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Posterior quadrantic disconnection maintains the activity of isolated temporal-parietal-occipital nerve tissue: neuroprotective measures in the surgical treatment of epilepsy 被引量:4
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作者 Shaoya Yin Keke Feng +2 位作者 Mei Feng Xueqing Zhang Yuqin Zhang 《Neural Regeneration Research》 SCIE CAS CSCD 2014年第4期447-448,共2页
Extensive lesions involving the posterior quadrant of the cerebral hemisphere (temporal, parietal, and occipital lobes) induce intractable epilepsy. These patients are potential candidates for surgical treatmenttu. ... Extensive lesions involving the posterior quadrant of the cerebral hemisphere (temporal, parietal, and occipital lobes) induce intractable epilepsy. These patients are potential candidates for surgical treatmenttu. Maintenance of isolated nerve tissue activity after surgery plays a crucial role in the neuroprotective effects of neurosurgery treatment. Disconnection surgery of the posterior quadrant is used to completely isolate nerve fibers, while blood supply at the isolated lobes is maintained. Subsequently, cavities caused by cystic or necrotic nerve tissues should be reduced as much as possible, 展开更多
关键词 MRI Posterior quadrantic disconnection maintains the activity of isolated temporal-parietal-occipital nerve tissue neuroprotective measures in the surgical treatment of epilepsy EEG Figure
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Pretreatment with low-frequency repetitive transcranial magnetic stimulation may influence neuronal Bcl-2 and Fas protein expression in the CA1 region of the hippocampus: A possible anti-epilepsy mechanism in a lithium-pilocarpine-induced epileptic rat mod 被引量:2
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作者 Sha Ke Hongning Zhao +6 位作者 Xiaoming Wang Junqiang Zhang Fang Chen Yuanxu Wang Xiaoqiong Zhao Hui Huang Jianxiu Hu 《Neural Regeneration Research》 SCIE CAS CSCD 2010年第12期895-900,共6页
BAOKGROUND: Bcl-2 and Fas proteins are well known as anti-apoptotic and pro-apoptotic factors respectively. However, whether the anti-epileptic mechanism of low-frequency repetitive transcranial magnetic stimulation ... BAOKGROUND: Bcl-2 and Fas proteins are well known as anti-apoptotic and pro-apoptotic factors respectively. However, whether the anti-epileptic mechanism of low-frequency repetitive transcranial magnetic stimulation (rTMS) involves an anti-apoptotic effect via regulating Bcl-2 and Fas protein expression remains to be determined. OBJECTIVE: To verify the correlation between the anti-epileptic mechanism following pretreatment of low-frequency rTMS and anti-hippocampal apoptosis. DESIGN, TIME AND SETTING: A randomized controlled animal experiment was performed at Institute of Neurological Disorders, Affiliated Hospital of North Sichuan Medical College between September 2007 and March 2008. MATERIALS: Pilocarpine (053K13011) was provided by Sigma, USA; lithium was provided by Shanghai Biotechnology Co., Ltd., China; Dantec Maglite-r25 rTMS instrument was provided by Dundee, Denmark. METHODS: A total of 21 adult male Wistar rats were randomly divided into control (n = 6), rTMS pretreatment (n = 9), and sham-stimulation (n = 6) groups. The rTMS pretreatment group was pretreated with low-frequency rTMS (0.5 Hz, 75% threshold intensity, 20 times/bundle, and 5 bundles/day), while the sham-stimulation group was sham-stimulated with a similar sound for 7 successive days to establish lithium-pilocarpine-induced epileptic state models. MAIN OUTCOME MEASURES: Epileptic stroke latency; neuronal morphology was observed using hematoxylin and eosin staining; mean positive-reactive cell number and mean absorbance of Bcl-2 and Fas protein in the hippocampal CA1 region was observed using immunohistochemistry. RESULTS: Epileptic latency in the rTMS pretreatment group was significantly enhanced (P 〈 0.01), and a number of degenerated neurons were observed to be apoptotic. Bcl-2 protein expression increased at each time point, but Fas protein expression decreased (P 〈 0.01). CONCLUSION: Low-frequency rTMS has an anti-epileptic effect, which may be via regulation of Bcl-2 and Fas protein expression in the hippocampal region. 展开更多
关键词 transcranial magnetic stimulation epileptic state Bcl-2 protein Fas protein brain injury neural regeneration
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