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Objective To explore the intracranial distribution of bone marrow-derived mesenchymal stem cells (BMSCs) and the ability of BMSCs shifting to glioma tissue.Methods We isolated BMSCs from the rats and constructed a BMSCsRL model that can stably express Renilla luciferase (RL).And 9L glioma cells marked with PKH26 were implanted into the brain parenchyma of Fischer rat using stereotactic surgery;7 d after that, the BMSCsRL was implanted into the contralateral brain parenchyma.The intracranial distribution of BMSCsRL was detected by using Xenogen bioluminescance imaging (BLI);at the same time,the migration of BMSCsRL into the glioma tissue was observed using Transwell plates.Results Phenotypical properties of the isolated BMSCs were CD90 and CD44 positive.BMSCs could be targeted to glioma tissue.In vivo BLI showed that the BMSCs shifted to the glioma tissue 0,7 and 14 d after transplantation and the junction area between tumor tissue and normal tissue was much more obvious than the other areas.Conclusion These results confirm the migratory capability of BMSCs over considerable distances, suggesting that BMSCs can be used as a delivery vehicle for targeted therapy of glioma.
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Objective To obtain eukaryotic expression vectors containing coding region of nephroblastoma over-expression gene (NOV) and detect its expression in dermal multipotent stem cells(DMSCs). Methods A 1 178 bp cDNA fragment was amplified from the total RNA of normal rat brain tissue by RT-PCR and cloned into eukaryotic expression vector pEGFP-N1. The cloned insert was identified by double digestion of the recombinant plasmid with restriction enzymes Hind Ⅲ and BamH Ⅰ.The recombinant plasmid was transfected into DMSCs with liposome. The expression of NOV gene was detected by RT-PCR. Results Eukaryotic expression vectors containing 1 178-bp coding region of NOV gene were successfully constructed. DMSCs transfected with the recombinant plasmid expressed NOV gene. Conclusions That eukaryotic expression vector containing coding region of NOV gene is constructed and expressed in DMSCs can provide a strong molecular tool for the studies on the NOV gene and DMSCs.
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@#Alzheimer's disease (AD) is a common progressive degenerative disease of the central nervous system. It's also a main cause for dementia in presenium and senectitude. In the past few years, the discoveries in vitro expansion of neural stem cells (NSCs) indicate a new way for recovery and replacement of damaged neurons as well as reconstruction of the neural circuit, and offer a useful future therapy for AD. There are two main promising approaches in NSCs replacement therapy. They are endogenetic approach, inducing proliferation and differentiation of endogenetic NSCs, improving self-repair of central nervous system, and exogenous approach, ransplantation of exogenous tissue and promoting proliferation of endogenous NSCs. However, it may not become truth before the mechanism of NSCs' proliferation, migration, differentiation and it's integration with the host tissues to be elucidated.
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<p><b>OBJECTIVE</b>To identify the mutation of Cu/Zn superoxide dismutase(SOD1) gene in an amyotrophic lateral sclerosis (ALS) family with unique phenotype.</p><p><b>METHODS</b>Five exons of SOD1 gene were amplified by PCR. The differences of these products were analyzed by PCR-single strand conformation polymorphism and visualized by silver staining.</p><p><b>RESULTS</b>Abnormal bands were found in exons 2 and 5 of SOD1 gene in several familial members. DNA sequence analysis verified that a base pair insertion occurred in the codon area of exon 2 and in the intron area of exon 5. And the insertion mutation of exon 2 led to a frameshift mutation and premature stop. It is a new type of SOD1 mutation which may be associated with familial amyotrophic lateral sclerosis.</p><p><b>CONCLUSION</b>Insertion mutation of exon 2 may be responsible for the disease of an ALS family in Chongqing.</p>
Subject(s)
Adult , Humans , Amyotrophic Lateral Sclerosis , Genetics , Mutation , Polymorphism, Single-Stranded Conformational , Superoxide Dismutase , Genetics , Superoxide Dismutase-1ABSTRACT
Objective To study the pattern of activities of microglia, the patholgical changes of chronically hypoperfused brain of rats and the interrelationship between them. Methods Model of chronically hypoperfused brain was established in rat by the ligation of both common carotid arteries, and the histopathological changes of brain were observed with light microscope. The activity of microglia of the brain were also observed with immunohistochemistry method and the number of microglia was measured with image analyzer. Results Extensive activation of microglia was observed after chronic cerebral hypoperfusion and the activation was increased with the elapse of time of hypoperfusion. There were obvious pathological change in the brain after the chronic cerebral hypoperfusion, such as myelinic degeneration and formation of glial nodule in white matter. After treated with cyclosporin A, the number of microglia was obviously reduced, but the pathological change was evidently decreased. Conclusion The activation of microglia resulted from chronic cerebral hypoperfusion is relates to the pathological changes of the brain. However, cyclosporin A can decrease the pathological change and inhibit the activation of microglia.
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Objective To study the pattern of activities of microglia, the patholgical changes of chronically hypoperfused brain of rats and the interrelationship between them. Methods Model of chronically hypoperfused brain was established in rat by the ligation of both common carotid arteries, and the histopathological changes of brain were observed with light microscope. The activity of microglia of the brain were also observed with immunohistochemistry method and the number of microglia was measured with image analyzer. Results Extensive activation of microglia was observed after chronic cerebral hypoperfusion and the activation was increased with the elapse of time of hypoperfusion. There were obvious pathological change in the brain after the chronic cerebral hypoperfusion, such as myelinic degeneration and formation of glial nodule in white matter. After treated with cyclosporin A, the number of microglia was obviously reduced, but the pathological change was evidently decreased. Conclusion The activation of microglia resulted from chronic cerebral hypoperfusion is relates to the pathological changes of the brain. However, cyclosporin A can decrease the pathological change and inhibit the activation of microglia.