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

The aim of the study was to analyse in TEM the evolution of changes in structural elements of synaptic junctions of the cerebellar cortex in rats in valproate encephalopathy induced by chronic 12-month administration of sodium valproate - VPA (once daily intragastrically, in a dose of 200 mg/kg b.w.) and after withdrawal of this antiepileptic for 1 and 3 months. After 9 and 12 months of the experiment, synaptic endings of both the symmetrical and asymmetrical synapses in the neuropil of the cerebellar cortex, especially in the molecular layer, showed signs of severe damage (mainly swelling) and even disintegration. They were mostly observed in axodendritic endings and axospinal endings on the dendritic spines of Purkinje cells, being manifested in the presence of large vacuolar structures, electron lucent areas and swollen mitochondria within the cytoplasm. A reduced number of axonal synaptic vesicles (with more type F vesicles preserved) could be seen. One and 3 months after the end of chronic application of VPA, the synaptic junctions did not show morphological exponents of the repair processes. The alterations observed in the synapticjunctions of the cerebellar cortex may suggest disorders in neurotransmission processes, such as exhaustion and damage caused by ischaemia due to damage to the blood-brain barrier induced by VPA and/or its toxic metabolites.
 ...
PMID:Ultrastructure of synaptic junctions in the cerebellar cortex in experimental valproate encephalopathy and after terminating chronic application of the antiepileptic. 1223 Feb 60

1,2-dichloroethane(1,2-DCE) is toxic, especially by inhalation due to its high vapour pressure. Inhalation of concentrated 1,2-DCE vapor can induce effects on the human nervous system, even encephalopathy. However, 1,2-DCE toxic encephalopathy has seldom been reported, and no adequate data were available to evaluate the encephalopathy of 1,2-DCE in experimental animals. The aim of the present study was to establish a toxic experimental animal model induced by 1,2-DCE. Dose effect and time effect of 1,2-DCE on the nervous system were detected. The rats were treated by 1,2-DCE at various concentrations of 0, 2.5, 5.0, 10.0 g/m3 for 6 h and treatment of rats at 10.0 g/m3 for 0, 3, 6, and 12 h. Morphology of brain tissue was observed by HE staining and TEM under light and electron microscope, besides water contents in the cortex and medulla of rats were analyzed. The results indicated that 1,2-DCE induced abnormal histopathology, and significantly higher water content were confirmed in the cerebral cortex of toxic animal model in a dose- and time-dependent manner. To declare that 1,2-DCE could induce toxic encephalopathy with a pathological feature of cerebral edema is very important for the medical rescue in urgent toxic accidents.
 ...
PMID:Establishment of a poisoned animal model of toxic encephalopathy induced by 1,2-dichloroethane. 2132 70