Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027121 (myositis)
 4,538 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Electromyographic and histopathologic studies were performed in Rockland mice chronically infected with CA-I Trypanosoma cruzi strain. At 4 months post-infection the emg failed to show spontaneous activity, but a diminished interference pattern was detected in half of the infected group, while mean motor unit potential amplitude and duration were increased, compared with controls. An active denervation was observed at 6 months which persisted up to 9 months, when motor unit potential showed a significantly lower mean activity and duration. At 12 months most of the infected mice developed a reduced interference pattern, polyphasic motor unit potential increase with higher duration and amplitude than controls. Histopathologic studies showed myositis with perivascular involvement as well as intramuscular neuritis, especially at 4 and 12 months. Atrophic and hypertrophic fibers were seen. Few amastigote nests were detected. Inflammatory neuropathy with the demyelinated fibers and scanty axonal degeneration were the most common features in all infected mice. Mild myelinated fiber loss was only evident after 12 months. Endoneural parasites were seen only in the perineural macrophagic cells. These findings suggest that the neurogenic mechanism involved in the pathogenesis of muscle damage in this experimental model of chronic Chagas' disease consistently has been overlooked. The features registered here suggest that T. cruzi-infected mice developed a bimodal muscle denervation with an early acute period at any time before month 4, followed by reinnervation with a subsequent new acute denervation period by month 6, followed in turn by a slow later reinnervation.
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PMID:Peripheral nervous system damage in experimental chronic Chagas' disease. 310 27

The aging-associated changes in hippocampal benzodiazepine (omega) receptor isotypes have been investigated in rats of the Wistar and Fischer 344 strains. Displacement experiments of [3H]flunitrazepam binding by zolpidem demonstrated that in hippocampal membranes from adult (3-month-old) Wistar strain rats, high (type I; omega 1)-, intermediate (type IIM; omega 2)-, and low (type IIL; omega 5)-affinity sites for this imidazopyridine account for 27.1 +/- 7.5, 44.2 +/- 7.5, and 28.8 +/- 5.1%, respectively. In hippocampal membranes from aged (24-month-old) rats of the same strain, the relative abundance of these sites was 42.8 +/- 9.3, 26.3 +/- 4, and 36.0 +/- 5.9%, respectively. In contrast, no significant difference was observed in the whole benzodiazepine (omega) binding site density between adult and aged rats. The increase in type I (omega 1) binding site density in the hippocampus of aged rats was also demonstrated in saturation experiments with [3H]zolpidem. This aging-induced increase in [3H]zolpidem binding was also observed in hippocampal membranes from Fischer 344 rats. Moreover, in both rat strains, GABA induced a greater enhancement of [3H]zolpidem (5 nM) binding to type I (omega 1) sites (GABA shift) in aged than in adult hippocampal membranes. Quantitative autoradiographic analysis of [3H]zolpidem binding to coronal brain sections from adult and aged Fischer 344 rats demonstrated that the aging-associated increases in the density of type I (omega 1) binding sites were restricted to the hippocampus. Moreover, increases in binding density were larger in the dentate gyrus and in the CA2 field than in the CA1 and CA3 fields.
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PMID:Aging-associated changes in the pharmacological properties of the benzodiazepine (omega) receptor isotypes in the rat hippocampus. 783 81

Weanling C3H/HeN mice were fed either a torula yeast-based diet deficient in selenium (Se) or the same diet supplemented with 0.2 ppm Se as sodium selenite. After 4 wk of feeding, the mice were inoculated intraperitoneally with the CA-I strain (clone K98) of Trypanosoma cruzi (TC). Before inoculation, mean serum Se levels were 430 versus 61 ng/ml in adequate and deficient mice, respectively. During the ascending phase of parasitemia, the Se-deficient mice exhibited significantly higher levels of parasites at 22-34 days postinfection (PI). However, no difference was found in the subsequent descending phase. As judged by visual examination at 2-mo-PI, some Se-deficient infected mice presented clinical signs of motor dysfunction. At 3-mo-PI, the end of the observation period, this chronic disease developed into a hind limb flaccid paralysis affecting 5 of 8 infected deficient mice. No signs of paralysis were seen in noninfected mice fed either diet or in infected mice fed the Se-adequate diet. At the histological level, both Se-adequate and Se-deficient infected mice showed mild myocarditis and moderate to severe myositis, with increasing intensity from 1- to 3-mo-PI in both groups. However, the severity of myositis was always more intense in the Se-deficient mice so that prominent areas of skeletal muscle replaced by fibrotic tissue were frequently observed. Thus, it can be concluded that Se deficiency in the murine host increases the severity of TC-induced myositis.
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PMID:Host selenium deficiency increases the severity of chronic inflammatory myopathy in Trypanosoma cruzi-inoculated mice. 1209 23