ABSTRACT
UNLABELLED: Our aim is to search the differential expression genes of genetic epilepsy and establish the groundwork of exploring the pathogenesis of epilepsy on the gene level by using cDNA array technology. METHODS: Gene expression profiles of the cerebral cortex of genetic epilepsy-prone P77PMC rats and normal Wistar rats were established using the Atlas Rat cDNA Expression Array. The difference between gene expression profiles was analyzed using an image analysis instrument. RESULTS: Fifteen genes exhibited a differential expression pattern between the P77PMC rats' and Wistar rats' cerebral cortex, while there maybe many other differential expression genes undiscovered due to having no image analysis software. Among them, the levels of expression of 13 genes were elevated in P77PMC rats as compared to their levels in Wistar rats, in contrast, the levels of expression of two genes were decreased in P77PMC rats. CONCLUSION: There were several differential expression genes between P77PMC rats and Wistar rats. All these genes could play important roles in the pathogenesis of epilepsy.
Subject(s)
DNA, Complementary/genetics , Epilepsy/genetics , Gene Expression/genetics , Animals , Genetic Predisposition to Disease , RNA/genetics , Rats , Rats, Wistar , Reverse Transcriptase Polymerase Chain ReactionABSTRACT
Objective To evaluate the quality of life and influenced factors in epileptic adults. Methods 106 adults with epilepsy and 64 healthy people as control were studied and tested by using QOLIE-30.Results Compared with control group, QOL score was lower in epileptic group (54?16 vs 77?15). Worrying about the seizure attacks and side effect of antiepileptic medication, having memory problems, they are unsatisfied with their lives, in a blue mood, easy to be tired and their social activities are limited. Comparing the QOL of patients between different sexes, duration of seizure, AEDs taken and seizure frequency, it was found that their medication and seizure frequency play an important role. QOL was negatively associated with the number of the AEDs taken and their seizure frequency.Conclusion QOL was lower in epileptic adults. Medication and seizure frequency play an important role. Adequate medications to control the attack of seizures is a key to improve the quality of life in epileptic patients.
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Objective To detect the protein expression of chemotactic monocyte chemotactic protein 1 (MCP 1), macrophage inflammatory protein 1 alpha (MIP 1alpha) and regulated on activation normal T cell expression secretion (RANTES) in the affected muscle of simple polymyositis (SPM), and analysed the relationship between the amount of these proteins and the stage, severity of SPM.Methods Immuohistochemical LAB technique was used to detect the expression of these chemotactic factor protein in SPM affected muscle specimens.The expression levels of these chemotactic factors were determined by Image Analyzer system.Results The expressions of these chemotactic factors protein in SPM were showed in SPM. The expression levels of MCP 1 increased remarkably in the chronic SPM group and the severer one (P0 05).Conclusion MCP 1 not only could play an important role in the chronic SPM,but also related to the severity of the disease,it might be as an index on the development and deterioration of the di sease;MIP 1alpha might contribute to the continuous development of the disease. RANTES might embody its role as a ubiquitous response to inflammation during the onset of SPM.
ABSTRACT
Objective To explore the expression and its significance of growth-associated protein(GAP-43 ) and brain-derived neurotrophic factor (BDNK) receptor TrkB gene in rat hippocampus after epilepsy induced by pilocarpine (PILO). Methods In situ hybrid histochemical method was used to observe the changes of the expression of GAP-43 and TrkB mRNA in hippocampus after status epilepticus( SE) induced by PIOL. Results At 3 - 6h following the onset of status epilepticus(SE), TrkB mRNA expression was dramatically high than control groups in the dentate gyrus granule cell and CA3,CA1 pyramidal cell layers(P