Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0013911 (emaciation)
 1,059 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hydrocephalus is known to produce progressive mental deterioration and other peculiar neurological symptoms and signs, such as gait disturbance, pyramidal and extrapyramidal signs and urinary incontinence. Alteration of energy metabolism in various cerebral regions in association with hydrocephalus, however, has not been fully understood. The quantitative carbon 14 deoxyglucose autoradiographic method was employed in kaolin induced hydrocephalus of rats. The hydrocephalic rats developed marked emaciation with normal physiological parameters. They showed reduced motor activity and muscle tone and sluggish reflexes. The animals remained conscious and displayed no seizure activity. The rates of local cerebral glucose utilization in the cortical areas and the thalamus were significantly lower than those of the control animals. In the limbic system, the hypothalamus, and basal ganglia, the values showed considerable variation, however, the degrees of reduction were relatively mild. The values in the brain stem were either lower or higher than those of the control animals. The lower values were seen in the sensory system and higher values in the nucleus raphe and locus ceruleus. Decrease of the glucose utilization rate in the cerebellum was moderate and uniform in all the cerebellar structures. Reductions of the metabolic rates in the white matter structures were relatively uniform throughout the brain.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Cerebral glucose metabolism studied with (14C)-deoxyglucose method in experimental hydrocephalus]. 662 86

Mice with the Otx2+/- mutation often die during the postneonatal period. Before death these animals, generated from TT2 ES cells and crossed with CBA mice, develop a dome-shaped head, weakness of the limbs, kyphosis, lethargy, drowsiness, and emaciation. Autopsy of these mice revealed eminent dilatation of lateral ventricles and a ballooned cerebrum. Histological analysis shows edematous change of the periventricular white matter. These results suggest that Otx2 functions as a head organizer, and a mutation of this gene is a likely cause of hydrocephalus in mammals. Additionally, craniobasal skeletal anomaly in half of the heterozygotes and dwarfism in some of the female heterozygotes are described.
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PMID:Hydrocephalus in the Otx2+/- mutant mouse. 939 63

The developmental toxicity of purified fumonisin B1 (FB1), a mycotoxin from the common corn fungus Fusarium moniliforme, was examined in Charles River rats. Pregnant rats were dosed orally on gestation days 3-16 at 0, 6.25, 12.5, 25 or 50 mg FB1/kg body weight/day. FB1 was not teratogenic at the doses tested. At 50 mg/kg, maternal toxicity (inappetence, emaciation, lethargy, death, resorption of entire litters) and foetal toxicity (increased number of late deaths, decreased foetal body weight, decreased crown rump length, increased incidence of hydrocephalus, increased incidence of skeletal anomalies) were seen. The foetal toxicity observed at 50 mg/kg may be related to maternal toxicity. Histopathological evaluation of tissues from dams of control and all treated groups revealed dose-related toxic changes in kidney and liver tissues. Acute toxic tubular nephrosis was seen in kidneys from all treated groups. Hepatocellular cytoplasmic alteration and individual cellular necrosis of the liver was seen in the two high-dose groups. Sphinganine (Sa) and sphingosine (So) were measured in day-17 adult and foetal tissues. Dose related increases in Sa/So ratios were seen in maternal liver, kidney, serum and brain, but there was no effect on foetal liver, kidney and brain. These data suggest that FB1 does not cross the placenta and further suggest that the observed foetal toxicity is a secondary response to maternal toxicity.
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PMID:Effects of fumonisin B1 in pregnant rats. Part 2. 973 18

Five cases of xanthomatosis in geckos were evaluated, one in a northern green gecko (Naultinus grayi) and the remaining four in three species of leaf-tailed geckos (two Uroplatus henkeli, one U. sikorae, one U. fimbriatus). All geckos were females 3-11 yr of age, were clinically ill on presentation, and either died or were euthanized. Necropsies showed emaciation in three geckos, with white nodular foci on coelomic surfaces in two of these geckos. The other two geckos had no gross abnormalities. Histopathologic examination revealed xanthomatosis involving the coelomic surfaces of four geckos and the ventricles of the brain in all geckos. Xanthomas in the brain were associated with various degrees of hydrocephalus. The lesions were comprised of stacks of clear clefts consistent with cholesterol crystals, and these structures were surrounded by epithelioid macrophages, multinucleated giant cells, and lymphocytes. Four geckos had active folliculogenesis, and two had foci of follicular degeneration and localized yolk coelomitis. In all cases, xanthomatosis was believed to have contributed significantly to morbidity and mortality.
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PMID:Xanthomatosis in geckos: five cases. 1057 73