Stem Cell Dynamics in an Experimental Model of Stroke / 전남의대학술지

We investigated the migration of endogenous neural stem cells (NSCs) toward an infarct lesion in a photo-thrombotic stroke model. The lesions produced by using rose bengal dye (20 mg/kg) with cold light in the motor cortex of Sprague-Dawley rats were also evaluated with sequential magnetic resonance imaging (MRI) from 30 minutes through 8 weeks. Migration of NSCs was identified by immunohistochemistry for nestin monoclonal antibody in the lesion cortex, subventricular zone (SVZ), and corpus callosum (CC). The contrast to noncontrast ratio (CNR) on MRI was greatest at 12 hours in DWI and decreased over time. By contrast, T1-weighted and T2-weighted images showed a constant CNR from the beginning through 8 weeks. MRI of the lesional cortex correlated with histopathologic findings, which could be divided into three stages: acute (edema and necrosis) within 24 hours, subacute (acute and chronic inflammatory cell infiltration) at 2 to 7 days, and chronic (gliofibrosis) at 2 to 4 weeks. The volume of the infarct was significantly reduced by reparative gliofibrosis. The number of nestin+ NSCs in the contralateral SVZ was similar to that of the ipsilateral SVZ in each group. However, the number of nestin+ NSCs in the ipsilateral cortex and CC increased at 12 hours to 3 days compared with the contralateral side (p<0.01) and was reduced significantly by 7 days (p<0.01). Active emigration of internal NSCs from the SVZ toward the infarct lesion may also contribute to decreased volume of the infarct lesion, but the self-repair mechanism by endogenous NSCs is insufficient to treat stroke causing extensive neuronal death. Further studies should be focused on amplification technologies of NSCs to enhance the collection of endogenous or transplanted NSCs for the treatment of stroke.

Stem Cell Dynamics in an Experimental Model of Stroke / 전남의대학술지

We investigated the migration of endogenous neural stem cells (NSCs) toward an infarct lesion in a photo-thrombotic stroke model. The lesions produced by using rose bengal dye (20 mg/kg) with cold light in the motor cortex of Sprague-Dawley rats were also evaluated with sequential magnetic resonance imaging (MRI) from 30 minutes through 8 weeks. Migration of NSCs was identified by immunohistochemistry for nestin monoclonal antibody in the lesion cortex, subventricular zone (SVZ), and corpus callosum (CC). The contrast to noncontrast ratio (CNR) on MRI was greatest at 12 hours in DWI and decreased over time. By contrast, T1-weighted and T2-weighted images showed a constant CNR from the beginning through 8 weeks. MRI of the lesional cortex correlated with histopathologic findings, which could be divided into three stages: acute (edema and necrosis) within 24 hours, subacute (acute and chronic inflammatory cell infiltration) at 2 to 7 days, and chronic (gliofibrosis) at 2 to 4 weeks. The volume of the infarct was significantly reduced by reparative gliofibrosis. The number of nestin+ NSCs in the contralateral SVZ was similar to that of the ipsilateral SVZ in each group. However, the number of nestin+ NSCs in the ipsilateral cortex and CC increased at 12 hours to 3 days compared with the contralateral side (p<0.01) and was reduced significantly by 7 days (p<0.01). Active emigration of internal NSCs from the SVZ toward the infarct lesion may also contribute to decreased volume of the infarct lesion, but the self-repair mechanism by endogenous NSCs is insufficient to treat stroke causing extensive neuronal death. Further studies should be focused on amplification technologies of NSCs to enhance the collection of endogenous or transplanted NSCs for the treatment of stroke.

C1772T polymorphism of hypoxia-inducible factor-1 alpha gene in Han ethnic population from Northern China / 浙江大学学报·医学版

<p><b>OBJECTIVE</b>To analyze the distribution of single nucleotide polymorphism C1772T (SNP/C1772T) in hypoxia-inducible factor -1 alpha (HIF-1 alpha) gene in Han ethnic population from Northern China.</p><p><b>METHODS</b>Allele frequencies in a sample of 206 healthy Chinese Hans were determined by polymerase chain reaction followed by restriction fragment length polymorphism.</p><p><b>RESULT</b>The genotype frequencies of C1772T observed in Chinese Hans were 93 % and 7% for CC and CT respectively; and allele frequencies were 96% and 4 %for C and T respectively. There was significant difference in distribution of allele frequencies between Chinese Hans and Caucasian.</p><p><b>CONCLUSION</b>The single nucleotide polymorphism of C1772T in HIF-1 alpha gene has difference in different ethnic population.</p>

Chronological Changes in Cerebral Infarction of Photochemical Thrombosis Model: Magnetic Resonance Imaging and Histopathological Correlation

OBJECTIVE: Authors investigated magnetic resonance imaging (MRI) and histological characteristics of photothrombotic infraction rat model (PIRM) on long term basis to provide a basis for further research. METHOD: Photothrombotic ischemia was induced in male Sprague-Dawley rats using Rose-bengal dye (20 mg/kg) and cold light. MRI was performed 1, 6, 12, 24 hours, 3, 7 days, 2, 3, 4, 6, and 8 weeks after photothrombosis and obtained T1- & T2-weighted and contrast-enhanced images. Also, T2* images were obtained after superparamagnetic iron oxide injection. After MRI, animals were sacrificed and the brain sections were stained for routine immunohistopathology. RESULTS: MRI and histological analysis revealed well induced lesion in the cortex and showed biological course of infarction. However, PIRM showed rapid development of infarction lacking collateral circulation. Infarction size reached maximum 12 hours after induction, progressively decreasing over 4 weeks. Interstitial and cytotoxic edema were evident at 6, 12, 24 hours, but decreasing afterwards. Neurogenic inflammation appeared on 3rd day and reached maximum on 5~7th day. Arachnoid membrane was characteristically invaded with inflammatory cells and later thickened with fibrosis. CONCLUSION: This study showed PIRM is ideal model to study subacute and chronic stages of cerebral infarction.