cytochrome oxidase/atrofie

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Delayed onset of neurologic deterioration following anoxia/ischemia coincides with appearance of impaired brain mitochondrial respiration and decreased cytochrome oxidase activity.

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We previously demonstrated markedly inhibited brain mitochondrial respiration only in cats that (a) were hyperglycemic at anoxia and (b) had neurologic signs, i.e., fasciculations in tongue or facial muscles or focal seizures following reoxygenation. However, since the relationship between time of

Neuronal degeneration in the brain of the brindled mouse. Histochemical demonstration of decreased cytochrome oxidase activity in the cerebellum and brain stem.

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In order to investigate the levels of cytochrome oxidase activity in neuronal mitochondria in the brain of the brindled mouse hemizygote (BM), the cerebella and brain stems from 12 pairs of brindled and normal littermates aged 13-16 days were examined. The diaminobenzidine method for light- and

Modular organization of human extrastriate visual cortex: evidence from cytochrome oxidase pattern in normal and macular degeneration cases.

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The human extrastriate occipital cortex contains several visual areas that are probably analogues of macaque areas V2, V3, VP, V4 and V5. Tracing of callosal connections has led to the anatomical identification of these areas and to the characterization of some of them by cyto- and myeloarchitecture

Progressive cerebral degeneration of childhood with liver disease (Alpers Huttenlocher disease) with cytochrome oxidase deficiency presenting with epilepsia partialis continua as the first clinical manifestation.

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A previously healthy and normally developed 17-year-old young female presented with a sudden onset of focal motor seizure status that proved to be refractory to anticonvulsive treatment. Severe encephalopathy with visual impairment leading to blindness, mental deterioration, and predominantly left

Resveratrol ameliorates motor neuron degeneration and improves survival in SOD1(G93A) mouse model of amyotrophic lateral sclerosis.

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Resveratrol has recently been used as a supplemental treatment for several neurological and nonneurological diseases. It is not known whether resveratrol has neuroprotective effect on amyotrophic lateral sclerosis (ALS). To assess the effect of resveratrol on the disease, we tested this agent on an

Fiber atrophy and hypertrophy in skeletal muscles of late middle-aged Fischer 344 x Brown Norway F1-hybrid rats.

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We examined young adult and late middle-aged male rats to test the hypothesis that gastrocnemius (a locomotor muscle) demonstrates reduced fiber size with aging, whereas soleus (a postural muscle) demonstrates atrophy of some fibers and compensatory hypertrophy in other fibers. Although body mass

Decreased brain protein levels of cytochrome oxidase subunits in Alzheimer's disease and in hereditary spinocerebellar ataxia disorders: a nonspecific change?

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Controversy exists as to the clinical importance, cause, and disease specificity of the cytochrome oxidase (CO) activity reduction observed in some patients with Alzheimer's disease (AD). Although it is assumed that the enzyme is present in normal amount in AD, no direct measurements of specific CO

The effects of age on atrophy and recovery in denervated fiber types of the rat nasolabialis muscle.

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This study investigates the effects of advancing age on responses of nasolabialis muscle fibers to denervation and reinnervation. The nasolabialis is innervated by the facial nerve and is responsible for the whisking movement of the animal's large vibrissae. In young adult (3-month) and middle-aged

Patterns of thalamocortical degeneration after ablation of somatosensory cortex in monkeys.

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We examined the pattern of cytochrome oxidase (CO), Nissl staining, and gamma-amino butyric acid (GABA) immunoreactivity in the ventroposterior lateral nucleus (VPL) of the thalamus in monkeys that received no, total, or subtotal, ablation of the hand representations in postcentral somatosensory

Unaltered cytochrome oxidase, glutamate dehydrogenase and glutaminase activities in platelets from patients with sporadic amyotrophic lateral sclerosis--a study of potential pathogenetic mechanisms in neurodegenerative diseases.

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Sporadic Amyotrophic Lateral Sclerosis (SALS) is a fatal neurologic disease characterized by degeneration of motor neurons in the spinal cord, brainstem and cortex. While familial cases of ALS exist, the sporadic form accounts for the majority of adult-onset cases. It has been hypothesized that the

Chronic intrastriatal dialytic administration of quinolinic acid produces selective neural degeneration.

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The excitotoxic hypothesis of Huntington's disease pathogenesis suggests that selective striatal neuronal loss results from excessive activation of striatal excitatory amino acid receptors. Using a microdialysis probe mated to an Alzet 2002 mini-osmotic pump three different concentrations of

Rapid but transient atrophy of brown adipose tissue in capsaicin-desensitized rats.

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Our previous studies showed atrophy of brown adipose tissue (BAT) in capsaicin-desensitized rats during the period 11-28 days after injections [Cui et al., Am. J. Physiol. 259 (Regulatory Integrative Comp. Physiol. 28): R324-R332, 1990]. The objective of the present studies was to assess the

Selective degeneration of the parvocellular-projecting retinal ganglion cells in a New World monkey, Saimiri sciureus.

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Selective degeneration of retinal ganglion cells projecting to parvocellular layers of the dorsal lateral geniculate nucleus (LGN) was observed in squirrel monkeys (Saimiri sciureus) exposed to a range of doses of acrylamide monomer. Similar acrylamide-induced neuronal loss has previously been

Effects of cortical and thalamic lesions upon primary afferent terminations, distributions of projection neurons, and the cytochrome oxidase pattern in the trigeminal brainstem complex.

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Early postnatal lesions of the primary somatosensory cortex alter the vibrissa-related cytochrome oxidase (CO) pattern in nucleus principalis (PrV) of the rat's trigeminal (V) brainstem complex (Erzurumlu and Ebner, '88: Dev. Brain Res. 44:302-308). At present, the reason for this change is not

Selective acrylamide-induced degeneration of color opponent ganglion cells in macaques.

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P beta (color opponent) retinal ganglion cells in macaques were found to degenerate as a result of oral administration of acrylamide. Histological examination, wheat germ agglutinin-horseradish peroxidase transport and cytochrome oxidase histochemistry indicate that other retinal ganglion cells and

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