neurodegenerative diseases/mrzlica

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L-ephedrine-induced neurodegeneration in the parietal cortex and thalamus of the rat is dependent on hyperthermia and can be altered by the process of in vivo brain microdialysis.

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Multiple doses of the dietary supplement L-ephedrine can cause severe hyperthermia and modest dopamine depletions in the rat brain. Since D-amphetamine treatment can result in neurodegeneration, the potential of L-ephedrine to produce similar types of degeneration was investigated. Adult male rats,

Role of hyperthermia in the protective action of clomethiazole against MDMA ('ecstasy')-induced neurodegeneration, comparison with the novel NMDA channel blocker AR-R15896AR.

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1. The immediate effect of administration of 3,4-methylenedioxymethamphetamine (MDMA or 'ecstasy') on rectal temperature and the effect of putative neuroprotective agents on this change has been examined in rats. The influence of the temperature changes on the long term MDMA-induced

Hyperthermia induced after recirculation triggers chronic neurodegeneration in the penumbra zone of focal ischemia in the rat brain.

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Chronic neurodegenerative processes have been identified in the rat forebrain after prolonged survival following hyperthermia (HT) initiated a few hours after transient global ischemia. Since transient global ischemia and ischemic penumbra share pathophysiological similarities, this study addressed

Protection against 3,4-methylenedioxymethamphetamine-induced neurodegeneration produced by glutathione depletion in rats is mediated by attenuation of hyperthermia.

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3,4-Methylenedioxymethamphetamine (MDMA) administration produces neurotoxic degeneration of serotonin terminals in rat brain. These effects occur only after systemic administration and not after central injection, suggesting that peripheral metabolism, possibly hepatic, is required for toxicity.

Heat shock protein (hsx70) mRNA expression in human brain: effects of neurodegenerative disease and agonal state.

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Heat shock proteins (hsps) are involved in the response by cells to stress including hyperthermia, hypoxia and injury. Previous work has demonstrated expression of messenger RNA (mRNA) encoding 70 kDa hsps (hsp70) in animal brain in response to stimuli such as these. We have used in situ

Treatment of rheumatoid and degenerative diseases with copper complexes: a review with emphasis on copper-salicylate.

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This review presents a historical account of the treatment of rheumatoid and other degenerative diseases with copper complexes. Clinical data obtained from 1940 to 1971 are provided for about 1,500 patients with rheumatoid arthritis (acute or chronic), rheumatic fever, ankylosing spondylitis,

The relationship between the degree of neurodegeneration of rat brain 5-HT nerve terminals and the dose and frequency of administration of MDMA ('ecstasy').

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The effect of varying the dose and frequency of administration of 3,4-methylenedioxymethamphetamine (MDMA or 'ecstasy') on both the acute hyperthermic response and the long term neurodegeneration of 5-hydroxytryptamine (5-HT) nerve terminals in the brain has been studied in Dark Agouti rats. A

Serial MRI alterations of pediatric patients with beta-propeller protein associated neurodegeneration (BPAN).

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Beta-propeller protein-associated neurodegeneration (BPAN) is one subtype of neurodegeneration with brain iron accumulation. It is difficult to diagnose BPAN due to the non-specificity of their clinical findings and neuroimaging in early childhood. We experienced four pediatric

Thermoregulatory profile of neurodegeneration-induced dementia of the Alzheimer's type using intracerebroventricular streptozotocin in rats.

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OBJECTIVE Here, we have extensively investigated the relationship between thermoregulation and neurodegeneration-induced dementia of the Alzheimer's type using intracerebroventricular injections of streptozotocin (icv-STZ). METHODS Male Wistar rats were treated with bilateral injections of icv-STZ,

Amphetamine- and methamphetamine-induced hyperthermia: Implications of the effects produced in brain vasculature and peripheral organs to forebrain neurotoxicity.

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The adverse effects of amphetamine- (AMPH) and methamphetamine- (METH) induced hyperthermia on vasculature, peripheral organs and peripheral immune system are discussed. Hyperthermia alone does not produce amphetamine-like neurotoxicity but AMPH and METH exposures that do not produce hyperthermia

Drugs of abuse-induced hyperthermia, blood-brain barrier dysfunction and neurotoxicity: neuroprotective effects of a new antioxidant compound H-290/51.

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The psychostimulants, morphine and methamphetamine are well known drugs of abuse that induce brain pathology and/or neurodegeneration resulting in a huge burden on our society. The possible mechanisms of psychostimulants induced neuropathology and neurodegeneration are still not well known. The

Methods to produce hyperthermia-induced brain dysfunction.

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The recent increase in the frequency and intensity of killer heat waves across the globe has aroused worldwide medical attention to exploring therapeutic strategies to attenuate heat-related morbidity and/or mortality. Death due to heat-related illnesses often exceeds >50% of heat victims. Those who

[Lesions in the central nervous system of the mouse caused by yellow fever 17 D. An animal model of the histological evaluation of viral encephalitis (author's transl)].

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Random-Bred-Swiss Mice were inoculated intracerebrally with 0.02 ml of a 10(-1) diluted suspension of yellow fever virus 17 D. The animals were sacrificed at selected times ranging from 1 day up to 168 days after inoculation. Brain sections were stained and then histologically investigated. Nerve

Peptide modulation of fever and inflammation within the brain.

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The importance of melanocortin peptides to host responses was recognized with the observation of the antipyretic effect of centrally administered alpha-melanocyte stimulating hormone (alpha-MSH). It is now clear that this neuropeptide also exerts remarkable antiinflammatory activity via direct

Effect of hyperthermia and anoxia on glucocorticoid and mineralocorticoid receptor expression in neonatal rat hippocampus.

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Brief periods of neonatal asphyxia are frequently observed. Within the CNS, the hippocampus is known to be particularly vulnerable to the damaging effects of hypoxia/ischaemia. The hippocampus contains the highest concentration of both mineralocorticoid (MR) and glucocorticoid (GR) receptors and the

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