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    15 October 2013, Volume 8 Issue 29 Previous Issue    Next Issue
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    Expression of synaptosomal-associated protein-25 in the rat brain after subarachnoid hemorrhage
    Gang Chen, Tong Hu, Qi Li, Jianke Li, Yang Jia, Zhong Wang
    2013, 8 (29):  2693-2702.  doi: 10.3969/j.issn.1673-5374.2013.29.001
    Abstract ( 242 )   PDF (567KB) ( 1330 )   Save

    Synaptosomal-associated protein-25 is an important factor for synaptic functions and cognition. In this study, subarachnoid hemorrhage models with spatial learning disorder were established through a blood injection into the chiasmatic cistern. Immunohistochemical staining and western blot analysis results showed that synaptosomal-associated protein-25 expression in the temporal lobe, hippocampus, and cerebellum significantly lower at days 1 and 3 following subarachnoid hemorrhage. Our findings indicate that synaptosomal-associated protein-25 expression was down-regulated in the rat brain after subarachnoid hemorrhage.

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    Why do stroke patients with negative motor evoked potential show poor limb motor function recovery?
    Zhibin Song, Lijuan Dang, Yanling Zhou, Yanjiang Dong, Haimao Liang, Zhengfeng Zhu, Suyue Pan
    2013, 8 (29):  2713-2724.  doi: 10.3969/j.issn.1673-5374.2013.29.003
    Abstract ( 240 )   PDF (324KB) ( 1249 )   Save

    Negative motor evoked potentials after cerebral infarction, indicative of poor recovery of limb motor function, tend to be accompanied by changes in fractional anisotropy values and the cerebral pe-duncle area on the affected side, but the characteristics of these changes have not been reported. This study included 57 cases of cerebral infarction whose motor evoked potentials were tested in the 24 hours after the first inspection for diffusion tensor imaging, in which 29 cases were in the negative group and 28 cases in the positive group. Twenty-nine patients with negative motor evoked potentials were divided into two groups according to fractional anisotropy on the affected side of the cerebral peduncle: a fractional anisotropy < 0.36 group and a fractional anisotropy ≥ 0.36 group. All patients underwent a regular magnetic resonance imaging and a diffusion tensor imaging examina-tion at 1 week, 1, 3, 6 and 12 months after cerebral infarction. The Fugl-Meyer scores of their hemiplegic limbs were tested before the magnetic resonance and diffusion tensor imaging exami-nations. In the negative motor evoked potential group, fractional anisotropy in the affected cerebral peduncle declined progressively, which was most obvious in the first 1–3 months after the onset of cerebral infarction. The areas and area asymmetries of the cerebral peduncle on the affected side were significantly decreased at 6 and 12 months after onset. At 12 months after onset, the area asymmetries of the cerebral peduncle on the affected side were lower than the normal lower limit value of 0.83. Fugl-Meyer scores in the fractional anisotropy ≥ 0.36 group were significantly higher than in the fractional anisotropy < 0.36 group at 3–12 months after onset. The fractional anisotropy of the cerebral peduncle in the positive motor evoked potential group decreased in the first 1 month after onset, and stayed unchanged from 3–12 months; there was no change in the area of the cer-ebral peduncle in the first 1–12 months after cerebral infarction. These findings confirmed that if the fractional anisotropy of the cerebral peduncle on the affected side is < 0.36 and the area asymme-tries < 0.83 in patients with negative motor evoked potential after cerebral infarction, then poor hemiplegic limb motor function recovery may occur.

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    Downregulation of caveolin-1 contributes to the synaptic plasticity deficit in the hippocampus of aged rats
    Yang Liu, Zhanhua Liang, Jing Liu, Wei Zou, Xiaoyan Li, Yachen Wang, Lijia An
    2013, 8 (29):  2725-2733.  doi: 10.3969/j.issn.1673-5374.2013.29.004
    Abstract ( 236 )   PDF (421KB) ( 1649 )   Save

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    Global view of transcriptome in the brains of aged NR2B transgenic mice
    Chunxia Li, Men Su, Huimin Wang, Yinghe Hu
    2013, 8 (29):  2734-2743.  doi: 10.3969/j.issn.1673-5374.2013.29.005
    Abstract ( 286 )   PDF (332KB) ( 1758 )   Save

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    Toll-like receptor 4-mediated signaling participates in apoptosis of hippocampal neurons
    Yue He, Ailing Zhou, Wei Jiang
    2013, 8 (29):  2744-2753.  doi: 10.3969/j.issn.1673-5374.2013.29.006
    Abstract ( 317 )   PDF (495KB) ( 1441 )   Save

    The phosphatidylinositol 3 kinase (PI3K)/protein kinase B (AKT) signaling pathway is considered important for cell survival and has been shown to mediate various anti-apoptotic biological effects. This study explored the role of the Toll-like receptor 4 (TLR4)-mediated PI3K/AKT-glycogen syn-thase kinase 3β (GSK-3β) signaling pathways in lipopolysaccharide-induced apoptosis in a primary culture of hippocampal neurons. Results demonstrated that the apoptotic ratio of hippocampal neurons stimulated by lipopolysaccharide was significantly higher compared with the control group. Both the expression of P-AKTSer473 and P-GSK-3βSer9 in hippocampal neurons stimulated by lipo-polysaccharide decreased compared with the control, while the level of active Caspase-3 and the ratio of Bax/Bcl-2 were significantly increased. The level of active Caspase-3 and the ratio of Bax/Bcl-2 in hippocampal neurons treated with TLR4 antibody or the GSK-3β inhibitor, LiCl, de-creased before intervention with lipopolysaccharide, but increased after treatment with the AKT in-hibitor, LY294002. These findings suggest that the TLR4-PI3K/AKT-GSK3β signaling pathway may be involved in lipopolysaccharide-induced apoptosis of hippocampal neurons.

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    Optimal dose of zinc supplementation for preventing aluminum-induced neurotoxicity in rats
    Hao Lu, Jianyang Hu, Jing Li, Wei Pang, Yandan Hu, Hongpeng Yang, Wenjie Li, Chengyu Huang, Mingman Zhang, Yugang Jiang
    2013, 8 (29):  2754-2762.  doi: 10.3969/j.issn.1673-5374.2013.29.007
    Abstract ( 163 )   PDF (245KB) ( 1809 )   Save

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    Development of the sexually dimorphic nucleus of the preoptic area and the influence of estrogen-like compounds
    Zhen He, Sherry Ann Ferguson, Li Cui, Lazar John Greenfield, Merle Gale Paule
    2013, 8 (29):  2763-2774.  doi: 10.3969/j.issn.1673-5374.2013.29.008
    Abstract ( 261 )   PDF (582KB) ( 1605 )   Save

    One of the well-defined sexually dimorphic structures in the brain is the sexually dimorphic nucleus, a cluster of cells located in the preoptic area of the hypothalamus. The rodent sexually dimorphic nucleus of the preoptic area can be delineated histologically using conventional Nissl staining or immunohistochemically using calbindin D28K immunoreactivity. There is increasing use of the calbindin D28K-delineated neural cluster to define the sexually dimorphic nucleus of the preoptic area in rodents. Several mechanisms are proposed to underlie the processes that contribute to the sexual dimorphism (size difference) of the sexually dimorphic nucleus of the preoptic area. Recent evidence indicates that stem cell activity, including proliferation and migration presumably from the 3rd ventricle stem cell niche, may play a critical role in the postnatal development of the sexually dimorphic nucleus of the preoptic area and its distinguishing sexually dimorphic feature: a signifi-cantly larger volume in males. Sex hormones and estrogen-like compounds can affect the size of the sexually dimorphic nucleus of the preoptic area. Despite considerable research, it remains un-clear whether estrogen-like compounds and/or sex hormones increase size of the sexually dimor-phic nucleus of the preoptic area via an increase in stem cell activity originating from the 3rd ventricle stem cell niche.

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    Treatment of malignant glioma using hyperthermia
    Jiahang Sun, Mian Guo, Hengyuan Pang, Jingtao Qi, Jinwei Zhang, Yunlong Ge
    2013, 8 (29):  2775-2782.  doi: 10.3969/j.issn.1673-5374.2013.29.009
    Abstract ( 243 )   PDF (284KB) ( 1265 )   Save

    Thirty pathologically diagnosed patients with grade III–IV primary or recurrent malignant glioma (tumor diameter 3–7 cm) were randomly divided into two groups. The control group underwent conventional radiotherapy and chemotherapy. In the hyperthermia group, primary cases received hyperthermia treatment, and patients with recurrent tumors were treated with hyperthermia in com-bination with radiotherapy and chemotherapy. Hyperthermia treatment was administered using a 13.56-MHz radio frequency hyperthermia device. Electrodes were inserted into the tumor with the aid of a CT-guided stereotactic apparatus and heat was applied for 1 hour. During 3 months after hyperthermia, patients were evaluated with head CT or MRI every month. Gliomas in the hyper-thermia group exhibited growth retardation or growth termination. Necrosis was evident in 80% of the heated tumor tissue and there was a decrease in tumor diameter. Our findings indicate that ra-dio frequency hyperthermia has a beneficial effect in the treatment of malignant glioma.

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