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1.
FASEB J ; 22(11): 3888-95, 2008 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-18711027

RESUMO

This pilot study examines noninvasive MR monitoring of tissue-engineered vascular grafts (TEVGs) in vivo using cells labeled with iron oxide nanoparticles. Human aortic smooth muscle cells (hASMCs) were labeled with ultrasmall superparamagnetic iron oxide (USPIO) nanoparticles. The labeled hASMCs, along with human aortic endothelial cells, were incorporated into eight TEVGs and were then surgically implanted as aortic interposition grafts in a C.B-17 SCID/bg mouse host. USPIO-labeled hASMCs persisted in the grafts throughout a 3 wk observation period and allowed noninvasive MR imaging of the human TEVGs for real-time, serial monitoring of hASMC retention. This study demonstrates the feasibility of applying noninvasive imaging techniques for evaluation of in vivo TEVG performance.


Assuntos
Aorta/citologia , Prótese Vascular , Meios de Contraste/farmacologia , Ferro/farmacologia , Angiografia por Ressonância Magnética/métodos , Músculo Liso Vascular/citologia , Miócitos de Músculo Liso/citologia , Nanopartículas , Óxidos/farmacologia , Engenharia Tecidual/métodos , Animais , Dextranos , Óxido Ferroso-Férrico , Humanos , Nanopartículas de Magnetita , Camundongos , Camundongos SCID
2.
Med Pediatr Oncol ; 35(6): 526-30, 2000 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-11107108

RESUMO

BACKGROUND: Hereditary predisposition to develop neuroblastoma segregates as an autosomal dominant Mendelian trait. PROCEDURE: We have performed linkage analysis on 10 families with neuroblastoma to localize a hereditary neuroblastoma predisposition gene (HNB1). RESULTS: A single genomic interval at chromosome bands 16p12-p13 was consistent with linkage (lod = 3.46), and identification of informative recombinants defined a 25.9-cM critical region between D16S748 and D16S3068. Loss of heterozygosity was identified in 5/12 familial (42%) and 55/259 nonfamilial (21%) neuroblastomas at multiple 16p polymorphic loci. A 12.8-cM smallest region of overlap of deletions was identified within the interval defined by linkage analysis (tel-D16S764-D16S412-cen). CONCLUSIONS: Taken together, these data suggest that HNB1 is located at 16p12-p13 and that inactivation of this gene may contribute to the pathogenesis of nonfamilial neuroblastomas.


Assuntos
Deleção Cromossômica , Mapeamento Cromossômico , Cromossomos Humanos Par 16/genética , Predisposição Genética para Doença/genética , Neuroblastoma/genética , Criança , Ligação Genética , Humanos , Perda de Heterozigosidade , Linhagem
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