AIM:To investigate the expression patterns of D-serine and N-methyl-D-aspartate (NMDA) receptor 1 in the temporal lobes of patients with intractable epilepsy.
MATERIAL and METHODS:Cortical temporal lobe brain tissue samples were collected from 20 patients with intractable epilepsy and 6 patients with brain trauma. The expression patterns of D-serine and NMDA receptor 1 were detected by immunofluorescence staining and western blot analysis.
RESULTS:A total of 20 patients (11 males, 9 females) were included in the present study. D-serine expression was significantly higher in the neurons and glial cells of patients with intractable epilepsy than in control individuals. The mean integrated optical density (IOD) value for the intractable epilepsy group (13.37 ± 1.88) was significantly higher than that for the control group (9.27 ± 0.62, p<0.05). The mean absorbance value of the NMDA receptor 1 protein strip obtained from intractable epileptic patients was 0.4175 ± 0.2321, which was significantly higher than the value of 0.2402 ± 0.1458 for the control group (p<0.05).CONCLUSION: D-serine and NMDA receptor 1 expressions increased significantly in patients with intractable epilepsy compared with control patients. Therefore, the D-serine signaling pathway may represent a potential neurochemical target for epilepsy treatment.
In an adult patient with RE, a favorable prognosis was achieved after functional hemispherectomy. The safety and efficacy of functional hemispherectomy in patients with RE is highlighted.
Abstract. Increasing evidence suggests that microRNAs are involved in human carcinogenesis as tumor suppressors or oncogenes. A growing number of reports has shown that an interest has been sparked in aberrant microRNA expression and how they can be used to treat human diseases, including cancer. However, their precise biological role remains largely unknown. In the present study, we aimed to identify micro-RNA species involved in the regulation of tumor growth. By performing quantitative reverse transcription-polymerase chain reaction (RT-PCR) analysis, we demonstrated that mir-663 was downregulated in human gastric cancer cell lines unlike in normal cells. A transient introduction of mir-663 into the human gastric cancer cell lines BGC823 and SNU5 induced morphology changes and suppression of proliferation of these cells. In addition, mir-663 alters the DNA content and induces phenotypes of mitotic catastrophe in tumor cells. Moreover, the liposome-mediated delivery of mir-663 suppressed the in vivo growth of the BGC823 and SNU5 cells. Western blot analyses performed after the introduction of mir-663 revealed upregulation of cyclin B following transfection with mir-663. Our results provide evidence that downregulation of mir-663 in tumor cells may contribute to aberrant cell hyperplasia, leading to the development of gastric cancer. Therefore, mir-663 might function as a potent suppressor of tumor growth.
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