Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030552 (paresis)
 5,831 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Botulinum toxin is widely used for the treatment of focal movement disorders, where chemodenervation is used to decrease hyperactivity in selected muscles. Beside a focal paresis, widespread effects on neuromuscular synaptic function have been demonstrated. However, reactions of motoneurons after neuromuscular chemodenervation without gross morphological lesions are largely unknown. Peripheral axotomy, in contrast, leads to profound changes in the expression of several genes, including those encoding neurotransmitters, in motoneurons. We therefore examined the expression of neurotransmitter genes in rat motoneurons six days after intramuscular botulinum toxin application in the right gastrocnemius muscle. Similar doses of botulinum toxin as used in human where injected. A focal bilateral increase in expression of the choline acetyltransferase gene and a widespread bilateral increase of the beta-calcitonin-gene-related peptide and the enkephalin genes was measured in motoneurons after botulinum toxin injection. Cholecystokinin had a lower expression after botulinum toxin injections. Growth-associated protein 43, nitric oxide synthase, somatostatin and proopiomelanocortin messenger RNA were not found in motoneurons of both groups. Our results demonstrate that changes in the expression of neurotransmitter genes in motoneurons also occur after chemodenervation but with different patterns to those found after mechanical nerve lesioning. These changes reflect focal and widespread modulative events. The knowledge of these events should lead to a better understanding of the focal paralysis and of the more widespread effects found in human after intramuscular injection of botulinum toxin.
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PMID:Expression of neurotransmitter genes in rat spinal motoneurons after chemodenervation with botulinum toxin. 914 3

Proinflammatory cytokines exert a number of important effects on vascular reactivity. At one end of the spectrum, certain cytokines may induce vascular paresis leading to profound vasodilatation and hyporesponsiveness to constrictor stimuli. This may be relevant to the pathogenesis of septic shock and other types of inflammatory vasodilatation. At the other end of the spectrum, inflammatory cytokines can impair endothelium-dependent dilatation and the endothelium may lose its ability to respond to circulating hormones or autacoids. This effect may case a predisposition to vessel spasm, thrombosis or atherogenesis. Studies in human vessels suggest that interleukin-1 is particularly important as a mediator of inflammatory dilatation; the underlying mechanisms include induction of the inducible isoform of nitric oxide synthase in vascular smooth muscle, or over-production of nitric oxide from the endothelial isoform of nitric oxide synthase. Induction of the enzyme GTP cyclohydrolase 1 and consequent production of tetrahydrobiopterin contributes to the increase in the activity of endothelial nitric oxide synthase. In contrast, tumour necrosis factor-alpha considerably impairs endothelium-dependent relaxation. The mechanisms of these effects are not yet fully understood, but tumour necrosis factor can induce endothelial dysfunction in human endothelial cells in culture, and human blood vessels in vitro and in vivo. The implications of these observations for cardiovascular disease are discussed.
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PMID:Effects of cytokines on nitric oxide pathways in human vasculature. 991 65