Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085584 (encephalopathy)
 18,178 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Granule laden astrocytes exhibiting an affinity for chrome alum hematoxylin and aldehyde fuchsin (Gomori stains) have been described in the periventricular brain of all terrestrial vertebrate species examined to date including humans. The astrocytic inclusions are rich in sulfhydryl groups, emit an orange-red autofluorescence, and stain intensely with diaminobenzidine, a marker of endogenous peroxidase activity. The distinct autofluorescence pattern and the absence of neutral lipid, acid phosphatase, and beta-glucuronidase activity exclude lipofuscin or lysosomes as components of these astrocytic granules. The emission of orange-red autofluorescence and the nonenzymatic nature of the peroxidase activity implicate the presence of porphyrins and metalloporphyrins such as heme as major constituents of these cytoplasmic gliosomes. The role of Gomori-positive astrocytes under normal and pathologic conditions is incompletely understood. In vivo, numbers of astrocytic granules increase as a function of advancing age, in response to chronic estrogen stimulation, and following X-irradiation. In vitro, these cells accumulate with increasing time in culture and following exposure to the sulfhydryl agent, cysteamine. Gomori-positive astrocytes may supply heme to neurons for the synthesis of cytochromes, catalases, and other heme enzymes. They may play a role in photostimulation of sexual cyclicity, the promotion of neuritic development, the degradation of toxic lipoperoxides, and the metabolism of various neurotransmitters. Conversely, these cells may contribute to the pathogenesis of several neurologic and neuroendocrine disorders. Examples of the latter include a) augmentation of goldthioglucose neurotoxicity, b) induction of hypothalamic anovulation and reproductive failure, c) exacerbation of porphyric encephalopathy, and d) potentiation of parkinsonism and other free radical-related neurodegenerations.
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PMID:Gomori-positive astrocytes: biological properties and implications for neurologic and neuroendocrine disorders. 171 59

We isolated brain microglia from newborn rabbits and maintained these cells in in vitro culture. Enriched populations of rabbit microglia share several characteristics of mononuclear phagocytes including intracellular staining for nonspecific esterase and acid phosphatase. Microglia express Fc receptors, generate superoxide anion, and stain positive with the lectin Ricinus communis. Rabbit brain microglia develop multinucleated giant cells and small colonies in in vitro culture. The cells are highly phagocytic in culture. Other investigators have recently demonstrated that rabbits can be infected with HIV-1 in vivo and that neurological symptoms occur only when HIV-1 infection was carried out in HTLV-1-infected rabbits. Brain microglia most likely play a central role in HIV-1 encephalopathy. The availability of rabbit brain microglia in in vitro culture, offers a valuable potential cell model to study HIV-1 infection in the central nervous system.
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PMID:Isolation and characterization of newborn rabbit brain-derived microglia. 202 95

Brains from AIDS patients with an HIV-induced encephalopathy but without opportunistic infections or indications for an inflammation were studied by immuno- and enzyme-histochemical methods. It was found that the macrophages of these brains expressed a lysosomal tartrate-resistant acid phosphatase which gave a good immunological cross-reaction with an antibody to the well-characterized iron-containing bovine spleen purple acid phosphatase, belonging to the group of purple phosphatases, which are regarded as a marker for a special phenotype of activated macrophages. It was discussed that the numerous brain macrophages found in AIDS encephalopathy derive from latently infected monocytes which are believed to be drawn to the brain from the bloodstream.
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PMID:Purple acid phosphatase of human brain macrophages in AIDS encephalopathy. 279 17

The rate of perinatal encephalopathy and the nature of its outcomes in relation to the syndrome of the acute period of the disease were studied in 102 children. Also examined were the cytochemical parameters of blood leukocytes, alkaline phosphatase of neutrophils, acid phosphatase of lymphocytes, succinate and alpha-glycerophosphate dehydrogenase of lymphocytes in prematurely born infants on the 8th-15th and the 30th-45th days of life. It has been ascertained that in addition to the comatose and convulsive syndromes the prognosis of the disease is the least favourable in the syndrome of total inhibition of the CNS in the acute period. Furthermore, the findings of the conducted study open the possibility of preliminary individual prognosis of the disease on the basis of the cytochemical picture at the end of the acute period.
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PMID:[Development of children with a history of perinatal encephalopathy]. 342 43

Oral administration of manganese chloride (25 mg/kg b. w. daily) to monkeys for a period of 18 months produced congestion and marked increase in weight of testis. Histopathologic examination revealed interstitial oedema and degeneration of seminiferous tubules. Activities of succinic dehydrogenase, glucose-6-phosphate dehydrogenase and acid phosphatase were significantly inhibited whereas NADH-diaphorase and alkaline phosphatase activities showed only slight inhibition in seminiferous tubules of treated monkeys. It was concluded that chronic exposure to manganese does not produce sever degenerative changes in the testis earlier than metal induced encephalopathy in primates.
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PMID:Manganese induced testicular changes in monkeys. 624 33

Encephalopathy was induced in 14-day-old chicks by a vitamin E-deficient diet containing 15% thermally oxidized safflower oil. Bound acid phosphatase activity in the cerebellum was markedly lower in affected chicks than in vitamin E-supplied control chicks. Free activity also tended to be lower in the deficient group. There were no differences in enzyme activities of cerebrum and liver between deficient and control chicks.
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PMID:Lysosomal acid phosphatase decrease in nutritional encephalopathy in chicks. 744 96

Diabetic encephalopathy is a type of central diabetic neuropathy resulting from diabetes mainly manifested as cognitive impairments. However, its underlying pathogenesis and effective treatment strategies remain unclear. In the present study, we investigated the effect of Lipin1, a phosphatidic acid phosphatase enzyme, on the pathogenesis of diabetic encephalopathy. We found that in vitro, Lipin1 exerts protective effects on high glucose-induced reductions of PC12 cell viability, while in vivo, Lipin1 is downregulated within the CA1 hippocampal region in a type I diabetes rat model. Increased levels of Lipin1 within the CA1 region are accompanied with protective effects including amelioration of dendritic spine and synaptic deficiencies, phosphorylation of the synaptic plasticity-related proteins, LIM kinase 1 (p-limk1) and cofilin, as well as increases in the synthesis of diacylglycerol (DAG), and the expression of phosphorylated protein kinase D (p-PKD). These effects are associated with the rescue of cognitive disorders as shown in this rat model of diabetes. In contrast, knockdown of Lipin1 within the CA1 region enhanced neuronal abnormalities and the genesis of cognitive impairment in rats. These results suggest that Lipin1 may exert neuroprotective effects involving the PKD/Limk/Cofilin signaling pathway and may serve as a potential therapeutic target for diabetic encephalopathy.
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PMID:Lipin1 Is Involved in the Pathogenesis of Diabetic Encephalopathy through the PKD/Limk/Cofilin Signaling Pathway. 3312 8