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Objective To investigate the diagnostic value of plasma ,peripheral blood mononuclear cell (PB-MC) and throat swab EB virus (SBV) load in the patients with infectious mononucleosis (IM ) aged over 16 years old .Methods The detection results in 130 patients with suspected IM aged over 16 years old of 3 differ-ent samples of plasma ,peripheral blood mononuclear cell(PBMC) and throat swab EB virus(SBV) load were analyzed retrospectively .Results Among 61 cases of IM verified by clinic and laboratory ,16 cases of IM were detected by plasma sample ,the detection rate of EBV-DNA was 26 .22％ ;in 31 cases of PBMC detection ,the EBV-DNA detection rate was 61 .29％ ;in 31 cases of throat swab detection ,the EBV-DNA detection rate was 83 .78％ .The EBV-DNA detection rate of the combined detection with one indicator or multiple indicators positive of plasma ,PBMC and throat swab as the basis was 100 .00％ .Conclusion The combined detection of plasma ,PBMC and throat swab can improve the positive rate in the patients with IM aged over 16 years old , w hich can provide more bases for pathogenic diagnosis and treatment for clinic .
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Objective To investigate the expression of microRNA-134 ( miR-134 ) , CREB and pCREB in the temporal lobe tissue of patients and epileptic rats and to explore their roles in pathogenesis of epilepsy.Methods Tempo-ral lobe tissue samples of 14 patients with refractory epilepsy and 10 non-epileptic patients, and hippocampus and brain tis-sue samples of 42 rats were used in this study.Forty-two healthy adult male Sprague-Dawley rats were randomly divided in-to 6 epilepsy groups (24 h, 72 h, 7 d, 14 d, 30 d, and 60 d after kindling epilepsy) and a normal control group (n=6 for all groups) .The rat model of epilepsy was generated by intraperitoneal injection of 127 mg/kg lithium chloride and 16-20 h later, 35 mg/kg pilocarpine.In the temporal lobe tissue of patients and hippocampal tissue of rats, the expression level of miR-134 was detected by real-time polymerase chain reaction.The expression levels of CREB and pCREB were de-termined by Western blot, and CREB and pCREB localization was assessed by immunohistochemistry.Results Compared with the control rats, the expression of miR-134 was significantly decreased in the temporal lobe tissue of experimental rats at 72 h,7 d,14 d, 60 d after kindling (P＜0.05),and no significant change at 24 h and 30 d after kindling (P>0.05). Expression of miR-134 in patients with refractory epilepsy was significantly lower than that of the controls ( P＜0.05 ) , while up-regulation of CREB expression was at the same time points (P＜0.05).Up-regulation of pCREB expression was at all the time points after kindling (P＜0.05).CREB and p-CREB expressions were seen in the nuclei of neurons, and significantly higher in patients with refractory epilepsy and epileptic rats.Conclusions The expression of miR-134 is sig-nificantly decreased and that of CREB and pCREB was significantly increased in the temporal lobe tissue of patients with re-fractory epilepsy and the hippocampal tissue of epileptic rats.These findings indicate that the signaling pathway of miR-134/CREB/pCREB may play an important role in the pathogenesis of epilepsy.
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<p><b>OBJECTIVE</b>To investigate the expression and activity of silent information regulator 1 (SIRT1) in the temporal lobe of epileptic patients and rat models and explore its role in the occurrence and progression of epilepsy.</p><p><b>METHODS</b>The temporal lobe tissue of epileptic patients and rat models (induced by lithium-pilocarpine) were examined for SIRT1 expression using immunohistochemistry and Western blotting and also for SIRT1 activity using SIRT1 Deacetylase Assay Kit.</p><p><b>RESULTS</b>Immunohistochemistry detected positive SIRT1 expression mainly in the cytoplasm of the neurons in both human and rat brains, and the epileptic groups showed stronger SIRT1 immunoreactivity than the control group. Western blotting and activity assay showed that the expression and activity of SIRT1 were significantly increased in the temporal lobe of patients with refractory epilepsy as compared with the tissues samples from non-epileptic patients (P<0.05). In the rat models of epilepsy, SIRT1 expression was up-regulated at 6, 24, and 72 h and at 7, 14, 30, and 60 days after kindling (P<0.05) and SIRT1 activity was significantly increased at 6, 24, and 72 h and at 7 and 14 days (P<0.05), with the peak level of SIRT1 expression and activity occurring at 72 h.</p><p><b>CONCLUSION</b>Up-regulation of SIRT1 expression and activity in the temporal lobe of epileptic patients and rat models may play an important role in the pathogenesis of epilepsy.</p>
Subject(s)
Adolescent , Adult , Animals , Female , Humans , Male , Rats , Young Adult , Disease Models, Animal , Epilepsy , Metabolism , Rats, Sprague-Dawley , Sirtuin 1 , Metabolism , Temporal Lobe , MetabolismABSTRACT
Objective To explore the pathogenic mechanisms of intractable epilepsy by searching for the differential cell signal transduction associated genes expression in intractable and non intractable epilepsy rat brain using cDNA microarray Methods Intractable epilepsy and non intractable epilepsy rat model were build The total RNAs were isolated from the brain tissues Both mRNAs from the brains of the intractable and non intractable epilepsy rats were reversely transcribed to the cDNA with the incorporation of fluorescent dUTP to prepare the hybridization probes The PCR products of 4 096 human genes were spotted on a chemical material coated glass plates in array The mixed probes were then hybridized to the cDNA microarray After high stringent washing, the cDNA microarray was scanned for the fluorescent signals and showed differences between 2 tissues Results Among the 4 096 target genes, 29 genes associated with cell signal transduction differentially expressed were identified, 10 were up regulated(34 48%) and 19 down regulated(65 52%) Conclusion cDNA microarray technology is an effective technique in screening the differentially expressed genes between intractable and non intractable epilepsy rat brain Disturbances of cell signal transduction play a role in the pathogenic mechanism of intractable epilepsy