Brain research
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Cerebral aneurysm (CA) rupture is a major cause of subarachnoid hemorrhage with high morbidity and mortality. Using an animal model, we examined the potential of endothelial colony-forming cells (ECFCs) transfusion on vascular degeneration after CA induction and underlying mechanisms. CA was induced in the right anterior cerebral artery-olfactory artery (ACA/OA) bifurcations in Sprague-Dawley rats with or without ECFCs transfusion. ⋯ ECFCs transfusion dramatically decreased VCAM-1 and NF-κB expression, increased eNOS expression and caused no change in MCP-1 expression, which was accompanied by reduced macrophages infiltration. Moreover, ECFCs transfusion reversed downregulation of Bcl-2 expression and upregulation of iNOS expression, and decreased SMCs apoptosis. Collectively, these findings suggest that ECFCs transfusion confers protection against degeneration of aneurysmal wall by inhibiting inflammatory cascades and SMCs apoptosis.
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Previous studies have demonstrated that the commonly used anesthetic ketamine can induce widespread neuroapoptosis in the neonatal brain and can cause persistent cognitive impairments as the animal matures. Therefore, searching for adjunctive neuroprotective strategies that inhibit ketamine-induced neuroapoptosis and persistent cognitive impairments is highly warranted. The primary goal of this study was to investigate the protective effect of 17β-estradiol against ketamine-induced neuroapoptosis and persistent cognitive impairments in adult rats. ⋯ Moreover, 17β-estradiol significantly reversed the learning and memory deficits observed at 60 days of age. In brief, our present data demonstrate that 17β-estradiol attenuates ketamine-induced neuroapoptosis and reverses long-term cognitive deficits in developing rats and thus may be a potential therapeutic and neuroprotective method for the treatment of neurodevelopmental disorders. This article is part of a Special Issue entitled SI: Brain and Memory.
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The aim of this study is to explore the white matter structure integrity in patients with mild traumatic brain injury (mTBI) using diffusion tensor imaging (DTI), and to analyze the relationship between the white matter structure integrity and cognitive impairment of patients with mTBI. Twenty-five patients with mTBI and 25 healthy control subjects were studied with conventional MR imaging and diffusion tensor imaging. Fractional anisotropy (FA) and mean diffusivity (MD) maps of patients with mTBI were calculated and compared, with these control maps using tract-based spatial statistics (TBSS). ⋯ There was a positive correlation between the FA value of the uncinate fasciculus and Mini Mental State Examination (MMSE) in the mTBI patient group (R(2)=0.36, P<0.05). TBSS analysis of DTI suggests that patients with mTBI have focal axonal injury, and the pathophysiology is significantly related to the MMSE and IQ of mTBI patients. Diffusion tensor imaging can be a powerful technique for in vivo detection of mTBI, and can help in the diagnosis of patients with mTBI.