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婴幼儿血管瘤和血管畸形组织中一氧化氮合酶的表达及意义 被引量:2

The expression and significance of nitric oxide synthases in hemangiomas and vascular malformations in infants
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摘要 目的:研究婴幼儿血管瘤和血管畸形组织中一氧化氮合酶(NOS)的表达差异及其意义。方法:采用免疫组织化学方法及图像分析,检测49例血管瘤和29例血管畸形组织中NOS1、2、3蛋白的表达。分别采用秩和检验的Mann-Whitney test和Kruskal-Wallis test法,比较两组和多组等级变量间的差异;使用标准正态分布统计量Z、X2确定P值,或直接用精确概率法计算P值,P<0.05为有显著性差异。全部资料的统计分析均使用SPSS8.0统汁软件包完成。结果:49例血管瘤组织中,NOS1、2、3蛋白的阳性率为分别为2%、38.8%和38.8%;29例血管畸形组织中,NOS1、2、3蛋白的阳性率分别为0、3.5%和3.5%;血管瘤组织中NOS2、3蛋白的阳性表达率均明显高于血管畸形(P<0.001)。增生期血管瘤组,NOS2、NOS3蛋白的阳性率及消退期血管瘤组NOS3蛋白的阳性率均明显高于血管畸形组(P值分别为0.000、0.000和0.007)。年龄<13个月组和<13-24个月组,血管瘤的NOS2蛋白的阳性表达率均明显高于>24个月组(p分别为0.009和0.003)。结论:血管瘤与血管畸形中NOS蛋白的表达不同,提示两者在病理生理方面存在差异。 PURPOSE:To investigate the difference and significance of nitric oxide synthases (NOS) expression in hemangioma (HA) and vascular malformation (VM) in infants. METHODS:Immunohistochemical staining was used to detect the expression of NOS1,2,3 proteins in 49 cases of HA and 29 cases of VM. Mann-Whitney test and Kruskal Wallis test were used for comparing the differences.The data were analysed statistically with SPSS8.0 package. RESULTS: Positive rates of NOS 1,2,3 proteins in 49 cases of HA was 1%,38% and 38% respectively, in 29 cases of VM was 0%,3% and 3% respectively. The expressive rates of NOS2,3 proteins of HA was significantly higher than that of VM (P<0.001). The positive rates of NOS2,3 proteins in HA of proliferative phase was significantly higher than that in VM (P=0.000). The positive rate of NOS3 protein in HA of involuting phase was significantly higher than that in VM (P= 0.007). The positive rates of NOS2 protein in HA patients below 13 months and between 13 and 24 months was significantly higher than that in HA patients over 24 months (P=0.009 and 0.003). CONCLUSIONS: Expression of NOS in HA is different from that in VM, which indicates that there is pathophysical difference between HA and VM.
出处 《中国口腔颌面外科杂志》 CAS 2004年第3期169-172,共4页 China Journal of Oral and Maxillofacial Surgery
关键词 血管瘤 血管畸形 一氧化氮合酶 免疫组织化学 Hemangioma Vascular malformation Nitric oxide synthase Immunohistochemistry
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  • 1刘耕陶,中华医学杂志,1996年,76卷,563页
  • 2Gallo O, Masini E, Morbidelli L, et al. Role of nitric oxide in angiogenesis and tumor progression in head and neck cancer [J]. J Natl Cancer Inst, 1998,90(8):587-596.
  • 3Rosbe J, Kristina W, Petrusz P, et al. Immunohistochemical characterzation of nitric oxide synthase activity in squamous cell carcinoma of the head and neck [J]. Otolaryngology Head & Neck Surgery, 1995,113(5):541-549.
  • 4Thomsen LL, James MJ, Scott, et al. Selective inhibition of inducible nitric oxide synthase inhibits tumor growth in vivo:studies with 1400W, a novel inhibitor [J]. Cancer Res, 1997,57:3300-3304.
  • 5Chin K, Kurashima Y, Ogura T, et al. Induction of Vascular endothelial growth factor by nitric oxide in human glioblastoma and hepatocellular Carcinoma Cells [J]. Oncogene,1997,15:437-442.
  • 6Meyer RE, Shan S, DeAngelo J, et al. Nitric oxide synthase inhibition irreversibly decreases perfusion in the R3230Ac rat mammary adenocarcinoma [J]. Br J Cancer,1995,11:1169-1174.
  • 7Lejeune P, Lagadec P, Onier N, et al. Nitric oxide involvment in tumor-induced immunosuppression [J]. J Immunol, 1994,152:5077-5083.
  • 8Yagihashi N, Kasajima H, Sugai S, et al. Increased in situ expression of nitric oxide synthase in human coorectal cancer [J]. Virchows-Arch,2000,436(2):109-114.
  • 9Orucevic A,Bechberger J,Green AM,et al.Nitric-oxide production by murine mammary adenocarcinoma cell promotes tumor-cell invasiveness [J]. Int J Cancer, 1999,81:889-896.
  • 10董长宪,李恭才,张宪生,徐泉,高亚,苏宝山.碱性纤维母细胞生长因子在血管瘤及血管畸形中的表达[J].中华小儿外科杂志,1997,18(6):322-324. 被引量:14

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  • 1[1]Mulliken JB, Glowacki J. Hemangiomas and vascular malformations in infants and children: a classification based on endothelial characteristics[J]. Plast Reconstr Surg, 1982,69(3):412-422.
  • 2[2]Tan ST, Velickovic M, Ruger BM ,et al. Cellular and extracellular markers of hemangioma [J]. Plast Reconstr Surg, 2000,106(3):529-538.
  • 3[3]Williams RL, Risau W, Zerwes HG,et al. Endothelioma cells expressing the polyoma middle T oncogene induce hemangiomas by host cell recruitment[J]. Cell, 1989,57(6):1053-1063.
  • 4[4]Taraboletti G, Belotti D, Dejana E,et al. Endothelial cell migration and invasiveness are induced by a soluble factor produced by murine endothelioma cells transformed by polyoma virus middle T oncogene[J]. Cancer Res, 1993,53(16):3812-3816.
  • 5[5]Martin-Padura I, De Castellarnau C, Uccini S ,et al. Expression of VE (vascular endothelial)-cadherin and other endothelial-specific markers in haemangiomas[J]. J Pathol, 1995,175(1):51-57.
  • 6[6]Takahashi K, Mulliken JB, Kozakewich HP,et al. Cellular markers that distinguish the phases of hemangioma during infancy and childhood[J].J Clin Invest,1994,93(6):2357-2364.
  • 7[7]Blei F, Walter J, Orlow SJ,et al. Familial segregation of hemangiomas and vascular malformations as an autosomal dominant trait[J]. Arch Dermatol, 1998,134(6):718-722.
  • 8[8]Walter JW, Blei F, Anderson JL,et al. Genetic mapping of a novel familial form of infantile hemangioma[J]. Am J Med Genet, 1999,82(1):77-83.
  • 9[9]Berg JN, Walter JW, Thisanagayam U ,et al. Evidence for loss of heterozygosity of 5q in sporadic hemangiomas: are somatic mutations involved in haemangioma formation? [J]. J Clin Pathol,2001, 54(3):249-252.
  • 10[10]Chang J, Most D, Bresnick S,et al. Proliferative hemangiomas:analysis of cytokine gene expression and angiogenesis [J]. Plast Recanstr Surg, 1999,103(1):1-9.

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