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 ...
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 ... There are two types of ischemia: focal ischemia, which is confined to a specific region of the brain; and global ischemia, ...
36-. ISBN 978-0-306-48644-9. Eugene I. Gusev; Veronika I. Skvortsova (30 April 2003). Brain Ischemia. Springer Science & ... It was under investigation by Acea Pharmaceuticals as a neuroprotective agent for the treatment of cerebral ischemia associated ...
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 ischemia/reperfusion injury is mediated via complex I impairment. Recently it was found that oxygen deprivation leads to ... May 2018). "Critical Role of Flavin and Glutathione in Complex I-Mediated Bioenergetic Failure in Brain Ischemia/Reperfusion ... September 2019). "Redox-Dependent Loss of Flavin by Mitochondrial Complex I in Brain Ischemia/Reperfusion Injury". Antioxidants ... Galkin A (November 2019). "Brain Ischemia/Reperfusion Injury and Mitochondrial Complex I Damage". Biochemistry. Biokhimiia. 84 ...
Galkin, A (2019). "Brain Ischemia/Reperfusion Injury and Mitochondrial Complex I Damage". Biochemistry. Biokhimiia. 84 (11): ... "Critical Role of Flavin and Glutathione in Complex I-Mediated Bioenergetic Failure in Brain Ischemia/Reperfusion Injury". ... dissociation of flavin mononucleotide from mitochondrial complex I has been shown to occur during ischemia/reperfusion brain ...
For example brain ischemia/reperfusion injury is mediated via complex I redox-dependent inactivation. It was found that lack of ... In neonatal in vivo model of brain ischemia/reperfusion, tissue injury can be alleviated by the administration of FMN precursor ... Ten, Vadim; Galkin, Alexander (October 2019). "Mechanism of mitochondrial complex I damage in brain ischemia/reperfusion injury ... Galkin, A (November 2019). "Brain Ischemia/Reperfusion Injury and Mitochondrial Complex I Damage". Biochemistry. Biokhimiia. 84 ...
Davide Ancilotto, 23, Italian basketball player, brain ischemia during game. Hardial Bains, 58, Indian-Canadian microbiology ... Lotus Weinstock, 54, American stand-up comedian, author, musician, and actress, brain tumor. People killed in the 1997 Pont de ...
"Intracranial hypertension and cerebral ischemia after severe traumatic brain injury". Neurosurgical Focus. 14 (4): e2. doi: ... In this condition the brain collapses on itself resulting in the collection of CSF or blood around the brain. This can cause ... All brain ventricles are candidates for shunting. The catheter is most commonly placed in the abdomen but other locations ... A cerebral shunt is a device permanently implanted inside the head and body to drain excess fluid away from the brain. They are ...
... of the small bowel is called mesenteric ischemia. Brain ischemia is insufficient blood flow to the brain, and can be ... Chronic ischemia of the brain may result in a form of dementia called vascular dementia. A sudden, brief episode (symptoms ... Ischemia or ischaemia is a restriction in blood supply to any tissue, muscle group, or organ of the body, causing a shortage of ... Inadequate blood supply to a limb may results in acute limb ischemia or chronic limb threatening ischemia. Reduced blood flow ...
... 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 ...
MLC901 can activate KATP channels, which has a neuroprotective effect against brain ischemia. Neuroaid is not effective in ... September 2011). "MLC901, a traditional Chinese medicine protects the brain against global ischemia". Neuropharmacology. 61 (4 ... Brain Injury. 30 (3): 267-70. doi:10.3109/02699052.2015.1118764. PMID 26890534. Siddiqui FJ, Venketasubramanian N, Chan ES, ... and neuroplasticity by amplifying endogenous processes of self-protection and self-repair of the brain. ...
This could lead to making the brain more vulnerable to ischemia. A 2015 review concluded that "Nicotine acts as a gateway drug ... Nicotine exposure during brain development may hamper growth of neurons and brain circuits, effecting brain architecture, ... Young people's brains build synapses faster than adult brains. Because addiction is a form of learning, adolescents can get ... These complex effects of nicotine on the brain are still not well understood. Nicotine interferes with the blood-brain barrier ...
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 ...
Brain ischemia is characterized by insufficient blood flow to the brain. Studies with ischaemic gerbils indicate that, after a ... Quinolinic acid has also been found in HAND patients' brains. In fact, the amount of quinolinic acid found in the brain of HAND ... there are microglia containing quinolinic acid within the brain. Following cerebral ischaemia, delayed neuronal death may occur ... neurodegenerative processes in the brain, as well as other disorders. Within the brain, quinolinic acid is only produced by ...
... 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). ...
"Deletion of TRAAK potassium channel affects brain metabolism and protects against ischemia". PLOS ONE. 7 (12): e53266. Bibcode: ... Chromosomal localization, tissue distribution and functional expression". Brain Research. Molecular Brain Research. 102 (1-2): ... Brain Research. Molecular Brain Research. 82 (1-2): 74-83. doi:10.1016/S0169-328X(00)00183-2. PMID 11042359. Hartley JL, Temple ... TRAAK is only expressed in neuronal tissue, and can be found in the brain, spinal cord, and retina, which suggests that it has ...
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 ...
"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 ...
In response to ischemia, the brain degenerates by the process of liquefactive necrosis. There are various classification ... The more rapidly blood flow is restored to the brain, the fewer brain cells die. In increasing numbers of primary stroke ... Even in cases where there is a complete blockage to blood flow of a major blood vessel supplying the brain, there is typically ... Computed tomography (CT) and MRI scanning will show damaged area in the brain, showing that the symptoms were not caused by a ...
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/ ...
Decreased levels of PTPN5 has been implicated in Huntington's disease, brain ischemia, alcohol use disorder, and stress ... The expression of PTPN5 is restricted to the brain. Differential expression of PTPN5 is found in many brain regions, with no ... "Neuroprotective role of a brain-enriched tyrosine phosphatase, STEP, in focal cerebral ischemia". The Journal of Neuroscience. ... Brain and Behavior. 11 (5): 586-600. doi:10.1111/j.1601-183X.2012.00781.x. PMC 3922131. PMID 22405502. Kurup P, Zhang Y, Xu J, ...
In response to ischemia, the brain degenerates by the process of liquefactive necrosis. Lung: Pulmonary infarction or lung ... The resulting ischemia (restriction in blood supply) and oxygen shortage, if left untreated for a sufficient period of time, ... Bowel: Bowel infarction is generally caused by mesenteric ischemia due to blockages in the arteries or veins that supply the ... Cerebral infarction is the ischemic kind of stroke due to a disturbance in the blood vessels supplying blood to the brain. It ...
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 typical 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 ...
2015). "Toxic role of prostaglandin E2 receptor EP1 after intracerebral hemorrhage in mice". Brain Behav. Immun. 46: 293-310. ... It also regulates angiogenic factors and vascular permeability after focal cerebral ischemia-reperfusion, and regulates matrix ... and angiogenic factors after focal cerebral ischemia: correlations with angiogenesis and cerebral edema". Neurochem. Int. 58 (8 ... "Src regulates angiogenic factors and vascular permeability after focal cerebral ischemia-reperfusion". Neuroscience. 262 (3): ...
After subarachnoidal bleedings, irritation of the blood vessels can lead to a vasospasm and thus to an ischaemia, an ... insufficient blood supply to brain tissue. One possible effect of this is, in turn, an ischaemic stroke. In a randomized trial ...
A high PRx indicating disturbed pressure autoregulation predicts poor outcome in traumatic brain injury. PRx varies with the ... whereas CPP values below CPPopt are believed to cause hypoperfusion and ischemia resulting in tissue damage. Cerebral ... in order to guide therapy to protect the brain from dangerously high or low cerebral blood flow. PRx uses mathematical ... Short pressure reactivity index versus long pressure reactivity index in the management of traumatic brain injury. J Neurosurg ...
Schlicker E, Betz R, Göthert M (May 1988). "Histamine H3 receptor-mediated inhibition of serotonin release in the rat brain ... 1999 H3 receptor cloned 2000 H3 receptors called "new frontier in myocardial ischemia" 2002 H3(-/-) mice (mice that do not have ... 1988 H3 receptor found to mediate inhibition of serotonin release in rat brain cortex. 1997 H3 receptors shown to modulate ... Levi R, Smith NC (Mar 2000). "Histamine H(3)-receptors: a new frontier in myocardial ischemia" (abstract). The Journal of ...
Hook G, Yu J, Toneff T, Kindy M, Hook V (2014). "Brain pyroglutamate amyloid-β is produced by cathepsin B and is reduced by the ... "Neurovascular and neuronal protection by E64d after focal cerebral ischemia in rats". Journal of Neuroscience Research. 84 (4 ... Hook G, Hook V, Kindy M (2011). "The cysteine protease inhibitor, E64d, reduces brain amyloid-β and improves memory deficits in ...
Cheon MS, Kim SH, Fountoulakis M, Lubec G (2004). Heart type fatty acid binding protein (H-FABP) is decreased in brains of ... "Release of fatty acid-binding protein from isolated rat heart subjected to ischemia and reperfusion or to the calcium paradox ... "Identification of post-mortem cerebrospinal fluid proteins as potential biomarkers of ischemia and neurodegeneration". ...
The cause of postpartum bipolar disorder breaks down into two parts - the nature of the brain anomalies that predispose to ... The primary pathology is in the placenta, which secretes an anti-angiogenic factor in response to ischaemia, leading to ... In fatal cases, there are arterial lesions in many organs including the brain. This is the second most frequent organic ... The pathology is damage to the core of the brain including the thalamus and mamillary bodies. Its most striking clinical ...
Simka M (May 2009). "Blood brain barrier compromise with endothelial inflammation may lead to autoimmune loss of myelin during ... Venous pathology is commonly associated with hypertension, infarcts, edema and transient ischemia, and occurs more often with ... Zamboni theorized that malformed blood vessels cause increased deposition of iron in the brain, which in turn triggers ... Lassmann H (July 2005). "Multiple sclerosis pathology: evolution of pathogenetic concepts". Brain Pathology. 15 (3): 217-22. ...
During a normal embryologic processes, or during cell injury (such as ischemia-reperfusion injury during heart attacks and ... wider chaperome interactome that functions as a proteostasis safeguard and that is repressed in aging brains and in the brains ... Alternatively, overexpression of Hsp70 can mitigate damage from ischemia-reperfusion in cardiac muscle, as well damage from ... shock protein 72 suppresses apoptosis by increasing the stability of X-linked inhibitor of apoptosis protein in renal ischemia/ ...
They have connections with the spinal cord and ultimately the brain, however. Most commonly autonomic neuropathy is seen in ... Direct injury to a nerve, interruption of its blood supply resulting in (ischemia), or inflammation also may cause ... meaning nerves beyond the brain and spinal cord. Damage to peripheral nerves may impair sensation, movement, gland, or organ ... ischemia, radiation therapy, excessive alcohol consumption, immune system disease, celiac disease, non-celiac gluten ...
... binds to α4β2 nicotinic acetylcholine receptors in the mouse brain cortex with IC50 = 5.86 μM. Experiments ... In Wistar rats with gravitational cerebral ischemia, Phenylpiracetam reduced the extent of neuralgic deficiency manifestations ... Savchenko AI, Zakharova NS, Stepanov IN (2005). "[The phenotropil treatment of the consequences of brain organic lesions]". ... traumatic brain injury and certain types of glioma. Phenylpiracetam reverses the depressant effects of the benzodiazepine ...
"Ischemia"-Stressed PC12 Pheochromocytoma Cells". Brain Sciences. 8 (2): 32. doi:10.3390/brainsci8020032. PMC 5836051. PMID ... and traumatic brain injury. Lazarovici also contributed to the characterization of NGF angiogenic properties and ... "Nerve growth factor reduces myocardial ischemia/reperfusion injury in rat hearts". Journal of Basic and Clinical Physiology and ... pan-hematopoietic subpopulation derived from human umbilical cord blood in a traumatic brain injury model". Cytotherapy. 20 (2 ...
Myocardial Ischemia/Infarction: A heart attack is often caused by a significant build-up of plaque (atherosclerosis) in the ... Progress in Brain Research. Vol. 182. Elsevier. pp. 343-73. doi:10.1016/s0079-6123(10)82015-1. ISBN 978-0-444-53616-7. PMC ... Norepinephrine causes vessels to narrow, thereby limiting blood flow and inducing ischemia. Multiple organ dysfunction syndrome ...
It may also be triggered by other conditions that result in ischemia of the retina or ciliary body. Individuals with poor blood ... that carries visual information from the eye to the brain, thereby causing changes in vision. Jindal A, Ctori I, Virgili G, ...
... traumatic brain injury, cerebral ischemia, fragile X syndrome, and Rett syndrome. Tropoflavin also shows efficacy in animal ... Brain Res. 257: 8-12. doi:10.1016/j.bbr.2013.09.029. PMID 24070857. S2CID 24088558. Andero R, Heldt SA, Ye K, Liu X, Armario A ... Brain and Behavior. 11 (5): 503-12. doi:10.1111/j.1601-183X.2012.00801.x. PMC 3389160. PMID 22530815. Colombo PS, Flamini G, ... attenuates cerebral ischemia and reperfusion injury in rats". J. Mol. Histol. 45 (2): 129-40. doi:10.1007/s10735-013-9539-y. ...
Liepzig: Ischemia Verlagsgesellschaft. Puustinen A, Wikström M. (1991). "The heme groups of cytochrome o from Escherichia coli ... ISBN 978-0-7167-7108-1. Hanafy, K.A. (2013). "Carbon Monoxide and the brain: time to rethink the dogma". Curr. Pharm. Des. 19 ( ...
Daffertshofer, M. (2005). "Transcranial low-frequency ultrasound-mediated thrombolysis in brain ischemia: increased risk of ... "Ultrasound Shown To Exert Remote Control Of Brain Circuits". ScienceDaily. Brain Circuits. Retrieved 23 October 2013. Tyler, ... Unlike deep brain stimulation or Vagus nerve stimulation, which use implants and electrical impulses, TPU is a noninvasive and ... This proves that this method is capable of controlling brain activity at a high cognitive level. It is clear that shorter waves ...
Other factors in secondary damage are breakdown of the blood-brain barrier, edema, ischemia and hypoxia. Ischemia is one of the ... Primary and secondary brain injury are ways to classify the injury processes that occur in brain injury. In traumatic brain ... These include ischemia (insufficient blood flow); cerebral hypoxia (insufficient oxygen in the brain); hypotension (low blood ... It occurs after a variety of brain injury including subarachnoid hemorrhage, stroke, and traumatic brain injury and involves ...
A complete occlusion of the artery can result in cerebral ischemia as the brain is depleted of oxygen-rich blood. Because the ... Vertebral artery dissection, a flap-like tear of the inner lining of the vertebral artery that supply blood to the brain and ... DeSai C, Hays Shapshak A (2021). "Cerebral Ischemia". StatPearls. Treasure Island (FL): StatPearls Publishing. PMID 32809345. ... a separation of the layers of the artery wall supplying oxygen-bearing blood to the head and brain. ...
A recently brain-dead man, aged 23, was selected for the transplant. Despite atrophy of blood vessels and nerves, the arteries ... Potential complications include ischaemia, thrombosis, and impotence. In serious cases the condition may result in gangrene, ... Brain centers that regulate urination include the pontine micturition center, periaqueductal gray, and the cerebral cortex. ...
Since psychosis is associated with greater levels of right brain hemisphere activation and a reduction in the usual left brain ... Zornberg GL, Buka SL, Tsuang MT (February 2000). "Hypoxic-ischemia-related fetal/neonatal complications and risk of ... Handford HA (February 1975). "Brain hypoxia, minimal brain dysfunction, and schizophrenia". Am J Psychiatry. 132 (2): 192-4. ... "It was also noted that individuals who experienced perinatal brain hypoxia constituted a population at risk for minimal brain ...
... although it may worsen neuronal damage following global ischemia after stroke or seizures. In comparison to the ampakines or ... for this action is thought to be through promoting the induction of long-term potentiation between synapses in the brain. IDRA- ...
In the 1960s Joseph Altman and coworkers published a series of papers reporting that some dividing cells in the adult brain ... "Holter Monitoring for the Assessment of Silent Cardiac Ischemia in Cerebrovascular Disease," Archives of Physical Medicine and ... In addition, the concept that there may be brain stem cells that could proliferate, migrate, and then differentiate into new ... His research using light and electron microscopy suggested that neurogenesis occurs in the brain of adult mammals, but his ...
This gene is also weakly expressed in many other tissues such as brain, placenta, testis, etc. Malonyl-CoA decarboxylase is ... secondary increase in glucose oxidation associated with an improvement in the functional recovery of the heart during ischaemia ... It causes many symptoms: brain abnormalities, mild mental retardation, seizures, hypotonia, metabolic acidosis, vomiting, ...
The production of GluCer from Cer was found to be important in the growth of neurons or brain cells. On the other hand, ... Elevations in either of these lipids causes analgesia and anti-inflammation and tissue protection during states of ischemia, ...
As the brain receives its plentiful supply of afferent information relating to ventilation, it is able to compare it to the ... In 85% of cases it is due to asthma, pneumonia, cardiac ischemia, interstitial lung disease, congestive heart failure, chronic ... It is believed the central processing in the brain compares the afferent and efferent signals; and dyspnea results when a " ... A low level of brain natriuretic peptide is useful in ruling out congestive heart failure; however, a high level, while ...
The OECs were taken from the patient's olfactory bulbs in his brain and then grown in the lab, these cells were then injected ... Causes include tumors, physical trauma, and ischemia. Cauda equina syndrome may also be caused by central disc prolapse or ... It results from lack of input from the brain that quells muscle responses to stretch reflexes. It can be treated with drugs and ... Its use in traumatic brain injury is also not recommended. Surgery may be necessary, e.g. to relieve excess pressure on the ...
Magistretti, P. J; Siesjö, Bo K; Bolis, C. L; World Health Organization. Division of Mental Health; WHO Meeting on Basic Science Issues in the Field of Stroke and Subarachnoid Haemorrhage (‎1996 : Geneva, Switzerland)‎ (‎World Health OrganizationWorld Health Organization, 1998)‎ ...
In this study, we assessed the expressions of NT-3 and trkC in focal cerebral ischemia. We also assessed the expression of NT-3 ... NT-3 has been shown to have neuroprotective effects in focal cerebral ischemia. Exercise also has ability to induce functional ... These results suggest that exercise-induced functional recovery in focal cerebral ischemia was related to NT-3 and trkC, but ... and trkC with treadmill exercise in focal cerebral ischemia. The results showed that, in a permanent middle cerebral artery ...
DBMR has added a new research report titled Brain Ischemia Market Size, Share, Growth, Trends, and Forecast 2021 to 2028 spins ... Based on the type, the brain ischemia market is segmented into focal brain ischemia and global brain ischemia. ... Global Brain Ischemia Market Scenario Brain ischemia or cerebral ischemia is an ailment that happens when there isnt enough ... Brain Ischemia Market Scope and Market Size. The brain ischemia market is segmented on the basis of type, treatment and end ...
Taken together, our results reveal a critical role of Mib2 in microglial activation and ischemia-induced brain injury, thus ... significantly alleviates ischemia-induced neuroinflammation and brain injury. ... p,Neuroinflammation plays a critical role in ischemia-induced brain injury. Mib2, an E3 ubiquitin ligase, has been reported to ... Mib2 Deficiency Inhibits Microglial Activation and Alleviates Ischemia-Induced Brain Injury. {{javascript:window.custom_author_ ...
Brain protection using autologous bone marrow cell, metalloproteinase inhibitors, and metabolic treatment in cerebral ischemia. ... Brain protection using autologous bone marrow cell, metalloproteinase inhibitors, and metabolic treatment in cerebral ischemia ... Brain protection using autologous bone marrow cell, metalloproteinase inhibitors, and metabolic treatment in cerebral ischemia ... Brain protection using autologous bone marrow cell, metalloproteinase inhibitors, and metabolic treatment in cerebral ischemia ...
Mesenchymal stromal cell-derived extracellular vesicles protect the fetal brain after hypoxia-ischemia. / Ophelders, Daan R.M.G ... Mesenchymal stromal cell-derived extracellular vesicles protect the fetal brain after hypoxia-ischemia. In: Stem Cells ... Mesenchymal stromal cell-derived extracellular vesicles protect the fetal brain after hypoxia-ischemia. Stem Cells ... title = "Mesenchymal stromal cell-derived extracellular vesicles protect the fetal brain after hypoxia-ischemia", ...
Differential effect of PARP-2 deletion on brain injury after focal and global cerebral ischemia. In: Journal of Cerebral Blood ... Differential effect of PARP-2 deletion on brain injury after focal and global cerebral ischemia. Journal of Cerebral Blood Flow ... Differential effect of PARP-2 deletion on brain injury after focal and global cerebral ischemia. / Kofler, Julia; Otsuka, ... title = "Differential effect of PARP-2 deletion on brain injury after focal and global cerebral ischemia", ...
... Journal Article * Overview ... Aim: To study the role and possible mechanism of He-Ne laser acupoint irradiation treatment on hypoxia ischemia brain damage ( ... Aim: To study the role and possible mechanism of He-Ne laser acupoint irradiation treatment on hypoxia ischemia brain damage ( ... Conclusion: He-Ne laser acupoint irradiation has a neuroprotective effect on brain after hypoxia-ischemia, and its action ...
... a Pittsburgh brain ischemia lawyer from Berger and Green may be able to fight for full compensation for your claim. We can ... If you or a loved one was injured by a careless health provider and suffered brain ischemia, ... Causes of Brain Ischemia. There are two main types of brain ischemia: focal cerebral ischemia and global cerebral ischemia. ... Medical Negligence and Brain Ischemia. Brain ischemia, or an ischemic stroke, occurs when the brain does not receive sufficient ...
... it is now beyond doubt that body temperature influences the outcome of brain damage. An elevated body temperature is often ... Although the function of fever is still unclear, it is now beyond doubt that body temperature influences the outcome of brain ... Regulation of body temperature and neuroprotection by endogenous interleukin-6 in cerebral ischemia J Cereb Blood Flow Metab. ... Cerebral ischemia rapidly induced neuronal interleukin-6 (IL-6) expression in mice. In IL-6-deficient mice, body temperature ...
Here, we examined this possibility using two models of transient focal ischemia: (i) the monofilament model of middle cerebral ... mGlu2 metabotropic glutamate receptors protects vulnerable neurons in the 4-vessel occlusion model of transient global ischemia ... tracked articles of a similar age in Molecular Brain ... the short-term outcome of cerebral transient focal ischemia. ...
keywords = "dietary restriction, hypoxic-ischemia, neonatal brain, underweight",. author = "Tu, {Yi Fang} and Lu, {Pei Jung} ... and microglia activation account for the hypoxic-ischemia (HI) susceptibility in neonatal brain. The p53 upregulation is ... and microglia activation account for the hypoxic-ischemia (HI) susceptibility in neonatal brain. The p53 upregulation is ... and microglia activation account for the hypoxic-ischemia (HI) susceptibility in neonatal brain. The p53 upregulation is ...
Neuroprotection against hypoxia-ischemia in neonatal rat brain by novel superoxide dismutase mimetics」の研究トピックを掘り下げます。これらがまとまって ... Neuroprotection against hypoxia-ischemia in neonatal rat brain by novel superoxide dismutase mimetics. In: Neuroscience Letters ... Neuroprotection against hypoxia-ischemia in neonatal rat brain by novel superoxide dismutase mimetics. Neuroscience Letters. ... Neuroprotection against hypoxia-ischemia in neonatal rat brain by novel superoxide dismutase mimetics
Expression of energy status of brain in ischemia. Indian Journal of Biochemistry & Biophysics. 1988 Dec; 25(6): 615-7. ...
Brain Res. 13, 199-206. 25. Kirino, T., 1982. Delayed neuronal death in the gerbil hippocampus following ischemia. Brain Res. ... Brain Res. 711, 184-192. 24. Kindy, M.A., Bhat, A.N., Bhat, N.R., 1992. Transient ischemia stimulates glial fibrillary acid ... oxidative stress, cerebral ischemia, glutathione, lipid peroxidation, antioxidants, brain. Subjects:. Neuroscience , ... Mangifera indica L. extract (QF808) reduces ischaemia-induced neuronal loss and oxidative damage in the gerbil brain. Free ...
Dive into the research topics of The protective effects of thiopental on brain stem ischemia. Together they form a unique ...
This effect was enhanced when the duration of postmortem ischemia was prolonged by 6.4 min prior to microwave fixation. Brains ... It is not known whether the brain-dissection process and its duration also alter these metabolites. We applied CO2 with or ... In nonmicrowave-irradiated brains, sEH metabolites and one CYP metabolite correlated positively and negatively with dissection ... This study presents new evidence that the dissection process and its duration increase brain oxylipin concentrations, and that ...
If your infant suffered brain ischemia caused by a birth injury, you may be eligible to pursue damages for their medical care ... Infant Brain Ischemia Lawyer Near Me 1-800-222-9529. Infant Brain Ischemia Types. Brain ischemia, or cerebral ischemia, occurs ... Infant Brain Ischemia Frequently Asked Questions. How do I know if my baby has infant brain ischemia?. Infant brain ischemia ... Infant Brain Ischemia Glossary Terms. *What is focal ischemia? Focal ischemia is localized brain damage caused by a lack of ...
Brain Ischemia / diagnostic imaging * Brain Ischemia / surgery * Cerebral Hemorrhage / diagnostic imaging* * Cerebral ... Clinical, imaging, and procedural characteristics were used for the analysis, including brain imaging systematically performed ...
TLR-1 protein was up-regulated in injured areas of the brain but TLR-1 KO animals were not protected from HI. In contrast, TLR- ... The expression of TLRs in the neonatal brain and their regulation after HI is unknown. Wild type C57BL/6, TLR 1 knockout (KO) ... mRNA expression was detected for all investigated TLRs (TLR1-9), both in normal and HI exposed brains. After HI, TLR-1 was down ... Neonatal HI triggers a broad inflammatory reaction in the brain, including activation of the innate immune system. Toll-like ...
The aim of this study was to investigate the neuroprotective effects of iloprost and piracetam on spinal cord ischemia/ ... Kirsh JR, Helfaer MA, Lange DC, Traystma RJ . Evidence for free radical mechanism of brain injury resulting from ischemia/ ... Ischemia/reperfusion procedure. The spinal cord ischemia model was established as described by Zivin and DeGirolami.8, 9 In ... Kalkan, E., Keskin, F., Kaya, B. et al. Effects of iloprost and piracetam in spinal cord ischemia-reperfusion injury in the ...
Early signs of brain ischemia on CT and MRI arent easy to spot. AI radiology software can quantify imaging biomarkers and ... Brain Ischemia - Imaging in Acute Stroke (2088). Available at: http://radiologyassistant.nl/en/p483910a4b6f14/brain-ischemia- ... Early brain ischemia signs on CT and MRI - can AI radiology help out?. July 26, 2018 by Ory Six ... Although it is significantly easier to recognize early signs of brain ischemia on MRI, and MRI facilitates detection at an ...
Source: Safar P. Resuscitation after brain ischemia. In: Grenvik A, Safar P, eds. Brain failure and resuscitation. New York, NY ... CPC 4. Coma or vegetative state. Any degree of coma without the presence of all brain death criteria. Unawareness, even if ... Because anoxic brain injury can occur within 4--6 minutes of collapse, communities with more favorable outcomes (CPC 1 or CPC 2 ... CPC 3. Severe cerebral disability. Conscious, dependent on others for daily support because of impaired brain function. Ranges ...
Introduction: The brain is an extraordinarily dynamic structure specially its physiology in response to pathological events. ... Objective: The purpose of the present work is to compile the advances in understanding of plasticity after brain lesion, mainly ... aspects related with neuroplasticity has been proposed as part of the pathophysiological bases to understand brain ischemia and ... Progress in understanding of the pathophysiology of brain lesion has required the use of experimental models to evaluate ...
Brain injury in preterm newborn infants is often attributed to hypoxia-ischemia even when neither hypoxia nor ischemia is ... Hypoxia-ischemia is not an antecedent of most preterm brain damage: the illusion of validity.. Gilles, Floyd; Gressens, Pierre ... WHAT THIS PAPER ADDS Fetal hypoxemia is rarely documented in brain injury studies. Animal studies fail to consider human-animal ... Encephalopathy of prematurity is preferable to hypoxia-ischemia as a term for this disorder. Encephalopathy of prematurity is ...
Pineyro MM, Furtenbach P, Lima R, Wajskopf S, Sgarbi N, Pisabarro R. Brain and Optic Chiasm Herniation into Sella after ... Cerebral ischemia in pituitary apoplexy. Acta Neurochir. 2008. 150:1193-6. *. ... Hori A. Suprasellar peri-infundibular ectopic adenohypophysis in fetal and adult brains. J Neurosurg. 1985 Jul. 63(1):113-5. [ ... Hori examined normal adult brains at autopsy and found ectopic pituitary cells in the leptomeninges of the peri-infundibular ...
Why do Purkinje cells die so easily after global brain ischemia? Aldolase C, EAAT4, and the cerebellar contribution to ... Fractionator studies on Purkinje cells in the human cerebellum: numbers in right and left halves of male and female brains.. *T ... Cerebellar Purkinje Cells are Reduced in a Subpopulation of Autistic Brains: A Stereological Experiment Using Calbindin-D28k. * ... It is demonstrated that a reduction in cerebellar PCs was not a consistent feature of these autistic brains and that it ...
... intravenous alteplase guided by a mismatch between diffusion-weighted imaging and FLAIR in the region of ischemia resulted in a ... Brain Ischemia / diagnostic imaging * Diffusion Magnetic Resonance Imaging * Female * Fibrinolytic Agents / adverse effects ... and the VIB-KU Leuven Center for Brain and Disease Research, Laboratory of Neurobiology (A.W., R.L.), Leuven, Belgium; and ... intravenous alteplase guided by a mismatch between diffusion-weighted imaging and FLAIR in the region of ischemia resulted in a ...
Ischemia. Pathologic Processes. Necrosis. Brain Infarction. Brain Ischemia. Cerebrovascular Disorders. Brain Diseases. Central ... REmote iSchemic Conditioning in acUtE BRAin INfarction Study (RESCUE-BRAIN). The safety and scientific validity of this study ... Brain MRI changes of DWI ( Diffusion-Weighted Imaging) brain infarction volume (cc) between baseline (,H6) and day 1 in the 2 ... The per-CID corresponds, in cases of cerebral ischemia, to iterative ischemia realization of a member with a cuff. In humans, ...
Key words: Brain ischemia/drug therapy Reperfusion injury/drug therapy Neurons Apoptosis Protein kinases/physiology Sirolimus/ ... Rapamycin ameliorates brain metabolites alterations after transient focal ischemia in rats[J]. Eur J Pharmacol, 2015, 757:28- ... Rapamycin treatment starting at 24 h after cerebral ischemia/reperfusion exhibits protective effect on brain injury in rats. J ... Rapamycin treatment starting at 24 h after cerebral ischemia/reperfusion exhibits protective effect on brain injury in rats. ...
  • Ovine fetuses were subjected to global hypoxia-ischemia by transient umbilical cord occlusion, followed by in utero intravenous administration of MSC-EVs. (tue.nl)
  • Aim: To study the role and possible mechanism of He-Ne laser acupoint irradiation treatment on hypoxia ischemia brain damage (HIBD). (edu.au)
  • Results: He-Ne laser acupoint irradiation was effective in inhibiting the loss of Nissl bodies in brain tissue and promoting the expression of ChAT and BDNF in brain tissue after hypoxia-ischemia. (edu.au)
  • Conclusion: He-Ne laser acupoint irradiation has a neuroprotective effect on brain after hypoxia-ischemia, and its action mechanism may be related to the expression of BDNF. (edu.au)
  • MetaPhore Pharmaceuticals) on infarct volume after hypoxia-ischemia injury (H/I) in immature rats. (elsevier.com)
  • Hypoxia-ischemia is not an antecedent of most preterm brain damage: the illusion of validity. (bvsalud.org)
  • Brain injury in preterm newborn infants is often attributed to hypoxia - ischemia even when neither hypoxia nor ischemia is documented, and many causative speculations are based on the same assumption. (bvsalud.org)
  • Encephalopathy of prematurity is preferable to hypoxia - ischemia as a term for this disorder. (bvsalud.org)
  • We investigated in utero free radical production and injury following hypoxia-ischemia to premature fetal brain utilizing a rabbit model of acute placental insufficiency. (uab.edu)
  • Acute fetal hypoxia-ischemia without reoxygenation results in increased nitrogen and oxygen free radical production that may cause brain injury. (uab.edu)
  • The central finding, which offers the potential for neuroprotective and neurorestorative interventions, is that brain damage after perinatal hypoxia-ischemia evolves slowly over time. (auckland.ac.nz)
  • Although brain cells may die during profound hypoxia-ischemia, even after surprisingly severe insults many cells show transient recovery of oxidative metabolism during a "latent" phase characterized by actively suppressed neural metabolism and activity. (auckland.ac.nz)
  • Critically, after moderate to severe hypoxia-ischemia, this transient recovery is followed after ~6 h by a phase of secondary deterioration, with delayed seizures, failure of mitochondrial function, cytotoxic edema, and cell death over ~72 h. (auckland.ac.nz)
  • 15. Zhu C, Wang X, Cheng X, Qiu L, Xu F, Simbruner G, Blomgren K. Post-ischemic hypotermia-induced tissue protection and diminished apoptosis after neonatal cerebral hypoxia-ischemia. (bvsalud.org)
  • 2005) Brain stem ischemia from intracranial dural arteriovenous fistula: Case report. (scirp.org)
  • Which leads to the limited oxygen supply or cerebral hypoxia and leads to the death of brain tissue, cerebral infarction, or ischemic stroke. (pharmiweb.com)
  • Despite advances in imaging, understanding the underlying pathways, and clinical translation of animal models of disease there remains an urgent need for therapies that reduce brain damage after stroke and promote functional recovery in patients. (elsevier.com)
  • Brain ischemia, or an ischemic stroke, occurs when the brain does not receive sufficient blood. (bergerandgreen.com)
  • This is the same type of brain damage an adult might suffer from a stroke or ministroke. (birthinjurylawyer.com)
  • Technically speaking, the ASPECT (Alberta Stroke Program Early CT) score is not a sign, but a tool to analyze hypoattenuation in different brain regions. (quantib.com)
  • In patients with acute stroke with an unknown time of onset, intravenous alteplase guided by a mismatch between diffusion-weighted imaging and FLAIR in the region of ischemia resulted in a significantly better functional outcome and numerically more intracranial hemorrhages than placebo at 90 days. (nih.gov)
  • Most often, stroke results from blockage of an artery in the brain leading to tissue infarction within the perfusion territory of the affected vessel. (avhandlingar.se)
  • Dr. Wu has used mechanismbased approach to develop therapeutic intervention for various brain diseases including stroke, Parkinson diseases, Alzheimer's disease and epilepsy. (fau.edu)
  • A stroke is what happens when blood flow to part of the brain is interrupted. (healthline.com)
  • A massive stroke can be fatal, as it affects large portions of the brain. (healthline.com)
  • An ischemic stroke results from a clot that blocks blood flow to a particular region of the brain. (healthline.com)
  • This means it forms elsewhere in the body and moves into the brain, leading to a stroke . (healthline.com)
  • A hemorrhagic stroke occurs when blood vessels in the brain rupture, causing blood to accumulate in the surrounding brain tissue. (healthline.com)
  • For patient education information, see eMedicineHealth's Brain and Nervous System Center as well as Stroke and Stroke-Related Dementia . (medscape.com)
  • To test this, we investigated the relationship between acute brain ischemia, lung inflammation, and CNS reperfusion injury in the middle cerebral artery occlusion (MCAO) model of stroke. (rochester.edu)
  • TgSOD3 mice exhibited reduced blood-brain barrier (BBB) damage and developed smaller infarct volumes 72 hours post-stroke. (rochester.edu)
  • Transient ischemic attack (TIA), often referred to as a mini-stroke , is when blood flow to part of the brain is blocked temporarily. (medicalnewstoday.com)
  • But the researchers of this latest study - including Dr. Jeffrey J. Perry of the University of Ottawa in Canada - say that all patients who have a mild stroke should receive a CT scan, given how the brain images can predict when patients will be at highest risk of a subsequent stroke. (medicalnewstoday.com)
  • The team analyzed the brain images of 2,028 patients who underwent CT scans in the 24 hours after experiencing a TIA or non-disabling stroke. (medicalnewstoday.com)
  • They found that patients with ischemia were 2.6 times more likely to have another stroke if the images showed they had acute ischemia - newly damaged tissue as a result of poor blood circulation - compared with patients without ischemia. (medicalnewstoday.com)
  • Ischemia patients were 5.35 times more likely to have a stroke if the images showed both chronic ischemia (previously damaged tissue) and acute ischemia, and they were 4.9 times more likely to have a stroke if the images showed any form of microangiopathy (small blood vessel damage) in the brain alongside acute ischemia. (medicalnewstoday.com)
  • What is more, the team found that ischemia patients were 8.04 times more likely to have a stroke if the images showed both acute and chronic ischemia alongside microangiopathy. (medicalnewstoday.com)
  • The team notes that 3.4% of study participants had a stroke in the 90 days following a TIA or non-disabling stroke, and that 25% of these displayed both chronic and acute ischemia and microangiopathy in their CT scan images. (medicalnewstoday.com)
  • During the 90-day period, and also within the first 2 days after the initial attack, patients did much worse in terms of experiencing a subsequent stroke if they had additional areas of damage along with acute ischemia," Dr. Perry adds. (medicalnewstoday.com)
  • All patients should get a CT scan of their brain after a TIA or non-disabling stroke. (medicalnewstoday.com)
  • These findings should prompt physicians to be more aggressive in managing patients with TIA or non-disabling stroke who are diagnosed with acute ischemia, especially if there is additional chronic ischemia and/or microangiopathy. (medicalnewstoday.com)
  • Medical News Today recently reported on a study in which researchers from the UK and China claim to have identified a drug target for prevention of stroke-related brain damage . (medicalnewstoday.com)
  • A stroke is the rapid loss of brain function(s) due to disturbance in the blood supply to the brain. (medicaldaily.com)
  • A stroke can cause major brain damage. (medicaldaily.com)
  • People with some brain impairment, such as dementia, have a significant 39 percent increased risk of stroke compared to people with normal brain function. (medicaldaily.com)
  • Low‐level light emitting diode (LED) therapy suppresses inflammasome‐mediated brain damage in experimental ischemic stroke. (shefayekhatam.ir)
  • Experimental NMDA - GLU receptor blockers such as MK-801 (dizocilpine) have also demonstrated the ability to reduce or eliminate brain damage from acute conditions such as stroke, ischaemia/hypoxia/anoxia, severe hypoglycaemia, spinal cord injury and head trauma (1-3). (antiaging-nutrition.com)
  • An ischemic stroke is death of an area of brain tissue (cerebral infarction) resulting from an inadequate supply of blood and oxygen to the brain due to blockage of an artery. (msdmanuals.com)
  • Ischemic stroke usually results when an artery to the brain is blocked, often by a blood clot and/or a fatty deposit due to atherosclerosis. (msdmanuals.com)
  • Overview of Stroke A stroke occurs when an artery to the brain becomes blocked or ruptures, resulting in death of an area of brain tissue due to loss of its blood supply (cerebral infarction) and symptoms that. (msdmanuals.com)
  • An ischemic stroke typically results from blockage of an artery that supplies blood to the brain, most commonly a branch of one of the internal carotid arteries. (msdmanuals.com)
  • When the large arteries that supply the brain are blocked, some people have no symptoms or have only a small stroke. (msdmanuals.com)
  • When blockages develop slowly and gradually (as occurs in atherosclerosis), new arteries may grow in time to keep the affected area of the brain supplied with blood and thus prevent a stroke. (msdmanuals.com)
  • In a rat model of transient cerebral ischemia (middle cerebral artery occlusion) gene delivery vectors were used to overexpress tissue inhibitor of matrix metalloproteinase 1 and 2 (TIMP1 and TIMP2) 3 days before ischemia. (elsevier.com)
  • The time course of oxidative damage in different brain regions was investigated in the gerbil model of transient cerebral ischemia. (southampton.ac.uk)
  • We have previously found that sphingosine 1-phospate receptor subtype 1 (S1P₁) in post-ischemic brain following transient middle cerebral artery occlusion (tMCAO) can trigger microglial activation, leading to brain damage. (bvsalud.org)
  • Background and Purpose-: Neurovascular damage, including neuronal apoptosis and blood-brain barrier (BBB) damage, and microglia activation account for the hypoxic-ischemia (HI) susceptibility in neonatal brain. (elsevier.com)
  • Similarly, hypoxic ischemia is insufficient blood flow causing reduced blood oxygen content. (nanavatimaxhospital.org)
  • Brains dissected from rats subjected to CO2 without microwave fixation showed greater increases in LOX, PGDH, CYP and sEH metabolites compared with all other groups, as well as increased cyclooxygenase metabolites. (omicsdi.org)
  • The present study aimed to investigate the protective effect of curdione on focal cerebral ischemia reperfusion-induced injury in rats and further exploring the underlying mechanisms. (dovepress.com)
  • We have reported that cytosolic redistribution of cytochrome c in vivo occurred after transient focal cerebral ischemia (FCI) in rats and preceded the peak of DNA fragmentation. (jneurosci.org)
  • Towards chronic deep brain stimulation in freely moving hemiparkinsonian rats: applicability and functionality of a fully implantable stimulation system. (mpg.de)
  • The aim of this study was to determine long-term functional outcomes after cerebral ischemia in rats, focusing on fine motor function, social and depressive behavior as clinically relevant measures. (elsevier.com)
  • In this study, we evaluated the impact of PARP-2 deletion on histopathological outcome from two different experimental models of cerebral ischemia. (elsevier.com)
  • Treatment options have proven efficient in preclinical models of cerebral ischemia but have failed in the clinical setting. (elsevier.com)
  • In particular, oxidative stress and neuron apoptosis after ischemia are the major pathways that drive neuronal cell death. (dovepress.com)
  • The per-conditioning remote ischemic (Per-CID) showed a neuroprotective effect in cerebral ischemia by reducing the final size of cerebral infarction animal models. (clinicaltrials.gov)
  • metabolic acidosis, arrhythmias, myocardial ischemia or infarction, and noncardiogenic pulmonary edema, although any organ system might be involved. (cdc.gov)
  • Prolonged ischemia is associated with BRAIN INFARCTION . (bvsalud.org)
  • In contrast, upregulating p53 by nutlin-3 in DR-HI pups increased apoptosis, BBB damage, and microglia activation, and worsened brain damage. (elsevier.com)
  • Gut-brain communication by distinct sensory neurons differently controls feeding and glucose metabolism. (mpg.de)
  • As you all may be aware of in very simple terms the brain is made of grey matter (comprising the cell bodies of the neurons) and white matter (fiber tracts). (braindiseases.blog)
  • Excitotoxins are biochemical substances (usually amino acids, amino acid analogs, or amino acid derivatives) that can react with specialized neuronal receptors - GLU receptors - in the brain or spinal cord in such a way as to cause injury or death to a wide variety of neurons (1-3, 8-10). (antiaging-nutrition.com)
  • This study examines whether the IF increases anti-inflammatory cytokines and protected neurons from ischemia-reperfusion injury. (il-13.com)
  • Under pathophysiological conditions, K ATP channels play cytoprotective role in cardiac myocytes and neurons during ischemia and/ or hypoxia. (chinaphar.com)
  • A molecule called orexin is made in the brain and regulates the activity of a group of neurons that control sleep. (elifesciences.org)
  • However, most brain cells are formed before birth but the trillions of connections between these nerve cells (neurons) are not developed until infancy. (nanavatimaxhospital.org)
  • Conclusions-: Moderate DR, but not extreme DR, reduces p53-mediated neurovascular damage after HI and confers long-term protection in neonatal brain. (elsevier.com)
  • The gut microbiota modulates brain network connectivity under physiological conditions and after acute brain ischemia. (mpg.de)
  • Focal Cerebral Ischemia: Focal brain ischemia affects only a localized part of the brain where a blockage or bleed occurred. (birthinjurylawyer.com)
  • Of these patients, 814 had brain damage as a result of ischemia - restricted blood supply to the brain. (medicalnewstoday.com)
  • Many studies have also demonstrated that neurotrophic factors play important roles in neuronal survival, proliferation, maturation, and outgrowth in the developing brain and neuroprotective function in mature brain insult [ 5 ]. (hindawi.com)
  • Cerebral ischemia rapidly induced neuronal interleukin-6 (IL-6) expression in mice. (nih.gov)
  • These data indicate that the SOD mimetics M40403 and M40401 have protective effects against hypoxic-ischemic brain injury, and suggest the involvement of superoxide anion in neuronal cell injury during H/I. (elsevier.com)
  • Shortage of oxygen and nutrients in the brain induces the release of glutamate and ATP that can cause excitotoxicity and contribute to neuronal and glial damage. (frontiersin.org)
  • Seizures are disorders characterized by temporary neurologic signs or symptoms resulting from abnormal, paroxysmal, and hypersynchronous electrical neuronal activity in the brain. (mhmedical.com)
  • This book provides a comprehensive overview of the latest research in the role of non-neuronal cells - astrocytes, oligodendrocytes, endothelial cells, pericytes, microglia, and other immune cells in ischemic brain injury and long-term recovery. (bookshare.org)
  • There are two main types of brain ischemia: focal cerebral ischemia and global cerebral ischemia. (bergerandgreen.com)
  • Global cerebral ischemia occurs when there is no or a decreased amount of blood flow to the entire brain. (bergerandgreen.com)
  • Global Cerebral Ischemia: Global brain ischemia affects large areas of the brain and could be deadly if left untreated. (birthinjurylawyer.com)
  • Emerging evidence implicates organ crosstalk in the pathology of delayed central nervous system (CNS) damage following global cerebral ischemia. (rochester.edu)
  • Cerebrovascular diseases (CVDs) are referred to as a group of conditions that eventually lead to a reduction of blood supply to the brain as a consequence of a blockage (thrombosis or atherosclerosis), malformation (aneurysm), hemorrhage, or transient ischemia. (frontiersin.org)
  • This can be due to ischemia (lack of blood flow) caused by blockage, or a hemorrhage. (medicaldaily.com)
  • Effects of glucose and fatty acids on myocardial ischaemia and arrhythmias. (revistasad.com)
  • We conclude that PARP-2 is a novel executioner of cell death pathways in focal cerebral ischemia, but might be a necessary survival factor after global ischemia to mitigate hippocampal delayed cell death. (elsevier.com)
  • NG-nitro-L-arginine protects against ischaemia-induced increases in nitric oxide and hippocampal neuro-degeneration in the gerbil. (southampton.ac.uk)
  • Concomitantly, in vitro cortical and hippocampal cell viability and ATP levels decreased, with an increase in brain edema in hypoxic brains. (uab.edu)
  • Fetuses delivered 24 h post-ischemia had increased hippocampal nuclear karyorrhexis on histology compared with controls. (uab.edu)
  • Progress in understanding of the pathophysiology of brain lesion has required the use of experimental models to evaluate cellular events that occur immediately after the lesion or later, to associate this changes with clinical observations and to propose pharmacological neuroprotection therapies. (univalle.edu.co)
  • Oxygen free radical involvement in ischemia and reperfusion injury to brain. (southampton.ac.uk)
  • Although available interventions improve recanalization rates, there remain no therapies to treat delayed ischemia-reperfusion injury (IRI). (rochester.edu)
  • Bisphenols accumulation in the white matter-enriched brain tissue could signify that they are able to cross the blood-brain barrier. (greenmedinfo.com)
  • The result is oxygen deprivation to brain tissue. (healthline.com)
  • A CT scan provides cross-sectional images of the brain, allowing a more in-depth analysis of blood circulation and tissue damage. (medicalnewstoday.com)
  • Localized reduction of blood flow to brain tissue due to arterial obstruction or systemic hypoperfusion. (bvsalud.org)
  • This prevents those areas of the brain from getting the oxygen they need, and the cells begin to die. (birthinjurylawyer.com)
  • It can leave part of your brain deprived of blood and oxygen. (healthline.com)
  • Objectives The aim of the study is to evaluate the effect of hyperbaric oxygen therapy (HBOT) in participants suffering from chronic neurological deficits due to traumatic brain injury (TBI) of all severities in the largest cohort evaluated so far with objective cognitive function tests and metabolic brain imaging. (bmj.com)
  • Its effects are caused not only by impaired oxygen delivery but also by disrupting oxygen utilization and respiration at the cellular level, particularly in high-oxygen demand organs (i.e., heart and brain). (cdc.gov)
  • Insufficient delivery of oxygen and destruction of red blood cells may cause cardiopulmonary complaints with the development of ischemia, arrhythmia and shock. (cdc.gov)
  • This means it forms at the site of the blockage in the brain. (healthline.com)
  • Preterm neonates are susceptible to perinatal hypoxic-ischemic brain injury, for which no treatment is available. (tue.nl)
  • Ina preclinical animal model of hypoxic-ischemic brain injury in ovine fetuses, we have demonstrated the neuroprotective potential of systemically administered mesenchymal stromal cells (MSCs). (tue.nl)
  • Therefore, we investigated in this study the protective effects of mes-enchymal stromal cell-derived extracellular vesicles (MSC-EVs) in a preclinical model of preterm hypoxic-ischemic brain injury. (tue.nl)
  • Our study results suggest that a cell-free preparation comprising neuroprotec-tive MSC-EVs could substitute MSCs in the treatment of preterm neonates with hypoxic-ischemic brain injury, thereby circumventing the potential risks of systemic administration of living cells. (tue.nl)
  • If you or a loved one suffered an ischemic brain injury, contact us at (412) 661-1400 . (bergerandgreen.com)
  • These results contribute significant information on the timing and factors that influence free radical formation following ischemic brain injury, an essential step in determining effective antioxidant intervention. (southampton.ac.uk)
  • Questionable whether intermittent fasting (IF) protects against ischemic brain injury. (il-13.com)
  • Here, we review the differential role of TNF-a in response to brain injury, with emphasis on neurodegeneration, and discuss the possible mechanisms for such diverse and region-specific effects. (cdc.gov)
  • In these cases, neurodegeneration and brain repair ar. (bookshare.org)
  • WHAT THIS PAPER ADDS Fetal hypoxemia is rarely documented in brain injury studies. (bvsalud.org)
  • Fetal brains were obtained immediately after ischemia for oxidative and acute-injury markers or 24 hours (h) post- ischemia for histopathology. (uab.edu)
  • It can result from pancerebral hypoperfusion caused by vasovagal reflexes, orthostatic hypotension, or decreased cardiac output, or from selective hypoperfusion of the brainstem resulting from vertebrobasilar ischemia. (mhmedical.com)
  • More than 20 specific cardiac disorders have been implicated in leading to brain embolism. (medscape.com)
  • Although the link between S1P₁ and microglial activation as a pathogenesis in cerebral ischemia had been clearly demonstrated, whether the pathogenic role of S1P₁ is associated with its regulation of M1/M2 polarization remains unclear. (bvsalud.org)
  • Brain ischemia or cerebral ischemia is an ailment that happens when there isn't enough blood flow to the brain to meet the metabolic demand. (pharmiweb.com)
  • Following proper protocols for labor and delivery and providing the accepted standard of care can limit the instances of brain ischemia and allow for quick diagnosis and treatment if it does occur. (birthinjurylawyer.com)
  • A significant amount of DNA laddering was detected 24 hr after ischemia and increased in Sod2 −/+ mice. (jneurosci.org)
  • In male C57Bl6J mice, ischemia-reperfusion was associated with pulmonary function changes, vascular inflammation, and airway immune infiltration. (rochester.edu)
  • If the results in mice can be reproduced in people, patients with traumatic brain injuries could receive the BCAAs in a drink. (pursuitofresearch.org)
  • The experiments show that the injected orexin is able to enter the brain, where it helps the mice to survive and recover from septic shock by restoring normal body temperature and boosting heart rate. (elifesciences.org)
  • Brain ischemia, or cerebral ischemia, occurs when the brain suffers damage because of reduced or blocked blood flow. (birthinjurylawyer.com)
  • Although various studies have investigated behavioral improvements and structural alterations in the brain with postinjury exercise therapy, little is known about the underlying mechanisms [ 4 ]. (hindawi.com)
  • To further improve outcomes, we need to better understand the mechanisms of brain injury. (auckland.ac.nz)
  • My research has been focused on exploring the mechanisms of cerebral ischemia and reperfusion induced brain damage, especially under diabetic/hyperglycemic conditions, and investigating novel therapeutic approaches for treating neurodegenerative diseases using cell culture models, animal models and transgenic approaches. (neuroscijournal.com)
  • Protective role of reactive astrocytes in brain ischemia. (medscape.com)
  • However, if this blood flow is not quickly restored, the victim may suffer permanent brain damage. (bergerandgreen.com)
  • After HI, the DR-HI, but not extreme DR-HI, pups had significantly lower p53, higher phospho-murine double minute-2, lower cleaved caspases, less BBB damage and microglia activation, and less brain volume loss than NL-HI pups. (elsevier.com)
  • Although the function of fever is still unclear, it is now beyond doubt that body temperature influences the outcome of brain damage. (nih.gov)
  • Oxidative damage in hippocampus was maximal at late stages after ischemia (48-96 h) coincident with a significant impairment in glutathione homeostasis. (southampton.ac.uk)
  • Role of oxidants in ischemic brain damage. (southampton.ac.uk)
  • If your child suffered brain damage before, during, or shortly after birth, let an attorney from your state review your case. (birthinjurylawyer.com)
  • The infarct size of animals was determined by the 2,3,5-triphenyltetrazolium chloride staining, and pathological brain damage was estimated by hematoxylin-eosin staining. (dovepress.com)
  • In all instances, a decrease in oxygenation and nutrient supply ultimately leads to brain damage. (frontiersin.org)
  • Central arterial stiffness and increased blood flow pulsatility alter microvasculature structure and function in the brain contributing to hypoperfusion and end-organ damage. (neurodegenerationresearch.eu)
  • Overall, these results revealed S1P₁-regulated M1/M2 polarization toward brain damage as a pathogenesis of cerebral ischemia. (bvsalud.org)
  • This causes damage to brain cells and to intellectual ability and cause lasting damage. (nanavatimaxhospital.org)
  • Pulsinelli WA, Waldman S, Rawlinson D, Plum F. Moderate hyperglycemia augments ischemic brain damage: a neuropathologic study in the rat. (revistasad.com)
  • Here, due to non-development of a protective skull that protects your brain is not fully formed at birth thus, making the brain vulnerable to physical injury . (nanavatimaxhospital.org)
  • Traumatic brain injury (TBI) is one of the leading causes of death and disability in the general population. (bmj.com)
  • Further experiments suggest that orexin is likely to regulate immune responses through multiple signaling pathways in the brain. (elifesciences.org)
  • Brain Ischemia Market 2021 Industry Trend, Size Estimatio. (pharmiweb.com)
  • DBMR has added a new research report titled Brain Ischemia Market Size , Share, Growth, Trends, and Forecast 2021 to 2028 spins around market dynamics, regional growth, competition, and other important aspects of the global market. (pharmiweb.com)
  • The Brain Ischemia Market is expected to gain market growth in the forecast period of 2021 to 2028. (pharmiweb.com)
  • LEAG: study conception, de datos PubMed y Cochrane, se incluyeron artículos originales, estudios aleatorizados y de revisión, en español y en inglés, manuscript design, publicados entre 2017-2021. (bvsalud.org)
  • The increasing burden of the ischemic strokes and the growth in the elderly population which turn is prone to brain ischemia, the growing number of the patient suffering from the diabetes, obesity hypertension and other linked diseases are the factors expected to boost the growth of the brain ischemia market in the forecast period. (pharmiweb.com)
  • Should white matter disease of the brain be treated: if the white matter disease of the brain represents ischemic white matter disease it may be prudent to address vascular risk factors such as better control of hypertension and diabetes, lowering the cholesterol and advising the patient to stop smoking. (braindiseases.blog)
  • When a minor-risk cardioembolic source is present in a patient with cerebral ischemia, the etiologic role must be viewed with skepticism and considered in the context of other diagnostic information. (medscape.com)
  • This narrative review describes the main applications of de la ultrasonografía en ultrasound in anesthesia, ultrasound-guided techniques, and current trends in the perioperative anesthetic management of anestesia the surgical patient. (bvsalud.org)
  • If you or your loved one is suffering these symptoms and you suspect brain ischemia, seek medical attention immediately. (bergerandgreen.com)
  • So, it can be defined as any condition that is caused by a dysfunction in part of the brain or nervous system, resulting in physical and/or psychological symptoms . (nanavatimaxhospital.org)
  • Diagnosis is usually based on symptoms and results of a physical examination and brain imaging. (msdmanuals.com)
  • Focal cerebral ischemia occurs when a blood clot obstructs a blood vessel, so there is less blood flow to a particular region of the brain. (bergerandgreen.com)
  • Brain ischemia is a type of brain injury that occurs because of reduced blood flow to the brain. (birthinjurylawyer.com)
  • Strokes occur when blood flow to your brain is interrupted. (healthline.com)
  • This study presents new evidence that the dissection process and its duration increase brain oxylipin concentrations, and that this is preventable by microwave fixation. (omicsdi.org)
  • In many cases, brain ischemia is preventable. (birthinjurylawyer.com)