emetine/atrofie

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Emetine myopathy in a patient with an eating disorder.

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OBJECTIVE To alert physicians to the dangers of a readily available, non-prescription drug by describing the clinical and pathological features of myopathy due to chronic poisoning with ipecac syrup in a patient with an eating disorder. METHODS A 27-year-old woman presented in 1991 with a right foot

Emetine-induced lactate dehydrogenase release, functional changes and electrocardiographic changes in the rat heart in vitro.

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Emetine is an old drug which is used primarily as a emetic in ipecac syrup and as an alternative amoebicide. The major problem with emetine is that chronic use causes severe cardiotoxicity. In order to explore the mechanism of emetine cardiotoxicity, simultaneous recordings of mechanical activity

Emetine-induced cardiomyopathy in rabbits.

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A correlative electrocardiographic and ultrastructural study of myocardium in rabbits, administered 1 mg/kg of emetine hydrochloride intramuscularly for 5 successive days of a week over 2 to 4 week period, was conducted. The study revealed electrocardiographic changes and a spectrum of

Cytotoxic effects of emetine hydrochloride in the kidney of Long-Evans rats.

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Emetine hydrochloride has been used to study its effects in the rat kidney, Sublethal doses of the drug at 10.0 mg/kg body weight of the animal were administered at 12 and 24 h intervals. Certain morphological changes occurred within the kidney. These changes involved the formation of vacuoles,

Nonsense-mediated messenger RNA decay of survival motor neuron 1 causes spinal muscular atrophy.

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Autosomal recessive proximal spinal muscular atrophy (SMA) is a neurodegenerative disorder resulting from functional loss of survival motor neuron 1 (SMN1). Homozygous absence of SMN1 due to deletion or gene conversion accounts for about 96% of SMA cases. In the remaining 4%, subtle SMN1 mutations

Emetine myopathy in the rat.

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1 (-)Emetine (0.25-2.0 mg/kg i.p.) was administered to rats for up to 220 days. 2 At doses of 1.0 mg/kg or less, the animals continued to gain weight but more slowly than the untreated control animals. The physiological changes in the muscles from these animals were minimal; there was a small

Effects of pharmacological interventions on emetine cardiotoxicity in isolated perfused rat hearts.

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The cardiotoxicity of emetine continues to be a significant clinical problem. The purpose of this study was to investigate the effect of several mechanistic interventions, including ICRF-187, an iron-chelating agent which protects against doxorubicin toxicity, atropine, and fructose-1,6-bisphosphate

Experimental (-) emetine myopathy. Ultrastructural and morphometric observations.

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The ultrastructural changes induced by (-) emetine hydrochloride were studied in two skeletal muscles of the rat. (-) Emetine was administered at a dose level of 2 mg/kg for periods ranging from one to four weeks. Changes were noted after the one week stage and were progressive with all muscle

Reversible emetine-induced myopathy with ECG abnormalities: a toxic myopathy.

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A young anorexic woman is described with a history of progressive muscle weakness following chronic ingestion of syrup of ipecac that was used in an attempt at weight control. Electrocardiogram (ECG) showed T-wave inversion in all leads and prolongation of the Q-T interval. Electromyography was

Toxic mechanisms of the heart: a review.

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Toxic injury is one of the many ways by which the functional integrity of the heart may become compromised. Any of the subcellular elements may be the target of toxic injury, including all of the various membranes and organelles. Understanding the mechanisms underlying cardiotoxicity may lead to

Programmed cell death triggered by insect steroid hormone, 20-hydroxyecdysone, in the anterior silk gland of the silkworm, Bombyx mori.

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Silk gland is a larval specific tissue of lepidopteran insects and begins to degenerate shortly before pupation. Programmed cell death (PCD) of the anterior silk gland of Bombyx mori last instar larvae was studied in vivo and in vitro, focusing on the effects of 20- hydroxyecdysone (20E). The glands

Protein synthesis inhibitors delay transneuronal death in the piriform cortex of young adult rats.

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It has been demonstrated that apoptotic cell death is an active process that is dependent on RNA and protein synthesis. The question remains as to whether neuronal death in adult, mammalian brains can also be demonstrated in vivo to be dependent on protein synthesis. To address this question we have

Disturbance of the determination of germinal and somatic nuclei by heat shock in Paramecium caudatum.

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During conjugation of Paramecium caudatum, nuclear determination occurs soon after the third postzygotic division: one of the four anterior nuclei becomes the micronucleus and the remaining three degenerate, while four posterior nuclei differentiate into macronuclear anlagen. Macronuclear

Inflammatory and toxic myopathy.

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Although muscle diseases are relatively rare, several treatable myopathies must be recognized by the clinician to maximize the possibility of restoring strength in affected patients. The inflammatory myopathies, including polymyositis, dermatomyositis, inflammatory necrotizing myopathy, and myositis

3-Nitropropionic acid induces apoptosis in cultured striatal and cortical neurons.

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Ingestion of 3-nitropropionic acid (3-NPA) in moldy sugar cane causes brain damage in children. The mechanism of 3-NPA toxicity is thought to be inhibition of energy production, leading to ATP depletion and excitotoxicity. We exposed cultured mouse striatal or cortical neurons to 1-2 mM 3-NPA for 48

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