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Neuron necrosis

S3fntichaki P, Tavemarakis N. The biochemistry of neuronal necrosis rogue biology Nat Rev Neurosci 2003 4 672-684. [Pg.114]

Following short-term inhalation exposure to 160 ppm [620 mg/m ] methyl bromide (6 h per day on five days per week for up to six weeks), B6C3F, mice were found to be more sensitive than Fischer 344/N rats 50% of male mice died after eight exposures and 50% of female mice after six exposures, while similar mortality was observed in male rats only after 14 exposures. Neuronal necrosis and testicular degeneration were observed in both species nephrosis was observed in nearly all mice, while necrosis of the olfactory epithelium was more marked in rats. Myocardial degeneration occurred in rats and to a lesser degree in male mice. In the adrenal cortex, there was cytoplasmic vacuolation in rats and inner zone atrophy in female mice (Eustis et al., 1988). [Pg.726]

Activation of calpain is usually associated with the progression of a necrotic type of cell death (Wang, 2000). However, neuronal necrosis and apoptosis occur in parallel after ischemic injury in vitro and in vivo (Charriaut-Marlangue et al., 1996). Retinal ischemia causes precocious necrosis of neurons in the ganglion cell layer (GCL) and INL, whereas apoptosis appears as the delayed component of neuronal death associated with transient retinal ischemia (Joo et al., 1999). [Pg.413]

Garcia J, Liu K-F, Ho K-L (1995) Neuronal necrosis after middle cerebral artery occlusion in Wistar rats progresses at different time intervals in the caudoputamen and the cortex. Stroke 26 636-643... [Pg.22]

Warner D. S., Deshpande J. K., andWielochT. (1986) The effectof isofluraneon neuronal necrosis following near-complete forebrain ischemia in the r t. Anesthesiology 64,19-23. [Pg.141]

Verschoyle RD, Brown AW, Ray DE, et al. 1987. The relationship between uncoupling of oxidative phosphorylation and neuronal necrosis within the CNS in rats dosed with trihalogenated imidazoles. Toxicol Appl Pharmacol 89 175-282. [Pg.156]

Kesslak JP, Frederickson CJ, Gage FH (1987) Quantification of hippocampal noradrenaline and zinc changes after selective cell destruction. Exp Brain Res 67 77-84 Kim EY, Koh JY, Kim YH, Sohn S, Joe E, Gwag BJ (1999) Zn2-l- entry produces oxidative neuronal necrosis in cortical cell cultures. Eur J Neurosci 11 327-334... [Pg.687]

In general, the California encephalitis subgroup viruses spread from the site of inoculation to skeletal muscles, which is the major site of replication. The virus then spreads to the lymphatic channels, thus spreading to additional skeletal muscles and cardiac muscles. Ultimately, the virus ends up in the CNS, where viral replication can occur in neurons and glial cells. Due to considerable neuronal necrosis, death can... [Pg.336]

A 51-year-old man underwent double lung transplantation for pulmonary fibrosis, accidentally received an infusion of ciclosporin 30 mg/hour instead of 3 mg/hour, and 3 hours later had bilateral reactive mydriasis and absence of tendon reflexes. A CT brain scan showed diffuse cerebral edema, and massive intracranial hjrpertension rapidly developed. He died 5 hours later from brainstem compression, and pathological examination showed diffuse cerebral edema with neuronal necrosis. [Pg.757]

Chronic camphor dosing in a mouse model has lead to development of neuronal necrosis. [Pg.383]

Hypotension (low blood pressure) and ischemia (restricted blood flow) associated with exposure reduces the delivery of oxygen to tissues and cells and may lead to sever damage and/or death of nerve cells (neuronal necrosis). [Pg.1357]

Mouse (B6C3F1) 104 wk ad lib (F) 0.14 M 0.69 M (sensory neuropathy cerebral and cerebellar neuronal necrosis posterior paralysis) Mitsumori et al. 1990 MMC... [Pg.120]

Neuropathological examination of the four patients who died indicated neuronal necrosis and astrocytosis, particularly in the hippocampus and the amygdaloid nucleus. All four victims also had lesions in the claustrum, secondary olfactory areas, the septal area, and the nucleus accumbens septi. Two had prominent thalamic damage, especially in the dorsal medial nucleus. The subfrontal cortex was also damaged in three of the patients. The authors noted that the pattern of damage in the hippocampus appeared to parallel that seen in animals that suffered neurotoxic reactions after administration of kainic acid (and domoic acid see above). [Pg.421]

Nevander G, Ingvar M, Auer R, Siesjo BK. Status epilepticus in well-oxygenated rats causes neuronal necrosis. Ann Neurol. 1985 18 281-290. [Pg.176]

Once the EEG goes flat, neuronal necrosis appears over 10-30 min (Auer et al., 1984a,b) as aspartate floods the extracellular space (Sandberg et al., 1986). These necrotic neurons can be stained with any acid histological stain, and the increased affinity for acid dyes will cause them to be acidophiUc. Since most histologic stains of the brain involve a pink or red acid dye, acidophiUc neurons are invariably red in routinely stained tissue sections. [Pg.37]

A conspicuous feature of hypoglycemic brain damage in the rat is neuronal necrosis in the dentate gyrus (Fig. 3.4) of the hippocampus (Auer et al., 1985). This seems to be due to the proximity of the NMDA receptors of the molecular layer of the dentate, to the CSF spaces containing the excitatory amino acid aspartate. A similar picture of dentate necrosis is seen sometimes, in human cases of hypoglycemic coma. Although the concept of excitotoxicity was unknown in 1938, toxicity of some kind was postulated by Arthur Weil, when he noticed dentate gyrus neurons near the CSF were necrotic in rabbits (Weil et al., 1938). [Pg.37]

Auer RN, Kalimo H, Olsson Y, Wieloch T. The dentate gyrus in hypoglycemia pathology implicating excitotoxin-mediated neuronal necrosis. Acta Neuropathol (Berl) 1985. 67 279-288 Baker AB. Cerebral lesions in hypoglycemia. 11. Some possibilities of irrevocable damage from insulin shock. Arch Pathol 1938. 26 765-776... [Pg.40]

Niquet, J., Baldwin, R. A., Allen, S. G., Fujikawa, D. G., Wasterlain, C. G. (2003) Hypoxic neuronal necrosis protein synthesis-independent activation of a cell death program. Proc. Natl. Acad. Sci. US 100 2825-2830. [Pg.14]

Olney, J. W., 1971, Glutamate-induced neuronal necrosis in the infant mouse hypothalamus. An electron microscopic study. /. Neuropathol. Exp. Neurol. 30 75-90. [Pg.267]

Neuronal necrosis can occur either from direct or iixlirect toxic effects on neurons. [Pg.31]

Mercury interferes with protein synthesis in the CNS. Blindness is associated with neuronal necrosis in the calcarine sulci of the visual cortex. [Pg.149]

The answer is 2 f/f 6 6 b (4)1. Mercury causes blindness by preventing protein synthesis and neuronal necrosis in the calcarine sulci... [Pg.154]


See other pages where Neuron necrosis is mentioned: [Pg.823]    [Pg.23]    [Pg.894]    [Pg.615]    [Pg.458]    [Pg.1545]    [Pg.179]    [Pg.6]    [Pg.105]    [Pg.135]    [Pg.139]    [Pg.256]    [Pg.19]    [Pg.233]    [Pg.823]    [Pg.58]    [Pg.367]    [Pg.144]    [Pg.335]    [Pg.69]    [Pg.237]    [Pg.33]    [Pg.34]    [Pg.36]    [Pg.113]   
See also in sourсe #XX -- [ Pg.24 , Pg.26 , Pg.117 ]




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