral ischemia". Brain Research. 997 (2): ... BDNF, brain-derived neurotrophic factor, ANON2, BULN2, Brain-derived neurotrophic factor, brain derived neurotrophic factor. ... Brain Research. Molecular Brain Research. 130 (1-2): 178-86. doi:10.1016/j.molbrainres.2004.07.019. PMID 15519688.. ... Brain-derived neurotrophic factor, also known as BDNF, is a protein[5] that, in humans, is encoded by the BDNF gene.[6][7] BDNF ...
Increased intracranial pressure (ICP) is one of the major causes of secondary brain ischemia that accompanies a variety of ... and can be used to identify patients who are at risk of developing cerebral ischemia in early phases of traumatic brain injury ... brain tissue, brain ventricles, and/or intracranial vessels). The common drawback of all these methods is that they measure ... Brain parenchyma tissue[edit]. More recently, multivariate methods have been proposed that derive ICP by combining the transit ...
In the highly metabolically active tissues of the heart and brain, irreversible damage to tissues can occur in as little as 3-4 ... Ischemia o Ischaemia es un restriction in le copia sanguinari ad texito causante un carentia de oxygeno que es necessario pro ... Ischemia or ischaemia is a restriction in blood supply to tissues, causing a shortage of oxygen that is needed for cellular ... Ischemia es generalmente causate per problemas con le vasso sanguinari, con resulta in damno o dysfunction de texito. Etiam ...
Ischemia. *Brain ischemia. *Ischaemic heart disease. *large intestine: Ischemic colitis. *small intestine: Mesenteric ischemia ...
The brain shows manifestations of increased pressure within the cranium, such as headache, nausea, vomiting, and/or ... The resulting ischemia prompts further release of vasoactive substances including prostaglandins, free radicals, and thrombotic ... In the brain, hypertensive encephalopathy - characterized by hypertension, altered mental status, and swelling of the optic ... Similar to hypertensive retinopathy, evidence of nerve fiber infarcts due to ischemia (cotton-wool spots) can be seen on ...
... the blood brain barrier prevents enzyme from reaching the brain, for example), and can sometimes be associated with allergic ... These compounds normally accumulate during exercise or ischemia, but are also elevated in patients with disorders of pyruvate ...
Wright JW, Harding JW (2015). "The Brain Hepatocyte Growth Factor/c-Met Receptor System: A New Target for the Treatment of ... HGF also promotes angiogenesis in ischemia injury.[12] HGF may further play a role as an indicator for prognosis of chronicity ...
In the brain, it slows metabolic activity by a combination of actions. Presynaptically, it reduces synaptic vesicle release ... cardioprotective in cardiac ischemia. *inhibition of neutrophil degranulation. *2-(1-Hexynyl)-N-methyladenosine ... as well as producing a sedative effect through action on A1 and A2A receptors in the brain. Xanthine derivatives such as ... These two receptors also have important roles in the brain,[5] regulating the release of other neurotransmitters such as ...
... traveling to the brain resulting in small ischemic strokes without symptoms, altered blood flow to the brain, inflammation, ... ischemia)). Other possible symptoms include congestive heart failure symptoms such as fatigue, shortness of breath, or swelling ... Emboli in the brain may result in an ischemic stroke or a transient ischemic attack (TIA). ... including bleeding in the brain) is similar to that of warfarin and DOACs despite its inferior efficacy.[81][88] ...
Gainer, J (2008). "Trans-sodium crocetinate for treating hypoxia/ischemia". Expert Opinion on Investigational Drugs. 17 (6): ... Brain Research. 1309: 136-145. doi:10.1016/j.brainres.2009.10.067. PMID 19891959. S2CID 25369069.. ... "Anti-inflammatory effects of crocin and crocetin in rat brain microglial cells". European Journal of Pharmacology. 648 (1-3): ... in patients with a form of brain cancer known as glioblastoma.[14] The drug is currently under investigation for its possible ...
... it is extremely sensitive to early changes in the brain resulting from ischemia (abnormally low blood flow), such as the ... "SPECT Brain Imaging". Retrieved January 12, 2016.. *^ a b c d Crosson B, Ford A, McGregor KM, Meinzer M, Cheshkov S, Li X, ... These measurements reflect the amount of brain activity in the various regions of the brain and allow to learn more about how ... PET scanning is also used for diagnosis of brain disease, most notably because brain tumors, strokes, and neuron-damaging ...
Ischemia[edit]. Main article: Ischemia. Ischemia, meaning insufficient blood flow to a tissue, can also result in hypoxia. This ... Cerebral hypoxia - Oxygen shortage of the brain or cerebral anoxia, a reduced supply of oxygen to the brain ... Erotic asphyxiation or autoerotic hypoxia, intentional restriction of oxygen to the brain for sexual arousal ...
Hum Brain Mapp. 16 (1): 14-23. doi:10.1002/hbm.10026. PMID 11870923. Archived from the original (PDF) on 2012-07-17.. ... 2009). "Wireless near-infrared spectroscopy of skeletal muscle oxygenation and hemodynamics during exercise and ischemia". ... In non-injured patients the brain absorbs the NIR light evenly. When there is an internal bleeding from an injury, the blood ... When a specific area of the brain is activated, the localized blood volume in that area changes quickly. Optical imaging can ...
Malformed aorta, slow pulse, ischemia: these cause reduced blood flow to the renal arteries, with physiological responses as ... the heart and brain.[1][2][3][4] It can be autosomal dominant or autosomal recessive, with the autosomal dominant form being ...
... cytochrome c in vulnerable hippocampal neurons after 4 hours of reperfusion following 10-minute complete brain ischemia". Acta ...
Brain: encephalopathy symptoms including agitation, confusion, coma; causes may include ischemia, bleeding, formation of blood ... In the central nervous system, direct damage of the brain cells and disturbances of neurotransmissions causes altered mental ... brain, urinary tract, skin, and abdominal organs.[3] Risk factors include being very young, older age, a weakened immune system ... Campaign recommended packed red blood cells transfusion for hemoglobin levels below 70 g/L if there is no myocardial ischemia, ...
"Brain. 124 (8): 1646-1656. doi:10.1093/brain/124.8.1646. PMID 11459755. Archived from the original on 2010-02-17.. ... and vasospasm of the blood vessels supplying the labyrinth or central vestibular pathways resulting in ischemia to these ... Benign paroxysmal positional vertigo (BPPV), Ménière's disease, labyrinthitis, stroke, brain tumors, brain injury, multiple ... brain tumors, brain injury, multiple sclerosis, migraines, trauma, and uneven pressures between the middle ears.[2][4][5] ...
... and ethical grounds that a person dies when brain death occurs.1Yet, the brain is highly vulnerable to a... ... The singular importance of the brain to life is exemplified by agreement on medical, legal, ... Brain Ischemia Global Ischemia Focal Ischemia Ischemic Brain Injury Global Brain Ischemia These keywords were added by machine ... Nemoto E.M. (1985) Brain Ischemia. In: Lajtha A. (eds) Alterations of Metabolites in the Nervous System. Springer, Boston, MA. ...
... in the brain. During ischemia, glutamate is released into the synaptic cleft and activates NMDA receptors, increasing calcium ... Schematic of mechanisms implicated in ischemia-induced neuronal death (in red) and the development of ischemic tolerance (in ...
It is well-established that ischemia leads to very complex and heterogenous changes in microcirculation and metabolism of the ... Raichle, M. A., 1983, The pathophysiology of brain ischemia, Ann. Neurol., 13: 2.PubMedCrossRefGoogle Scholar ... Middle Cerebral Artery Brain Cortex Sham Control Ischemic Brain Damage Stroke Group These keywords were added by machine and ... Microcirculation and Mitochondrial Function in Focal Brain Ischemia. In: Longmuir I.S. (eds) Oxygen Transport to Tissue VIII. ...
This reduction in blood flow restricts oxygen to the brain and may result in dead brain tissue, cerebral infarction... ... Cerebral or brain ischemia occurs when there is not enough blood flow to the brain. ... Brain ischemia may be categorized as focal ischemia or global ischemia, and the cause for ischemia can range from congenital ... brain ischemia may result in irreversible brain damage, stroke or cardiac arrest. Treatments for brain ischemia include ...
Brain ischemia is an interruption of the supply of blood to the brain, which disrupts the flow of oxygen and nutrients that are ... Brain ischemia is an interruption of the supply of blood to the brain, disrupting the flow of oxygen and nutrients needed to ... Most commonly, brain ischemia involves not the carotid artery, but one of the smaller blood vessels in the brain. Blood vessels ... When brain ischemia involves the areas of the brain responsible for regulating functions such as breathing and heart rate, this ...
Due to different susceptibility to ischemia of various brain regions, a global brain ischemia may cause focal brain infarction ... During brain ischemia, the brain cannot perform aerobic metabolism due to the loss of oxygen and substrate. The brain is not ... The causes of brain ischemia vary from sickle cell anemia to congenital heart defects. Symptoms of brain ischemia can include ... A closely related disease to brain ischemia is brain hypoxia. Brain hypoxia is the condition in which there is a decrease in ...
Role of oxygen free radicals in carcinogenesis and brain ischemia.. Floyd RA1. ... may be a key event in stroke-induced brain injury. Oxygen free radicals may play a key role in carcinogenesis by mediating ... recent results show that oxidative damage plays a key role in brain injury that occurs in stroke. Subtle changes, such as ...
... Call for Papers. Brain injury of diverse ... Transient global ischemic brain injury may result from cardiac arrest where cerebral perfusion diminishes to the point that ... How different or similar the mechanisms of these two brain injuries and their management are and whether they can be grouped ... We invite our peers to submit original research and review articles that seek to define the mechanisms of brain injury after ...
This project is supported by the Canadian Institutes of Health Research (award #111062), Alberta Innovates - Health Solutions, and by The Metabolomics Innovation Centre (TMIC), a nationally-funded research and core facility that supports a wide range of cutting-edge metabolomic studies. TMIC is funded by Genome Alberta, Genome British Columbia, and Genome Canada, a not-for-profit organization that is leading Canadas national genomics strategy with funding from the federal government. Maintenance, support, and commercial licensing is provided by OMx Personal Health Analytics, Inc. Designed by Educe Design & Innovation Inc. ...
Brain Ischemia: Alzheimers Disease Mechanisms. Ryszard Pluta, MD, PhD (Editor). Head of Laboratory of Ischemic and ... Chapter 9. Dual Role of Autophagy in Ischemia-Reperfusion Brain Injury: Linking Ischemic Autophagy to Alzheimers Disease. ( ... Dual Role of Mitophagy Following Ischemia-Reperfusion Brain Injury: Ischemic Mitophagy Link to Alzheimers Disease. (Marzena ... Chapter 4. Alzheimers Disease-Related Proteins Following Ischemia-Reperfusion Brain Injury. (Ryszard Pluta, MD, PhD, Marzena ...
... Ling-Hua Tang, Zhong-Yuan Xia ... It has been confirmed that PCr is effective in preventing and treating cardiac and renal ischemia-reperfusion injury. In this ... indicated that PCr can decrease the morphological damage and the neuron apoptosis of the ischemia-reperfusion injury brain ... Compared with sham-operated group (sham group), TUNEL-positive cells, MDA, and level of CaM activity increased in ischemia- ...
Affiliations: Center of Excellence for Aging & Brain Repair, Department of Neurosurgery & Brain Repair, University of South ... Rather than the conventional cell replacement mechanism, we advance alternative pathways of graft-mediated brain repair ...
... brain disorder) abbreviated? H/I stands for Hypoxia-Ischemia (brain disorder). H/I is defined as Hypoxia-Ischemia (brain ... New trends in brain hypoxia ischemia research. Effects of the 21-amino steroid tirilazad mesylate (U-74006F) on brain damage ... and practitioners contribute nine chapters on recent and significant research on brain hypoxia-ischemia. ... S.v. "H/I." Retrieved March 21 2019 from https://www.acronymfinder.com/Hypoxia_Ischemia-(brain-disorder)-(H%2fI).html ...
Using an intranasal administration route in a rat model of focal cerebral ischemia, we demonstrate that nose-to-brain delivery ... surgery results in the delivery and retention of FBP in Fas-expressing ischemic areas of the brain. A single intranasal ... reduced neurologic deficit scores and recovery from cerebral ischemia. Intranasally delivered FBP might be a promising strategy ... that by obstructing Fas signaling in cerebral ischemia inhibits apoptosis. ...
Brain ischemia may be analyzed from two different perspectives: that of oxygen deprivation (hypoxic damage per se) and that of ... Brain ischemia may be analyzed from two different perspectives: that of oxygen deprivation (hypoxic damage per se) and that of ... is one of the players deregulated after ischemia and OGD. In addition, neuroprotective intervention either by estradiol or by ... Intense efforts are being undertaken to understand the pathophysiological mechanisms triggered after brain ischemia and to ...
... studies have suggested both exercise and mitochondrial biogenesis contribute to improved post-ischemic recovery of brain ... In the ischemia-exercise group, only peroxisome proliferator activated receptor coactivator-1 (PGC-1) expression was increased ... On the other hand, the benefit of exercise-induced mitochondrial biogenesis in brain has been confirmed. In this study, we ... We subjected adult male rats to ischemia, followed by either treadmill exercise or non-exercise and analyzed the effect of ...
... in brain tissue in simulated ischemia in rats. The study seeks to cast light on NO as a signalling molecule in a modeled ... "The development of brain ischemia is often commonly referred to not only by physicians, but also other "specialists" as James ... In this new study, the team of scientists conducted experimental analysis of NO role in brain tissue in simulated ischemia in ... Nitric oxide: Experimental analysis of its role in brain tissue in simulated ischemia. Pensoft Publishers ...
Novel docosanoids inhibit brain ischemia-reperfusion-mediated leukocyte infiltration and pro-inflammatory gene expression.. ... Docosahexaenoic acid released from membrane phospholipids during brain ischemia is a major source of lipid peroxides. Leukocyte ... The newly discovered brain messenger 10,17S-docosatriene potently inhibited leukocyte infiltration, NFkappaB, and ... These results challenge the view that docosahexaenoate only participates in brain damage and demonstrate that this fatty acid ...
What to look for to determine whether you have a childbirth brain injury case and the settlement value of these medical ... Causes of Infant Brain Ischemia Infant brain ischemia can occur when blood and oxygen flood to the baby are cut off or ... Brain ischemia occurs when brain cells are permanently damaged due to a lack of adequate blood flow. The human brain requires a ... Types of Injuries Caused by Infant Brain Ischemia Brain ischemia is not an injury but rather the name of a medical condition ( ...
PGD(2) DP1 receptor protects brain from ischemia-reperfusion injury.. [Sofiyan Saleem, Hean Zhuang, Artur J de Brum-Fernandes, ... Development of drugs to stimulate the DP1 receptor in brain could provide a new therapeutic strategy against cerebral ischemia ... Ischemia-reperfusion injury was produced by a 90-min occlusion of the right middle cerebral artery followed by a 4-day ... Therefore, in this study, the effect of the DP1 receptor on the outcome of cerebral ischemia in wildtype (WT) and DP1 knockout ...
... a cerebral ischemia-reperfusion (I/R) group, and (iii) an I/R+bexarotene group. Brain water content was measured by the dry wet ... Results After 24 h, 48 h, and 72 h post-I/R, several effects were observed with bexarotene administration: (i) brain water ... in the ischemic brain. The retinoid X receptor agonist bexarotene suppresses MMP-9 expression in endothelial cells and displays ... over-expression disrupts the blood-brain barrier (BBB) ... Brain damage Is the Subject Area "Brain damage" applicable to ...
A TIGAR-Regulated Metabolic Pathway Is Critical for Protection of Brain Ischemia. Mei Li, Meiling Sun, Lijuan Cao, Jin-hua Gu, ... We hypothesized that TIGAR plays a neuroprotective role in brain ischemia as neurons do not rely on glycolysis but are ... We found that TIGAR was highly expressed in brain neurons and was rapidly upregulated in response to ischemia/reperfusion ... Supplementation of NADPH also reduced ischemia/reperfusion brain injury and alleviated TIGAR knockdown-induced aggravation of ...
2. Brain Ischemia Overview. 3. Pipeline Therapeutics*An Overview of Pipeline Products for Brain Ischemia ... Pipeline Therapeutics assessment of products for Brain Ischemia. The report assesses the active Brain Ischemia pipeline ... Brain Ischemia - Pipeline Insight, 2018 report offers comprehensive Insight of the pipeline (under development) therapeutics ... Table 1: Total Products for Brain Ischemia. Table 2: Products in Clinical Stage. Table 3: Products in Non-clinical Stage. Table ...
... activity and pathological outcome following transient cerebral ischemia, which was induced in 33 chronically … ... Outcome after ischemia in the developing sheep brain: an electroencephalographic and histological study Ann Neurol. 1992 Jan;31 ... The length of this depression correlated with the duration of ischemia (r = 0.88). After 30 or 40 minutes of ischemia, EEG ... After 10 or 20 minutes of ischemia, EEG activity was depressed and then progressively recovered and mild selective neuronal ...
This frequently occurs in conjunction with brain hypoxia (HYPOXIA, BRAIN). Prolonged ischemia is associated with BRAIN ... Localized reduction of blood flow to brain tissue due to arterial obstruction or systemic hypoperfusion. ... Brain Ischemia (Cerebral Ischemia). Subscribe to New Research on Brain Ischemia Localized reduction of blood flow to brain ... Cerebral Ischemia; Encephalopathy, Ischemic; Ischemia, Cerebral; Brain Ischemias; Cerebral Ischemias; Ischemia, Brain; ...
1993) Antagonism of the NMDA and non-NMDA receptors in global versus focal brain ischemia. Prog Brain Res 96:125-135. ... 1993) A2A adenosine receptor gene expression in developing rat brain. Brain Res Mol Brain Res 20:313-327. ... A2A Adenosine Receptor Deficiency Attenuates Brain Injury Induced by Transient Focal Ischemia in Mice. Jiang-Fan Chen, Zhihong ... A massive release of these excitatory amino acids during brain ischemia plays a critical role in subsequent neuronal death. A1 ...
Marijuana can lead to temporary cerebrovascular ischemia, but this is not directly affected by most pain medications. Pain ... Can microvascular ischemia in the brain related to marijuana use be triggered by pain medication?. ... A: Drug use can damage the liver, lungs, brain, throat and stomach. Drug use also causes addiction, which can results in ... The microvascular ischemia caused by marijuana is generally short-lived, according to the American Journal of Neuroradiology. ...
Expression of caveolins was decreased in MCAo brain tissue, whereas the levels of iNOS and glial fibrillary acidic protein ( ... To investigate whether changed expression of caveolins has a pivotal role in focal cerebral ischemia, we induced middle ... These results suggest that forced exercise may be beneficial for promoting functional recovery following cerebral ischemia ... rats were used to compare the effects of hypertension on focal cerebral ischemia. All MCAo groups showed neurological ...
Reperfusion was done 2 h after ischemia. Twenty-four hours after ischemia phospholipase A2 (PLA2) levels and metabolic changes ... spectroscopy of brain tissues. MCAo in rats was induced by insertion of nylon filament. One hour after ischemia, rapamycin (250 ... Perchloric acid extraction was performed on the brain of all animals (n=7; sham, vehicle; DMSO and rapamycin 250 μg/kg) and the ... In all 44 metabolites were assigned in the proton NMR spectrum of rat brain tissues. In the vehicle group, we observed ...
Cerebral ischemia is followed by a local inflammatory response that is thought to participate in the extension of the tissue ... Inducible nitric oxide synthase gene expression in brain following cerebral ischemia J Cereb Blood Flow Metab. 1995 May;15(3): ... In the ischemic brain, there was expression of iNOS mRNA that began at 12 h, peaked at 48 h, and returned to baseline at 7 days ... Cerebral ischemia is followed by a local inflammatory response that is thought to participate in the extension of the tissue ...
  • Exercise induces mitochondrial biogenesis after brain ischemia in rats. (biomedsearch.com)
  • We subjected adult male rats to ischemia, followed by either treadmill exercise or non-exercise and analyzed the effect of exercise on the amount of mitochondrial DNA (mtDNA), expression of mitochondrial biogenesis factors, and mitochondrial protein. (biomedsearch.com)
  • A joint study conducted by scientists at the National Academy of Sciences in Belarus and Kazan Federal University in Russia, looks at the role of nitric oxide (NO) in brain tissue in simulated ischemia in rats. (eurekalert.org)
  • In this new study, the team of scientists conducted experimental analysis of NO role in brain tissue in simulated ischemia in rats. (eurekalert.org)
  • Particularly, spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto (WKY) rats were used to compare the effects of hypertension on focal cerebral ischemia. (mdpi.com)
  • Effect of Baicalin-loaded PEGylated cationic solid lipid nanoparticles modified by OX26 antibody on regulating the levels of baicalin and amino acids during cerebral ischemia-reperfusion in rats. (curehunter.com)
  • The effects of exercise preconditioning on cerebral blood flow change and endothelin-1 expression after cerebral ischemia in rats. (curehunter.com)
  • Synthesis and protective effect of scutellarein on focal cerebral ischemia/reperfusion in rats. (curehunter.com)
  • We also investigated two members of the Bcl-2 protein family, which are largely responsible for the outcome of the apoptotic process.Using a model for unilateral cerebral hypoxia-ischemia (HI) in 7-day-old rats, the expression of calpastatin was investigated by western blotting, immuno-histochemistry and quantitative RT-PCR. (avhandlingar.se)
  • Retigabine protects the blood-brain barrier by regulating tight junctions between cerebral vascular endothelial cells in cerebral ischemia-reperfusion rats. (bioportfolio.com)
  • To investigate the effect of retigabine on the blood-brain barrier permeability in rats with cerebral ischemia-reperfusion and its mechanism. (bioportfolio.com)
  • Postnatal day 7 (P7) rats were used to establish classical hypoxia-ischemia animal models, and C16 postconditioning with 100 ug/kg was performed immediately after hypoxia. (medscimonit.com)
  • C16 can protect immature rats against hypoxia-ischemia-induced brain damage by modulating neuroinflammation. (medscimonit.com)
  • Thus, 30 male Wistar rats were divided into three groups by simple random sampling (using a random-number table): Control group (n = 10), Reperfusion ischemia group (n = 10), and Reperfusion ischemia + adenosine group (n = 10). (magiran.com)
  • A single intravenous injection of bio-bFGF/OX26-SA, equivalent to a dose of 25 μg/kg bFGF, produces an 80% reduction in infarct volume in the brain of rats subjected to permanent occlusion of the middle cerebral artery in parallel with a significant improvement of neurologic deficit. (aspetjournals.org)
  • Zhao F, Qu Y, Liu J, Liu H, Zhang L, Feng Y, Wang H, Gan J, Lu R and Mu D: Microarray profiling and co-expression network analysis of LncRNAs and mRNAs in neonatal rats following hypoxic-ischemic brain damage. (spandidos-publications.com)
  • Ischaemia was induced by pMCAO model, and rats were separated in to three groups. (termedia.pl)
  • We found that BDNF gene was down regulated in EE-housed rats when compared to the rats housed in standard cages at 2~12 days after cortical brain ischemia in peri-infarct cortex, contralateral cortex and bilateral hippocampus. (lu.se)
  • The mRNA expression of NGFI-A showed a similar pattern of BDNF except for an increase at 30 d after induction of brain ischemia in EE-housed rats. (lu.se)
  • Ischemia-induced reduction of GR was prevented in the rats housed in EE condition. (lu.se)
  • Methods: Transient focal cerebral ischemia was induced in rats by 60 minutes middle cerebral artery occlusion, followed by 23 hours reperfusion. (sid.ir)
  • This neuroprotective mechanism occurs in rats in which a harmful brain ischemia is followed by a sub-lethal ischemic insult applied at the femoral artery level. (unina.it)
  • Rats subjected to M.oleifera extract at all doses used in this study significantly decreased brain infarct volume both at cortical and subcortical structures in accompany with the elevation of SOD activity in both hippocampus and striatum while only the rats exposed to the extract at doses of 100 and 400 mg kg -1 BW showed the increased GSHPx activity in hippocampus. (thescipub.com)
  • To investigate the expression of autophagy markers of brain cells and the effect of propofol on autophagy during myocardial ischemia-reperfusion in type 2 diabetic rats. (ijpsonline.com)
  • Propofol can up-regulate the level of Phosphorylated mammalian target of rapamycin and down-regulate the expression of mechanistic target of rapamycin to alleviate the damage of brain cells after myocardial ischemia and reperfusion in normal rats and type 2 diabetic rats. (ijpsonline.com)
  • Once 4-CIN was establish to cross the blood-brain barrier, rats were treated with the inhibitor 60 min prior to a 5-min TGI. (deepdyve.com)
  • P7 Sprague-Dawley (SD) rats that underwent right common carotid artery ligation and rat brain microvascular endothelial cells (RBMECs) were used for the assessment of Na + -K + -Cl − co-transporter1 (NKCC1) expression, BBB permeability, cytokine expression, and neutrophil infiltration by western blot, q-PCR, flow cytometry (FCM), and immunofluorescence respectively. (biomedcentral.com)
  • Furthermore, brain electrical activity in freely moving rats was recorded by electroencephalography (EEG). (biomedcentral.com)
  • Vitexin also significantly suppressed brain electrical activity in neonatal rats. (biomedcentral.com)
  • In this study, we investigated the effects of IL-1RA and a novel protein (IL-1RA-PEP) that was fused to IL-1RA with a cell penetrating peptide, on blood-brain barrier integrity, in male rats subjected to transient middle cerebral artery occlusion. (springermedizin.de)
  • Collectively, our results demonstrated that IL-1RA-PEP could effectively penetrate the brain of rats with middle cerebral artery occlusion and ameliorate blood-brain barrier disruption. (springermedizin.de)
  • The results were tested in a whole animal (male Long Evans rats) model of global brain I/R using in situ antibodies and mRNA staining methods, in viv0 protein synthesis and Western blots. (wayne.edu)
  • This study aimed to investigate the effects of agmatine on brain apoptosis, astrogliosis and edema in the rats with transient cerebral ischemia. (oalib.com)
  • Four days after reperfusion, both motor and proprioception functions were assessed and then all rats were sacrificed for determination of brain infarct volume (2, 3, 5-triphenyltetrazolium chloride staining), apoptosis (TUNEL staining), edema (both cerebral water content and amounts of aquaporin-4 positive cells), gliosis (glial fibrillary acidic protein [GFAP]-positive cells), and neurotoxicity (inducible nitric oxide synthase [iNOS] expression). (oalib.com)
  • Conclusions The data suggest that agmatine may improve outcomes of transient cerebral ischemia in rats by reducing brain apoptosis, astrogliosis and edema. (oalib.com)
  • The effects of diabetes mellitus (DM) on the dynamics and intensity of neuronal and glial apoptosis were studied in the frontal, parietal and temporal lobes of the cerebral cortex of rats after ischemia-reperfusion injury. (begellhouse.com)
  • Rats were randomly divided into 4 groups : sham, ischemia-reperfusion (I/R), I/R plus 20 mg/kg resveratrol and I/R plus 40 mg/kg resveratrol. (jkns.or.kr)
  • Schematic of mechanisms implicated in ischemia-induced neuronal death (in red) and the development of ischemic tolerance (in blue) in the brain. (jci.org)
  • Ischemic stroke-induced neuronal cell death results in the permanent disabling of brain function. (nature.com)
  • A single intranasal administration of 2 mg/kg FBP resulted in significantly reduced neuronal cell death by inhibiting Fas-mediated apoptosis leading to decreased infarct volumes, reduced neurologic deficit scores and recovery from cerebral ischemia. (nature.com)
  • There is ample evidence to suggest that apoptosis, in addition to coagulation necrosis, contributes to the neuronal cell death that occurs after brain ischemia 6 . (nature.com)
  • Using in vivo and neuronal OGD models, it was recently established that mTORC1 (mammalian Target of Rapamycin Complex-1), a protein complex downstream of PI3K-Akt pathway, is one of the players deregulated after ischemia and OGD. (frontiersin.org)
  • To further address whether the DP1 protective role in the brain could be extended to neurons, mouse primary corticostriatal neuronal cultures were exposed to the DP1-selective agonist, BW245C, which provided dose-dependent protection against excitotoxicity induced by glutamate. (sigmaaldrich.com)
  • After 10 or 20 minutes of ischemia, EEG activity was depressed and then progressively recovered and mild selective neuronal loss was seen. (nih.gov)
  • Transient global cerebral ischemia causes delayed neuronal death in the hippocampal CA1 region. (mdpi.com)
  • Enriched environment (EE) housing significantly ameliorates neurological deficits induced by cortical brain ischemia without changing infarction size, suggesting that EE-related functional benefits are associated with neuronal plasticity events in the remaining tissue. (lu.se)
  • The receptor for advanced glycation end-products (RAGE) is expressed on human brain endothelial cells (HBEC) and is implicated in neuronal cell death after ischemia. (researchmap.jp)
  • We report that endogenous secretory RAGE (esRAGE) is a splicing variant form of RAGE that functions as a decoy against ischemia-induced neuronal cell damage. (researchmap.jp)
  • It has been also hypothesized, based on in vitro studies, that lactate, produced by glia in large amounts during activation and/or ischemia/hypoxia, is transported via specific glial and neuronal monocarboxylate transporters into neurons for aerobic utilization. (deepdyve.com)
  • Neuronal nitric oxide synthase (nNOS) and nitric oxide (NO) are implicated in neuronal injury following acute hypoxia-ischemia (HI). (figshare.com)
  • The subacute brain slice model could be a tool for studying the mechanisms involved in ongoing neuronal injury, and for rapidly assessing potential neuroprotectants. (figshare.com)
  • Neuronal death following brain I/R injury is a result of a variety of damage pathways. (wayne.edu)
  • Activation of CPP32-like caspases contributes to neuronal apoptosis and neurological dysfunction after traumatic brain injury. (semanticscholar.org)
  • In control animals (without diabetes mellitus), the level of apoptotic processes in neurons and gliocytes has been found to be unchanged in the frontal cortex after 20 minutes of carotid ischemia with one-hour reperfusion, whereas in the parietal lobe apoptosis was activated in neuronal cells, and in the temporal lobe, it was activated in both neuronal and glial cells. (begellhouse.com)
  • The NVU controls blood-brain barrier (BBB) permeability and cerebral blood flow, and maintains the chemical composition of the neuronal 'milieu', which is required for proper functioning of neuronal circuits. (scienceopen.com)
  • Pericytes are uniquely positioned within the neurovascular unit to serve as vital integrators, coordinators and effectors of many neurovascular functions, including angiogenesis, blood-brain barrier (BBB) formation and maintenance, vascular stability and angioarchitecture, regulation of capillary blood flow and clearance of toxic cellular byproducts necessary for proper CNS homeostasis and neuronal function. (scienceopen.com)
  • It has been confirmed that PCr is effective in preventing and treating cardiac and renal ischemia-reperfusion injury. (hindawi.com)
  • In this study, rat cerebral ischemia-reperfusion injury models were constructed. (hindawi.com)
  • This study indicated that PCr can decrease the morphological damage and the neuron apoptosis of the ischemia-reperfusion injury brain through attenuating abnormalities of calcium balance and production of oxygen free radicals. (hindawi.com)
  • PGD(2) DP1 receptor protects brain from ischemia-reperfusion injury. (sigmaaldrich.com)
  • Ischemia-reperfusion injury was produced by a 90-min occlusion of the right middle cerebral artery followed by a 4-day reperfusion. (sigmaaldrich.com)
  • Researchers have struggled to discover an effective therapeutic approach because the pathophysiologic mechanism of forebrain ischemia/reperfusion injury is very complex, especially in the aged population [ 3 ]. (mdpi.com)
  • Xiu-Ju Luo, Bin Liu, Qi-Lin Ma and Jun Peng, "Mitochondrial Aldehyde Dehydrogenase, A Potential Drug Target for Protection of Heart and Brain from Ischemia/Reperfusion Injury", Current Drug Targets (2014) 15: 948. (eurekaselect.com)
  • Current options to treat clinical relapse in inflammatory central nervous system (CNS) conditions such as cerebral ischemia-reperfusion injury are limited, and agents that are more effective are required. (springermedizin.de)
  • This finding might represent its novel therapeutic potential in the treatment of the cerebral ischemia-reperfusion injury. (springermedizin.de)
  • Reperfusion injury stimulates many pathological mechanisms such as leukocyte infiltration, oxidative stress, inflammation, destruction of blood-brain barrier, platelet activation, nitric oxide release, and apoptosis 29 31 34) . (jkns.or.kr)
  • Consequently, a potent anti-inflammatory and antioxidant mediators may be beneficial in the treatment of cerebral ischemia and reperfusion injury. (jkns.or.kr)
  • Transient global ischemic brain injury may result from cardiac arrest where cerebral perfusion diminishes to the point that blood supply can no longer meet the metabolic demand of brain or from aneurysmal subarachnoid hemorrhage where bleed from an intracranial aneurysm elevates the intracranial pressure above the blood pressure leading to at least momentary perfusion arrest. (hindawi.com)
  • Together, our results show that TIGAR protects ischemic brain injury via enhancing PPP flux and preserving mitochondria function, and thus may be a valuable therapeutic target for ischemic brain injury. (jneurosci.org)
  • Extracellular adenosine critically modulates ischemic brain injury, at least in part through activation of the A 1 adenosine receptor. (jneurosci.org)
  • Using line-scan diffusion imaging (LSDI), we investigated perinatal ischemic brain injury. (ajnr.org)
  • Despite technological improvements in obstetric and perinatal care, ischemic brain injury remains a major cause of infant morbidity and mortality (1-3) . (ajnr.org)
  • The findings suggest that ERK is an important mediator of hyperglycemic-ischemic brain injury and possible target for future interventions. (openthesis.org)
  • Mehta SL, Kim T and Vemuganti R: Long noncoding RNA FosDT promotes ischemic brain injury by interacting with REST-associated chromatin-modifying proteins. (spandidos-publications.com)
  • BBB leakage is a key issue in the injury cascade, which exacerbates ischemic brain injury. (biomedcentral.com)
  • If you or a loved one has suffered ischemic brain injury because of a doctor's negligence, you may be entitled to compensation. (marylandmedicalmalpracticeattorneyblog.com)
  • She maintains that this overall failure to monitor enabled her child's ischemic brain injury. (marylandmedicalmalpracticeattorneyblog.com)
  • The child was diagnosed with a severe hypoxic-ischemic brain injury due to oxygen deprivation. (marylandmedicalmalpracticeattorneyblog.com)
  • In this study, we describe the neuroprotective effects of a Fas-blocking peptide (FBP) that by obstructing Fas signaling in cerebral ischemia inhibits apoptosis. (nature.com)
  • This review summarizes the state-of-the-art of the complex kinase mTORC1 focusing in upstream and downstream pathways, their role in central nervous system and their relationship with autophagy, apoptosis and neuroprotection/neurodegeneration after ischemia/hypoxia. (frontiersin.org)
  • We will revise their connexion of mTORC1 with autophagy, apoptosis and neuroprotection/neurodegeneration, mostly focused on ischemia/hypoxia. (frontiersin.org)
  • Geniposide treatment significantly inhibited cell apoptosis, reduced serum IgG leakage into brain tissue, attenuated astrogliosis and microgliosis, prevented loss of pericytes, loss of tight junction and adherens junction proteins. (medworm.com)
  • When injured, neurons of the newborn brain are prone to undergo programmed cell death, apoptosis, since this genetic program is normally activated in some cells during development of the nervous system, even in the perinatal period. (avhandlingar.se)
  • Apoptosis is a programmed cell death that occurs due to various factors such as reperfusion ischemia. (magiran.com)
  • Also, adenosine injection seems to be effective in reducing oxidative stress and apoptosis induced by cerebral reperfusion ischemia. (magiran.com)
  • Level of oxidative stress, inflammatory mediators, and markers of apoptosis were estimated in the brain tissues. (termedia.pl)
  • Treatments with PtA attenuate the activity of antioxidant enzyme, and the level of inflammatory mediators and markers of apoptosis in the brain tissues of ischaemia-induced brain injury. (termedia.pl)
  • In vivo optical imaging of early-stage apoptosis in mouse brain after transient cerebral ischemia. (semanticscholar.org)
  • Detection of DNA damage induced by apoptosis in the rat brain following incomplete ischemia. (semanticscholar.org)
  • Apoptosis, a genetically programmed cellular event which occurs after ischemia and leads to biochemical and morphological changes in cells. (jkns.or.kr)
  • Pathological events like ischemia cause necrosis but can also induce apoptosis 20) . (jkns.or.kr)
  • Recent researches prove that activation of the cysteine protease caspases is critical for apoptosis in ischemia-induced brain injury 21) . (jkns.or.kr)
  • Using an intranasal administration route in a rat model of focal cerebral ischemia, we demonstrate that nose-to-brain delivery of FBP after middle cerebral artery occlusion (MCAO) surgery results in the delivery and retention of FBP in Fas-expressing ischemic areas of the brain. (nature.com)
  • To investigate whether changed expression of caveolins has a pivotal role in focal cerebral ischemia, we induced middle cerebral artery occlusion (MCAo)-reperfusion and examined expression of caveolins, inflammatory activation markers, and mediators of autophagic cell death. (mdpi.com)
  • Two hours after the last dose, each main group was subdivided into middle cerebral artery occlusion (MCAO) operated for infarct volume assessment and intact subgroup for the assessment of brain and serum antioxidant activity and lipid proxidation of brain and serum, respectively. (magiran.com)
  • We have previously found that sphingosine 1-phospate receptor subtype 1 (S1P 1 ) in post-ischemic brain following transient middle cerebral artery occlusion (tMCAO) can trigger microglial activation, leading to brain damage. (kstudy.com)
  • In the 2-hour middle cerebral artery occlusion model with 3-hour recirculation, we have identified 28 known ischemia-hypoxia response genes that are upregulated and 6 that are downregulated, together with 35 upregulated and 41 downregulated genes newly connected with ischemia. (pptaglobal.org)
  • We here used the oxidative chain inhibitor 3-nitropropionic acid (NPA) to induce ischemia tolerance in a rat middle cerebral artery occlusion (MCAO) stroke model. (uzh.ch)
  • 1 Yet, the brain is highly vulnerable to a variety of insults such as stroke, cardiac arrest, trauma, near-drowning, carbon monoxide poisoning, etc. with high morbidity and mortality. (springer.com)
  • This reduction in blood flow restricts oxygen to the brain and may result in dead brain tissue, cerebral infarction or stroke, according to the Columbia University Medical Center. (reference.com)
  • In severe cases, brain ischemia may result in irreversible brain damage, stroke or cardiac arrest. (reference.com)
  • The human brain, including blood vessels that can be involved in a stroke. (wisegeek.com)
  • 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)
  • 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)
  • Using a combination of these newer methods collectively focused on one model, recent results show that oxidative damage plays a key role in brain injury that occurs in stroke. (nih.gov)
  • Subtle changes, such as oxidative damage-induced loss of glutamine synthetase activity, may be a key event in stroke-induced brain injury. (nih.gov)
  • We invite our peers to submit original research and review articles that seek to define the mechanisms of brain injury after transient global cerebral ischemic stroke and aneurysmal subarachnoid hemorrhage (aSAH). (hindawi.com)
  • These findings present strong evidence that Fas ligand/receptor pathway promotes cell death following brain ischemia and inhibition of Fas ligand/receptor interaction may provide significant neuroprotection affording a new treatment modality in ischemic stroke injury. (nature.com)
  • The newly discovered brain messenger 10,17S-docosatriene potently inhibited leukocyte infiltration, NFkappaB, and cyclooxygenase-2 induction in experimental stroke and elicited neuroprotection. (nih.gov)
  • In animal and cellular stroke models, ischemia/reperfusion increased mitochondrial localization of TIGAR. (jneurosci.org)
  • Together with complimentary pharmacological studies, these data suggest that A 2A receptors play a prominent role in the development of ischemic injury within brain and demonstrate the potential for anatomical and functional neuroprotection against stroke by A 2A receptor antagonists. (jneurosci.org)
  • These findings, in concert with our recent demonstration that inhibition of iNOS reduces infarct volume in the same stroke model, indicate that NO production may play an important pathogenic role in the progression of the tissue damage that follows cerebral ischemia. (nih.gov)
  • Ferrer Therapeutics has made available CerAxon Oral Solution, a medical food containing citicoline, for the dietary management of brain ischemia due to stroke or traumatic brain injury in patients who have difficulty swallowing. (empr.com)
  • We investigated whether stroke changes the circRNAs expression profile in the mouse brain. (ovid.com)
  • New Rochelle, NY -Researchers have shown that following a stroke-induced ischemic injury to the human brain, stem cells are produced that have the potential to differentiate and mature to form neurons that can help repair the damage to the brain. (healthcanal.com)
  • The new clinical study that provides direct evidence of ischemia-induced stem cells (iSCs) in brain tissue removed during treatment of post-stroke patients is published in Stem Cells and Development , a peer-reviewed journal from Mary Ann Liebert, Inc., publishers . (healthcanal.com)
  • In the article entitled " Identification of Multipotent Stem Cells in Human Brain Tissue Following Stroke ," Kotaro Tatebayashi, Yasue Tanaka, Akiko Nakano-Doi , and coauthors from Hyogo College of Medicine, Nishinomiya, Japan, present this first clinical report describing the isolation of iSCs from the post-stroke human brain. (healthcanal.com)
  • The stem cells were situated near blood vessels in areas of the brain containing neurons that had died as a result of stroke-related lack of oxygen. (healthcanal.com)
  • This excellently performed demonstration in the human brain confirms previous work in the mouse that showed cerebral ischemia induced multipotent stem cells that were restricted to areas of the brain damaged by stroke," says Editor-in-Chief Graham C. Parker, PhD , The Carman and Ann Adams Department of Pediatrics, Wayne State University School of Medicine, Detroit, MI. (healthcanal.com)
  • However, the infant brain displays a unique profile of sensitivity and resistance compared to adult ischaemic stroke patients. (intechopen.com)
  • In this study, post-mortem brain slices from ischemic stroke patients were obtained corresponding to infarcted (IC) and contralateral (CL) areas. (mcponline.org)
  • Therefore, the quantitative proteomes of neurons and the BBB (or proteotypes) after human brain ischemia presented here contribute to increasing the knowledge regarding the molecular mechanisms of ischemic stroke pathology and highlight new proteins that might represent putative biomarkers of brain ischemia or therapeutic targets. (mcponline.org)
  • Ischemic stroke represents ∼85% of all stroke cases and is characterized by the impairment of blood flow to a specific region of the brain parenchyma caused by the occlusion of a cerebral artery ( 1 ). (mcponline.org)
  • Brain injury due to ischemic stroke is a major cause of permanent behavioral disabilities. (sciencemag.org)
  • Two cases of brain stem stroke involving the upper pons and the ponto-mesencephalic junction presented with transient excessive pathological yawning, associated with gait ataxia and in one subject with upper limb and facial hemiparesis. (ebscohost.com)
  • e.g. brief induced limb ischemia protects the brain from an otherwise more severe stroke. (bioportfolio.com)
  • Hypoxia and ischemia play a major role in the pathogenesis of cerebrovascular diseases such as stroke. (eurekaselect.com)
  • Brain injury caused by ischaemic stroke is a major cause of disability and death throughout the world. (termedia.pl)
  • Introduction: Brain edema is one of the most important mechanisms responsible for brain damage and mortality after ischemic stroke. (sid.ir)
  • CONCLUSION: The careful study of rodent ischemia models can yield valuable, clinically relevant insights into the pathophysiology of ischemic stroke. (pptaglobal.org)
  • Blood brain barrier (BBB) breakdown and neuroinflammation are key events in ischemic stroke morbidity and mortality. (strath.ac.uk)
  • Brain ischemia and reperfusion (I/R) occurs primarily following resuscitation from cardiac arrest and stroke and presents one of the most significant clinical challenges. (wayne.edu)
  • There has been extensive research on persistent TA in global models of brain I/R, whereas research in focal ischemia, as occurs in stroke, has not been as extensive. (wayne.edu)
  • The blood-brain barrier after stroke: structural studies and the role of transcytotic vesicles. (springermedizin.de)
  • Ischemic stroke induced matrixmetallo-proteinase-9 (MMP-9) upregulation, which increased blood-brain barrier permeability. (biomedcentral.com)
  • The resulting lack of oxygen can cause brain tissue death, a cerebral infarction or ischemic stroke. (marylandmedicalmalpracticeattorneyblog.com)
  • Untreated brain ischemia can lead to a stroke, cardiorespiratory arrest and even permanent brain damage. (marylandmedicalmalpracticeattorneyblog.com)
  • The focus of the 2012 symposium was widened from stroke and traumatic brain injury to neurodegenerative diseases, notably dementia, and more generally the ageing brain. (scienceopen.com)
  • Thereby, emphasis was given on neurovascular aspects of neurodegeneration and stroke including the blood-brain barrier, recent findings regarding the pathomechanism of Alzheimer's disease, and brain imaging approaches. (scienceopen.com)
  • A brief episode of ischemia affecting the brain is called a transient ischemic attack (TIA), often called a mini-stroke. (wikipedia.org)
  • and global ischemia, which encompasses wide areas of brain tissue. (wikipedia.org)
  • Finally, analysis of literature and results of conducted experiments demonstrated that comprehensive approach and application of precision methods of NO level measurement in brain tissue contributed to real data acquisition on the complex dynamics of NO production in nerve tissue in health and disease. (eurekalert.org)
  • Localized reduction of blood flow to brain tissue due to arterial obstruction or systemic hypoperfusion. (curehunter.com)
  • Expression of caveolins was decreased in MCAo brain tissue, whereas the levels of iNOS and glial fibrillary acidic protein (GFAP) increased. (mdpi.com)
  • Cerebral ischemia is followed by a local inflammatory response that is thought to participate in the extension of the tissue damage occurring in the postischemic period. (nih.gov)
  • Brain edema was measured on day 5 by MRI, histochemical staining of brain sections and tissue water content determination (n=7, each experiment). (sigmaaldrich.com)
  • On the left a patient with hypoattenuating brain tissue in the right hemisphere. (radiologyassistant.nl)
  • Cerebral ischemia entails rapid tissue damage in the affected brain area causing devastating neurological dysfunction. (mcponline.org)
  • Regional brain tissue prostaglandin (PG) levels have been measured during ischaemia produced by bilateral carotid occlusion for 1 hour and following restoration of flow. (ahajournals.org)
  • In the normal gerbil, the frontal cortical levels of PGF2 alpha were: 6.7 +/- 1.3 pg/mg and for PGE2: 6.4 +/- 1.1 pg/mg of brain tissue protein. (ahajournals.org)
  • However, neutrophil location and access to the damaged brain tissue is not yet entirely understood. (csic.es)
  • Brain tissue was taken to detect its levels of mechanistic target of rapamycin, phosphorylated mammalian target of rapamycin and Beclin-1 by Western blot. (ijpsonline.com)
  • Intracerebral transplantation of bone marrow stromal cells ameliorates tissue plasminogen activator-induced brain damage after cerebral ischemia in mice detected by in vivo and ex vivo optical imaging. (semanticscholar.org)
  • Neonatal hypoxic-ischemic brain damage, characterized by tissue loss and neurologic dysfunction, is a leading cause of mortality and a devastating disease of the central nervous system. (biomedcentral.com)
  • Moreover, it preserved blood-brain barrier integrity, attenuated changes in expression and localization of tight junction proteins and matrix metalloproteinases, and enhanced angiogenesis in ischemic brain tissue. (springermedizin.de)
  • Suzuki Y, Nagai N, Umemura K. A review of the mechanisms of blood-brain barrier permeability by tissue-type plasminogen activator treatment for cerebral ischemia. (springermedizin.de)
  • Ischemia or ischaemia is a restriction in blood supply to tissues, causing a shortage of oxygen that is needed for cellular metabolism (to keep tissue alive). (wikipedia.org)
  • Ischemia is generally caused by problems with blood vessels, with resultant damage to or dysfunction of tissue. (wikipedia.org)
  • Without immediate intervention, ischemia may progress quickly to tissue necrosis and gangrene within a few hours. (wikipedia.org)
  • Ischemia is a vascular disease involving an interruption in the arterial blood supply to a tissue, organ, or extremity that, if untreated, can lead to tissue death. (wikipedia.org)
  • Brain injury of diverse etiologies is frequently encountered in the clinical setting and requires diverse management. (hindawi.com)
  • FasL mutant mice (gld) are strongly protected from cerebral ischemic injury, and FasL deficiency does not appear to affect brain development or anatomy in these mice 13 . (nature.com)
  • The results indicate that exercise can promote mitochondrial biogenesis after ischemic injury, which may serve as a novel component of exercise-induced repair mechanisms of the brain. (biomedsearch.com)
  • Understanding the molecular basis for exercise-induced neuroprotection may be beneficial in the development of therapeutic approaches for brain recovery from the ischemic injury. (biomedsearch.com)
  • Brain ischemia is not an injury but rather the name of a medical condition (reduction of blood supply to the brain) that causes various types of injuries. (millerandzois.com)
  • Supplementation of NADPH also reduced ischemia/reperfusion brain injury and alleviated TIGAR knockdown-induced aggravation of ischemic injury. (jneurosci.org)
  • Promoting neurogenesis via Wnt/β-catenin signaling pathway accounts for the neurorestorative effects of morroniside against cerebral ischemia injury. (curehunter.com)
  • The present study investigated whether the PGI2 IP receptor plays an important role in brain injury after global cerebral ischemia in aged mice. (mdpi.com)
  • This study aims to investigate whether Geniposide has therapeutic potential to HI brain injury and the underlying mechanisms. (medworm.com)
  • Geniposide could protect against HI-induced brain injury, which might be through the activation of PI3K/Akt signaling pathway. (medworm.com)
  • Hypoxic ischaemic injury can damage the brain at any age. (intechopen.com)
  • With new revelations in the biology of brain injury in perinates and neonates being discovered, as global mortality and morbidity increases research funding into infant brain injury, it is important to raise awareness of the unparalleled challenge of treating these young patients. (intechopen.com)
  • If the injury occurs prior to 36 gestational weeks, the condition is described as perinatal hypoxia ischaemia. (intechopen.com)
  • Between 0.7 and 1.2 million infants are born with evidence of hypoxic ischaemic brain injury every year, accounting for 23% of global infant mortality [ 21 ]. (intechopen.com)
  • However, the molecular mechanisms underlying remapping after brain injury and the consequences of its modulation are poorly understood. (sciencemag.org)
  • ME may protect ischemia/reperfusion induced brain injury by increase in antioxidant activity, decrease in lipid proxidation and reduction in infarction volume. (magiran.com)
  • The cause of mechanisms underlying perinatal brain injury is not fully known, but it results in a wide variety of neurological impairments in the affected children. (avhandlingar.se)
  • The aim of this thesis was to elucidate the possible interaction between the classic necrotic and apoptotic cell death pathways in an animal model of perinatal brain injury. (avhandlingar.se)
  • Aim: To investigate the relation between brain ischemia and persistent vegetative state after severe traumatic brain injury. (neuroskills.com)
  • Persistent coma after severe brain injury is associated with bilateral thalamic ischemia. (neuroskills.com)
  • DL-3-n-butylphthalide protects the blood-brain barrier against ischemia/hypoxia injury via upregulation of tight junction proteins. (bioportfolio.com)
  • With the advent of sensitive imaging modalities such as diffusion-weighted magnetic resonance imaging (MRI), there has been an increasing awareness of injury to the brain in patients without major symptoms. (onlinejacc.org)
  • Hypoxic/ischemic (HI) brain damage (HIBD) is a major cause of acute neonatal brain injury, leading to high mortality and serious neurological deficits. (spandidos-publications.com)
  • Cell Counting Kit‑8 assays, Hoechst staining, calcein‑AM/PI staining, immunostaining, water maze tests and rotarod tests demonstrated that BDNF‑AS silencing protected against hypoxia‑induced primary hippocampal neuron injury in vitro and HI‑induced brain injury in vivo. (spandidos-publications.com)
  • Johnston MV, Trescher WH, Ishida A and Nakajima W: Neurobiology of hypoxic-ischemic injury in the developing brain. (spandidos-publications.com)
  • Zhao RB, Zhu LH, Shu JP, Qiao LX and Xia ZK: GAS5 silencing protects against hypoxia/ischemia-induced neonatal brain injury. (spandidos-publications.com)
  • The present study evaluates the neuroprotective effect of pseudopterosin A (PtA) against ischaemia-induced brain injury. (termedia.pl)
  • Repositioning drugs for traumatic brain injury - N-acetyl cysteine and Phenserine. (termedia.pl)
  • Kong X, Gong S, Su L, Li C, Kong Y. Neuroprotective effects of allicin on ischemia-reperfusion brain injury. (termedia.pl)
  • These data suggest that brain injury in cerebral malaria may be due in part to secondary systemic and intracranial factors as well as to the direct effect of intravascular sequestration. (bmj.com)
  • Diabetes can promote the autophagy of brain cells during myocardial ischemia-reperfusion and aggravate the brain injury. (ijpsonline.com)
  • In animal myocardial or cerebral ischemia/ reperfusion (I/R) models, accumulation of toxic aldehydes, such as 4-hydroxy-2-nonenal and malondialdehyde, is thought to be an important mechanism for myocardial and cerebral I/R injury. (eurekaselect.com)
  • Thus, ALDH2 might be a potential drug target for protection of the heart or brain from I/R injury. (eurekaselect.com)
  • Indeed, some of the newly identified ALDH2 activators (such as Alda-1) have demonstrated beneficial effects on heart and brain I/R injury. (eurekaselect.com)
  • The main purpose of this review is 1) to summarize recent findings regarding the role of ALDH2 in protection of heart or brain from I/R injury, 2) to list the available ALDH2 activators with their potency, selectivity and clinical potentials, and 3) to provide a rationale for ALDH br cells in clinical therapeutic value. (eurekaselect.com)
  • We have previously shown that vitexin has been attributed various medicinal properties and has been demonstrated to have neuroprotective roles in neonatal brain injury models. (biomedcentral.com)
  • Using an in vivo model of mast cell deficiency, this is the first study showing that mast cells promote BBB breakdown in focal ischemia in mice, and opens up future opportunities for using mice to identify specific mechanisms of mast cell-related BBB injury. (strath.ac.uk)
  • Below, I will review our current understanding of I/R brain injury and how diabetes worsens outcome. (wayne.edu)
  • Background Although agmatine therapy in a mouse model of transient focal cerebral ischemia is highly protective against neurological injury, the mechanisms underlying the protective effects of agmatine are not fully elucidated. (oalib.com)
  • Her colon was ruptured during the procedure, resulting in cerebral hypoxic-ischemia and a fatal brain injury. (marylandmedicalmalpracticeattorneyblog.com)
  • The defense denied any malpractice and asserted that the child's brain injury occurred prior to labor or delivery. (marylandmedicalmalpracticeattorneyblog.com)
  • APOE4 is a major genetic risk factor for Alzheimer's disease and is associated with Down's syndrome dementia and poor neurological outcome after traumatic brain injury and haemorrhage. (scienceopen.com)
  • In mice, lack of Apoe leads to blood-brain barrier (BBB) breakdown, whereas APOE4 increases BBB susceptibility to injury. (scienceopen.com)
  • Therefore, in this study, the effect of the DP1 receptor on the outcome of cerebral ischemia in wildtype (WT) and DP1 knockout (DP1(-/-)) C57Bl/6 mice was investigated. (sigmaaldrich.com)
  • Early Upregulation of NLRP3 in the Brain of Neonatal Mice Exposed to Hypoxia-Ischemia: No Early Neuroprotective Effects of NLRP3 Deficiency. (umassmed.edu)
  • Then mice at P18 were sacrificed and brain tissues were collected for further analysis. (medworm.com)
  • show that sensory deprivation in mice (through whisker trimming) after focal cerebral ischemia improved sensorimotor recovery through accelerated remapping to the somatosensory cortex representing the whiskers. (sciencemag.org)
  • Results In SBI-induced mice, we found abnormal activation of the coagulation cascade (factor XIII activity) and increased inflammation (myeloperoxidase activity) close to where emboli lodge in the brain. (onlinejacc.org)
  • In addition, fluorescent neutrophils obtained from reporter DsRed (discosoma red fluorescent protein) mice were transferred intravenously to wild-type mice after ischemia. (csic.es)
  • Mice received transcardial paraformaldehyde perfusion, the brain was cryoprotected, frozen, and cryostat sections were studied by immunofluorescence and confocal microscopy. (csic.es)
  • Adult male C57BL6/J wild type (WT) and mast cell-deficient (C57BL6/J KitWsh/Wsh (Wsh)) mice underwent tMCAo and BBB breakdown, brain edema and neutrophil infiltration were examined after 4 hours of reperfusion. (strath.ac.uk)
  • There was no effect of cromoglycate versus vehicle in Wsh mice, validating specificity of cromoglycate on brain mast cells. (strath.ac.uk)
  • The results showed that mesenchymal stem cell therapy attenuated blood-brain barrier disruption in mice after ischemia. (biomedcentral.com)
  • Common symptoms of brain ischemia include weakness in the body, coordination problems, blindness, unconsciousness and speech impairments. (reference.com)
  • Symptoms of brain ischemia vary, depending on the area of the brain involved. (wisegeek.com)
  • The main symptoms of Brain ischemia involve impairments in vision, body movement, and speaking. (wikipedia.org)
  • The symptoms of brain ischemia reflect the anatomical region undergoing blood and oxygen deprivation. (wikipedia.org)
  • The symptoms of brain ischemia range from mild to severe. (wikipedia.org)
  • Within all the considered experimental protocols, the one in which 100 minutes of MCAO were followed by 10 minutes reperfusion and 20 minutes occlusion of the femoral artery was the most effective in reducing brain infarct, resulting in almost 50% reduction in the infarct volume if compared to animals subjected to 100' MCAO alone. (unina.it)
  • In order to test this hypothesis, we aimed to determine the protective effect of M.oleifera leaves extract in animal model of focal cerebral ischemia induced by permanent occlusion of right middle cerebral artery. (thescipub.com)
  • The singular importance of the brain to life is exemplified by agreement on medical, legal, and ethical grounds that a person dies when brain death occurs. (springer.com)
  • Cerebral or brain ischemia occurs when there is not enough blood flow to the brain. (reference.com)
  • Focal ischemia is isolated to a particular region of the brain and occurs when a brain vessel is blocked by the formation of a blood clot. (reference.com)
  • Global ischemia covers wide portions of the brain and occurs when blood flow to the brain is severely reduced or stopped. (reference.com)
  • If the brain becomes damaged irreversibly and infarction occurs, the symptoms may be permanent. (wikipedia.org)
  • Brain ischemia occurs when brain cells are permanently damaged due to a lack of adequate blood flow. (millerandzois.com)
  • This frequently occurs in conjunction with brain hypoxia (HYPOXIA, BRAIN). (curehunter.com)
  • Brain damage after hypoxia-ischemia (HI) occurs in an age-dependent manner. (bioportfolio.com)
  • Prolonged ischemia is associated with BRAIN INFARCTION. (curehunter.com)
  • MR diffusion-weighted imaging provides early demonstration of neonatal brain infarction. (ajnr.org)
  • Recent studies have documented that diffusion-weighted imaging can show areas of infarction in perinatal brain ischemia before abnormalities are apparent on conventional MR images (7, 11, 12) . (ajnr.org)
  • MCA infarction: on CT an area of hypoattenuation appearing within six hours is highly specific for irreversible ischemic brain damage. (radiologyassistant.nl)
  • The TTC stain for infarction area and TUNEL stain for apoptotic cells were assayed 24 h after the brain hypoxia. (medscimonit.com)
  • Such investigations should lead to a better understanding and insight into the sequential early changes in the brain parenchyma after ischemia, which could be used for identifying new targets for neuroprotection. (epfl.ch)
  • In conclusion, neuroprotection in regional brain ischemia is possible following the delayed intravenous injection of low doses of bFGF providing the neurotrophin is conjugated to a BBB drug-targeting system. (aspetjournals.org)
  • Adventures in the Pathophysiology of Brain Ischemia: Penumbra, Gene Expression, Neuroprotection: The 2002 Thomas Willis Lecture. (pptaglobal.org)
  • Dóra E., Greenberg J.H., Tanaka K., Gonatas N.H., Reivich M. (1986) Microcirculation and Mitochondrial Function in Focal Brain Ischemia. (springer.com)
  • Neuroprotective strategies, including the early use of pharmacologic agents and induced cerebral hypothermia, may help to decrease the deleterious effects of brain ischemia (3) . (ajnr.org)
  • Our aim was to test whether immediate treatment with cannabidiol and hypothermia act through complementary brain pathways in hypoxic-ischemic newborn piglets. (frontiersin.org)
  • The present study demonstrated that cannabidiol and hypothermia act complementarily and show additive effects on the main factors leading to hypoxic-ischemic brain damage if applied shortly after the insult. (frontiersin.org)
  • It therefore appears that hypothermia can prevent effectively mitochondrial dysfunction due to ischemia. (springer.com)
  • Mild brain hypothermia (32 degrees C target temperature, for 5 hours) is highly neuroprotective even when initiated at the onset of recirculation. (pptaglobal.org)
  • We compared the effects of normothermia (38℃, group A), mild-hypothermia (33℃, group B), and severe-hypothermia (28℃, group C) on the central nervous functions after the global brain ischemia using 24 mongrel dogs (BW 13.5±3.4 kg). (nii.ac.jp)
  • Conclusion: Our findings show that administration of AG in early phase of transient focal cerebral ischemia reduces brain edema. (sid.ir)
  • Development of drugs to stimulate the DP1 receptor in brain could provide a new therapeutic strategy against cerebral ischemia and potentially other neurological conditions. (sigmaaldrich.com)
  • Brain injuries induced by hypoxia-ischemia in neonates contribute to increased mortality and lifelong neurological dysfunction. (medscimonit.com)
  • Rosenberg GA. Neurological diseases in relation to the blood-brain barrier. (springermedizin.de)
  • Previous studies have suggested both exercise and mitochondrial biogenesis contribute to improved post-ischemic recovery of brain function. (biomedsearch.com)
  • On the other hand, the benefit of exercise-induced mitochondrial biogenesis in brain has been confirmed. (biomedsearch.com)
  • In this study, we attempted to determine whether treadmill exercise induces functional improvement through regulation of mitochondrial biogenesis after brain ischemia. (biomedsearch.com)
  • Suppression of mitochondrial fission in experimental cerebral ischemia: The potential neuroprotective target of p38 MAPK inhibition. (curehunter.com)
  • The purpose of this work was to study the effects of warm (37°C) and cold (4°C) ischemia on different mitochondrial functions in rat brain, liver and kidney. (springer.com)
  • After l0 to 60 minutes of ischemia at 37°C the energy coupled respiration as well as the ADP-induced malate-aspartate shuttle activity in brain and liver mitochondria or the rate of mitochondrial ATP synthesis in kidney were significantly decreased. (springer.com)
  • When the temperature during the indicated ischemic periods was decreased to 4°C, in brain and liver no significant alterations of these mitochondrial functions were found in comparison with the non-ischemic controls. (springer.com)
  • Boime J, Smith EE, Hunter Jr FE: The role of fatty acids in mitochondrial changes during liver ischemia. (springer.com)
  • JI-8 decreased NO production in brain slices and also showed significant preservation of mitochondrial function at both 3 and 6 days (p (figshare.com)
  • We believe this new template may be important because it's showing different mechanisms of action-different ways to interact with neurons, possibly with a good therapeutic effect for such diseases as epilepsy, hypoxia-ischemia and several neurodegenerative disorders," said Alban Pereira, a postdoctoral researcher in Scripps' CMBB. (acronymfinder.com)
  • At present, the therapeutic outcome of cerebral ischemia is still not in the satisfaction level. (thescipub.com)
  • Another highly protective agent is human albumin, administered in doses of 1.25 to 2.5 g/kg-a therapy that reduces infarct volume in this ischemia model by 60% to 65%, markedly diminishes brain swelling, and has a therapeutic window extending to 4 hours. (pptaglobal.org)
  • Our study provides a strong rationale for the further development of vitexin as a promising therapeutic candidate treatment for epilepsy in the immature brain. (biomedcentral.com)
  • The blood-brain barrier: structure, function and therapeutic approaches to cross it. (springermedizin.de)
  • Clinical manifestations of acute limb ischemia (which can be summarized as the "six P's") include pain, pallor, pulseless, paresthesia, paralysis, and poikilothermia. (wikipedia.org)
  • Lack of blood flow to a limb results in acute limb ischemia. (wikipedia.org)
  • Marijuana can lead to temporary cerebrovascular ischemia, but this is not directly affected by most pain medications. (reference.com)
  • Brain ischemia is also known as cerebral ischemia or cerebrovascular ischemia. (sbwire.com)
  • What many people don't know is that strokes arise from several possible conditions, including brain ischemia (commonly referred to as cerebral or cerebrovascular ischemia). (marylandmedicalmalpracticeattorneyblog.com)
  • How different or similar the mechanisms of these two brain injuries and their management are and whether they can be grouped together is the focus of this special issue. (hindawi.com)
  • Intense efforts are being undertaken to understand the pathophysiological mechanisms triggered after brain ischemia and to develop effective pharmacological treatments. (frontiersin.org)
  • These results suggest that forced exercise may be beneficial for promoting functional recovery following cerebral ischemia through caveolin-dependent mechanisms or interactions between caveolins and these signaling molecules in ischemic brain regions. (mdpi.com)
  • Writing All disadvantages like the download mechanisms of secondary brain damage in cerebral, but these 'm the ordnance slowly. (nooranch.com)
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  • At present, there are no clinically effective pharmacologic interventions to halt brain damage following I/R. The major Aim of this dissertation will be to investigate possible mechanisms involved in neuron death following brain I/R, which may potentially lead to the development of effective therapies. (wayne.edu)
  • The purpose of this Dissertation is to investigate mechanisms of TA in the brain following focal ischemia, with and without diabetes. (wayne.edu)
  • I will discuss clinical outcomes, the major mechanisms, and especially focus on TA following brain I/R. The most current ideas on TA link it to intracellular stress responses and the formation of subcellular particles involved in mRNA metabolism such as stress granules and mRNA granules. (wayne.edu)
  • My Background discussion will lead to my hypotheses about mechanisms of prolonged TA following focal brain I/R and the possible effect of diabetes on these mechanisms. (wayne.edu)
  • The information presented here studies the mechanisms that underlie persistent translation arrest (TA) following global brain ischemia and reperfusion (I/R). To summarize the main findings I have discovered a new mechanism for prolonged post-ischemic TA that correlated exactly with in vivo translation rates and correlated precisely with cell outcome. (wayne.edu)
  • Chronic microvascular ischemic change is a term that describes areas in the brain where tiny blood vessels have ruptured or clotted off, causing limited bl. (reference.com)
  • What is microvascular ischemia? (reference.com)
  • Microvascular ischemia is a condition associated with reduced blood flow in some areas of the brain. (reference.com)
  • What are some symptoms of chronic microvascular ischemia? (reference.com)
  • Can microvascular ischemia in the brain related to marijuana use be triggered by pain medication? (reference.com)
  • The microvascular ischemia caused by marijuana is generally short-lived, according to the American Journal of Neuroradiology. (reference.com)
  • Morroniside improves microvascular functional integrity of the neurovascular unit after cerebral ischemia. (curehunter.com)
  • Sphingosine-1-phosphate protects against brain microvascular endothelial junctional protein disorganization and barrier dysfunction caused by alcohol. (bioportfolio.com)
  • Zhang J, Yuan L, Zhang X, Hamblin MH, Zhu T, Meng F, Li Y, Chen YE and Yin KJ: Altered long non-coding RNA transcriptomic profiles in brain microvascular endothelium after cerebral ischemia. (spandidos-publications.com)
  • Brain ischemia may be categorized as focal ischemia or global ischemia, and the cause for ischemia can range from congenital heart defects to sickle cell anemia. (reference.com)
  • The causes of brain ischemia vary from sickle cell anemia to congenital heart defects. (wikipedia.org)
  • Individuals with sickle cell anemia, compressed blood vessels, ventricular tachycardia, plaque buildup in the arteries, blood clots, extremely low blood pressure as a result of heart attack, and congenital heart defects have a higher predisposition to brain ischemia in comparison their healthy counterparts.Sickle cell anemia may cause brain ischemia associated with the irregularly shaped blood cells. (wikipedia.org)
  • Therefore, our results demonstrates the potential benefit of M.oleifera leaves to decrease oxidative stress damage and brain infarct volume. (thescipub.com)
  • Neurobehavioral outcome, infarct volume, and blood-brain barrier permeability were measured after ischemia. (biomedcentral.com)
  • Delivery of drugs through the systemic route to the brain is restricted due to the presence of blood brain barrier (BBB), which is composed of specialized endothelial cells that are selective in permitting diffusion into the central nervous system (CNS). (nature.com)
  • Is the Subject Area "Blood-brain barrier permeability assay" applicable to this article? (plos.org)
  • By means of laser microdissection, neurons and blood brain barrier structures (BBB) were isolated and analyzed using label-free quantification. (mcponline.org)
  • The increased permeability of the blood-brain barrier (BBB) induced by ischemia/hypoxia is generally correlated with alteration of tight junctions (TJs). (bioportfolio.com)
  • Blood-brain barrier pericytes as a target for HIV-1 infection. (bioportfolio.com)
  • Sphingosine-1-phosphate (S1P) has known endothelial barrier protective properties, but whether this extends to the blood-brain barrier (BBB) is unclear. (bioportfolio.com)
  • The choroid plexus (CP), main component of blood-cerebrospinal fluid barrier (BCSFB), protects the brain from peripheral inflammation similar to the blood-brain barrier. (bioportfolio.com)
  • The purpose of this research study is to determine if sunitinib can get past the blood-brain barrier and into the brain tumor. (bioportfolio.com)
  • The purpose of this study is to evaluate the safety and efficacy of the ExAblate® Model 4000 Type 2.0 system as a tool to open the blood-brain barrier (BBB) in patients with probable Alzh. (bioportfolio.com)
  • Basic fibroblast growth factor (bFGF) has minimal pharmacological effects in the central nervous system in the absence of blood-brain barrier (BBB) disruption. (aspetjournals.org)
  • To elucidate the dynamic transfer of esRAGE into the brain, we used the blood-brain barrier (BBB) system (PharmaCo-Cell) with or without RAGE knockdown in endothelial cells. (researchmap.jp)
  • The blood-brain barrier (BBB) plays an important role in brain damage. (biomedcentral.com)
  • Disruption of the blood-brain barrier is an early feature of lesion formation that correlates with clinical exacerbation and facilitates the entry of inflammatory medium and inflammatory cells. (springermedizin.de)
  • However, the effect of IL-1RA on blood-brain barrier disruption following ischemia-reperfusion has not been reported. (springermedizin.de)
  • Further study suggested that the effects of IL-1RA-PEP on preserving blood-brain barrier integrity might be closely correlated with the p65/NF-κB pathway, as evidenced by the effects of the inhibitor JSH-23. (springermedizin.de)
  • Gu Y, Dee CM, Shen J. Interaction of free radicals, matrix metalloproteinases and caveolin-1 impacts blood-brain barrier permeability. (springermedizin.de)
  • Yang Y, Rosenberg GA. Blood-brain barrier breakdown in acute and chronic cerebrovascular disease. (springermedizin.de)
  • Almutairi MM, Gong C, Xu YG, Chang Y, Shi H. Factors controlling permeability of the blood-brain barrier. (springermedizin.de)
  • Rempe RG, Hartz AM, Bauer B. Matrix metalloproteinases in the brain and blood-brain barrier: versatile breakers and makers. (springermedizin.de)
  • Studies demonstrated that mesenchymal stem cell therapy protected blood-brain barrier disruption from several cerebrovascular diseases. (biomedcentral.com)
  • We therefore hypothesized that mesenchymal stem cells reduced blood-brain barrier destruction by inhibiting matrixmetallo-proteinase-9 and it was related to intercellular adhesion molecule-1 (ICAM-1). (biomedcentral.com)
  • These data suggest that following ischemia, IP receptor deletion contributes to memory and cognitive deficits regulated by the CREB pathway and that treatment with IP receptor agonists could be a useful target to prevent harmful consequences. (mdpi.com)
  • We aimed to investigate neutrophil location in a mouse model of cerebral ischemia/reperfusion. (csic.es)
  • Previous studies have shown AG neurprotective effect in experimental model of cerebral ischemia. (sid.ir)
  • These results challenge the view that docosahexaenoate only participates in brain damage and demonstrate that this fatty acid is also the endogenous precursor to a neuroprotective signaling response to ischemia-reperfusion. (nih.gov)
  • We found that TIGAR was highly expressed in brain neurons and was rapidly upregulated in response to ischemia/reperfusion insult in a TP53-independent manner. (jneurosci.org)
  • 4 Thus, brain damage is a major public health problem deserving every effort towards understanding its pathogenesis and treatment. (springer.com)
  • Caveolin is the principal protein of caveolae and has been implicated in the pathogenesis of cerebral ischemia. (mdpi.com)
  • Although the link between S1P 1 and microglial activation as a pathogenesis in cerebral ischemia had been clearly demonstrated, whether the pathogenic role of S1P 1 is associated with its regulation of M1/M2 polarization remains unclear. (kstudy.com)
  • Overall, these results revealed S1P 1 -regulated M1/M2 polarization toward brain damage as a pathogenesis of cerebral ischemia. (kstudy.com)
  • To clarify the pathogenesis and molecular basis of ischemia-related nerve cell death, we examined the occurrence of DNA fragmentation as a hallmark of apoptotic cell death following incomplete ischemia in the rat brain by means of in situ end labeling of fragmented DNA. (semanticscholar.org)
  • The 6 groups are: diabetic rat with sham operation group, diabetic rat with myocardial ischemia reperfusion group, diabetic rat with myocardial ischemia reperfusion+propofol group, normal rat with sham operation, normal rat with myocardial ischemia reperfusion group, normal rat with myocardial ischemia reperfusion+propofol group[1]. (ijpsonline.com)
  • In addition, ALDH activity is present at high levels in some stem or progenitor cells, known as ALDH bright (ALDH br ) cells, which possess potential value in treating patients with myocardial ischemia. (eurekaselect.com)
  • Duration versus severity of ischemia as critical factors of cortical cell damage, in: Cerebro-vascular Diseases, Reivich, M. and Hurtig, H. I., eds. (springer.com)
  • Effects of the 21-amino steroid tirilazad mesylate (U-74006F) on brain damage and edema after perinatal hypoxia-ischemia in the rat. (acronymfinder.com)
  • Treadmill exercise ameliorates ischemia-induced brain edema while suppressing Na⁺/H⁺ exchanger 1 expression. (sigmaaldrich.com)
  • In this study, the effects of forced treadmill exercise with electric shock on ischemic brain edema were investigated. (sigmaaldrich.com)
  • The reason we see ischemia on CT is that in ischemia cytotoxic edema develops as a result of failure of the ion-pumps. (radiologyassistant.nl)
  • However, effects AG on cerebral edema almost have not yet been investigated in transient model of focal cerebral ischemia. (sid.ir)
  • Pune, India -- ( SBWIRE ) -- 02/01/2018 -- MarketResearchFuture.com adds "Brain Ischemia Market -2018 Global Analysis, Growth, Trends and Opportunities Research Report Forecasting to 2023" reports to its database. (sbwire.com)
  • Bedside intracerebral microdialysis monitoring of patients with subarachnoid hemorrhage and signs of delayed ischemia revealed dramatic changes in extracellular concentrations of glucose, lactate, and glycerol that could be directly correlated to the clinical status of the patients. (unboundmedicine.com)
  • We hypothesized that TIGAR plays a neuroprotective role in brain ischemia as neurons do not rely on glycolysis but are vulnerable to oxidative stress. (jneurosci.org)
  • Six hours after treatment, brains were processed to quantify the number of damaged neurons by Nissl staining. (frontiersin.org)
  • Reverse transcription‑quantitative PCR (RT‑qPCR) assays indicated that BDNF‑AS expression was significantly upregulated in HI‑injured neonatal brains and hippocampal neurons. (spandidos-publications.com)
  • However, BDNF expression was downregulated in HI‑injured neonatal brains and hippocampal neurons. (spandidos-publications.com)
  • The neurovascular unit (NVU) comprises brain endothelial cells, pericytes or vascular smooth muscle cells, glia and neurons. (scienceopen.com)
  • Freshly oxygenated blood travels up the carotid arteries to the head and neck, providing a steady supply of blood to the brain. (wisegeek.com)
  • Most commonly, brain ischemia involves not the carotid artery , but one of the smaller blood vessels in the brain. (wisegeek.com)
  • Ischemia within the arteries branching from the internal carotid artery may result in symptoms such as blindness in one eye, weakness in one arm or leg, or weakness in one entire side of the body. (wikipedia.org)
  • We examined the relationships between the time course of parasagittal electroencephalographic (EEG) activity and pathological outcome following transient cerebral ischemia, which was induced in 33 chronically instrumented fetal sheep by occluding the carotid arteries after ligation of the vertebral-carotid anastomoses. (nih.gov)
  • Ischemia was induced in animals by closing the carotid artery for 45 min. (magiran.com)
  • Incomplete ischemia was produced by permanently occluding one carotid artery, while temporarily occluding the other. (semanticscholar.org)
  • Transient global cerebral ischemia, arising in humans, can be an aftermath of cardiac arrest or severe systemic hypotension. (mdpi.com)
  • To test the role of lactate as an aerobic energy substrate postischemia in vivo, we employed the cardiac-arrest-induced transient global cerebral ischemia (TGI) rat model and the monocarboxylate transporter inhibitor α-cyano-4-hydroxycinnamate (4-CIN). (deepdyve.com)
  • To evaluate the diffusion changes occurring in neonatal brain ischemia, we used a robust quantitative diffusion technique, line-scan diffusion imaging (LSDI), which has been shown previously to yield high-quality images in neonates, children, and adults without the use of head restraints, cardiac gating, or specialized hardware (13-17) . (ajnr.org)
  • Both pathology and response to treatment are uniquely affected by the molecular landscape of the neonatal brain. (intechopen.com)
  • The Arginase Pathway in Neonatal Brain Hypoxia-Ischemia. (bioportfolio.com)
  • Cerebral morphology, as well as vascular and physiological measures (before, during, and after ischemia) did not differ between A 2A receptor knock-out and wild-type littermates. (jneurosci.org)
  • A RAGE-dependent transfer of esRAGE was demonstrated from the vascular to the brain side. (researchmap.jp)
  • Chronic ischemia of the brain may result in a form of dementia called vascular dementia. (wikipedia.org)
  • mean age, 2.6 days) with perinatal brain ischemia were evaluated using LSDI (1520/62.5/1 [TR/TE/excitations]) ( b maximum = 750 s/mm 2 ) and T1- and T2-weighted spin-echo (conventional) MR imaging. (ajnr.org)
  • The neurologic sequelae of perinatal brain ischemia include seizures, spasticity, behavioral disturbances, and developmental delay. (ajnr.org)
  • This suggests that diffusion imaging may be useful in the early detection of perinatal brain ischemia and likely is to become crucial in the effective and safe use of neuroprotective strategies (7, 11, 12) . (ajnr.org)
  • In this study, we describe the evolution of diffusion changes in neonates with suspected perinatal brain ischemia and some potential limitations of early diffusion-weighted imaging. (ajnr.org)
  • We reviewed the clinical records, laboratory results, and neuroimaging studies of 19 term neonates (between 38 and 42 weeks postconceptional age) ( Table 1 ) who were referred for MR imaging within the first 8 days of life to evaluate suspected perinatal brain ischemia. (ajnr.org)
  • Neuroprotective Effects of Endogenous Secretory Receptor for Advanced Glycation End-products in Brain Ischemia. (researchmap.jp)
  • These findings suggested that esRAGE is associated with heparan sulphate proteoglycans and is transferred into the brain via BBB to exert its neuroprotective effects in ischemia. (researchmap.jp)
  • A number of things can cause brain ischemia, including strokes, trauma to the brain, and blood vessel abnormalities. (wisegeek.com)
  • Even brief interruptions can cause brain ischemia, and potentially result in a situation called an ischemic cascade , where brain cells with inadequate blood supply start dying and releasing toxins that damage neighboring cells, causing them to rupture and release toxins of their own, creating a ripple effect across the brain. (wisegeek.com)
  • citation needed] A heart attack can also cause brain ischemia due to the correlation that exists between heart attack and low blood pressure. (wikipedia.org)
  • citation needed] Congenital heart defects may also cause brain ischemia due to the lack of appropriate artery formation and connection. (wikipedia.org)
  • What is chronic brain ischemia? (reference.com)
  • The aim of the study was to assess the cognitive function in patients with chronic brain ischemia and metabolic syndrome (MC ) during the treatment of hyperlipidemia with atorvastatin. (umj.com.ua)
  • In models of inflammation, expression of the inducible isoform of nitric oxide synthase (iNOS) is responsible for cytotoxicity through the production of large amounts of nitric oxide (NO). In this study, therefore, we sought to establish whether iNOS is expressed in the ischemic brain. (nih.gov)
  • Yilin Yang, Harleen K Sandhu, Feng Zhi, Fei Hua, Min Wu and Ying Xia, "Effects of Hypoxia and Ischemia on MicroRNAs in the Brain", Current Medicinal Chemistry (2015) 22: 1292. (eurekaselect.com)
Ischemic Stroke: MedlinePlus