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Neurons stroke

SirabeUa R, Secondo A, Pannaccione A, ScorzieUo A, Valsecchi V, Adometto A, Bilo L, Di Renzo G, Annunziato L (2009) Anoxia-induced NF-kappaB-dependent upregulation of NCXl contributes to Ca refining into endoplasmic reticulum in cortical neurons. Stroke 40(3) 922-929 22 Jan 2009 [Epub ahead of print]... [Pg.64]

Many derivatives of 4-hydroxy-3-nitro-l,X-naphthyridin-2(lH)-ones (X = 5,6,7, and 8) were claimed to have been used for treating or preventing neuronal loss associated with stroke, ischemia, CNS trauma, hypoglycemia, and surgery as well as for treating neurodegenerative diseases, chronic pain, convulsion, anxiety, and opiate tolerance (96MI2). [Pg.339]

NS AIDs Cyclooxygenases (COX-1, COX-2) l Prostaglandins l Thromboxanes l Sensitization of sensory neurons f Inhibition of spinal neurons Nonselective gastrointestinal ulcers, perforation, bleeding, renal impairment COX-2 thrombosis, myocardial infarction, stroke... [Pg.76]

Antiepileptics are used in neuropathic pain resulting from lesions to the peripheral (e.g., diabetes, heipes) or central nervous system (e.g., stroke). Such syndromes have been attributed to ectopic activity in sensitized nociceptors from regenerating nerve sprouts, recruitment of previously silent nociceptors, and/or spontaneous neuronal activity. This may result in sensitization... [Pg.77]

Excitotoxicity is the over-activity of the glutamatergic system responsible for the large number of dead neurons observed after ischemia (stroke) or epileptic seizures. This neuronal death is due to an overexcitation of the neurons and the massive Ca2+ entry... [Pg.487]

On the pathophysiological side, hyperactive nNOS has been implicated in A/-methyl-D-aspartate (NMDA)-receptor-mediated neuronal death in cerebrovascular-stroke. Some disturbances of smooth muscle tone within the gastrointestinal tract (e.g., gastroesophageal reflux disease) may also be related to an overproduction of NO by nNOS in peripheral nitrergic nerves. [Pg.863]

Thored P, Arvidsson A, Cacd E, Ahlenius H, KaUur T, Darsaha V, Ekdahl CT, Kokaia Z, LindvaU O (2006) Persistent production of neurons from adult brain stem cells during recovery after stroke. Stem Cells 24 739-747... [Pg.219]

A series of dihydrodibenzoxepines, represented by AJ3941, was tested in animal models of global ischaemia and hypoxia, and found to be protective. AJ3941 is an inhibitor of lipid peroxidation (Kurakawa etal., 1991). A novel quinazoline fumarate (KB56666, was found to inhibit lipid peroxidation in rat brain homogenates and isolated mitochondria. In a rat focal stroke model, KE56666 prevented brain oedema and neuronal damage in the ischaemic zone (Hara etal., 1991). [Pg.271]

Uyama, O., Matsuyama, T., Michishita, H., Nakamura, H. and Sugita, M. (1992). Protective effects of human recombinant SOD on transient ischemic injury of CAl neurons in gerbils. Stroke 23, 75-81. [Pg.277]

Narahashi T Northwestern University Medical School, Chicago, IL The effects of therapeutic drugs and toxins on neuronal ion channels National Institute of Neurological Disorders and Stroke... [Pg.364]

Neuronal function depends on a constant supply of oxygen. Hypoxia, a decrease in oxygen availability, depresses neuronal activity. Interruption of blood flow to the brain for only a few seconds leads to unconsciousness. A prolonged lack of blood flow, which is characteristic of stroke, leads to permanent brain damage in the affected area. [Pg.41]

Neurodegeneration Localised or widespread death of neurons, a feature of a number of brain disorders, such as Alzheimer s disease, Parkinson s disease and cerebrovascular stroke. It can also be caused by neurotoxic drugs like MDMA/Ecstasy, although there is debate over whether this occurs in humans as well as laboratory animals. [Pg.246]


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See also in sourсe #XX -- [ Pg.456 ]




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