肥厚性瘢痕

  • 网络hypertrophic scar;HTS
肥厚性瘢痕肥厚性瘢痕
  1. 肥厚性瘢痕胶原降解的研究

    A Study on the Catabolism Degradation of Collagen in Hypertrophic Scar

  2. 肌成纤维细胞凋亡与肥厚性瘢痕消退的关系

    Relationship between apoptosis of myofibroblasts and regression of hypertrophic scar

  3. 机械性压力对肥厚性瘢痕的作用效果:前列腺素E2的释放

    Effects of mechanical compression on hypertrophic scars : prostaglandin E_2 release

  4. 脉冲Nd∶YAG激光对培养肥厚性瘢痕成纤维细胞胶原合成的选择性抑制作用研究

    Selectively inhibitor effects of pulsed Nd ∶ YAG laser on collagen synthesis of cultured fibroblasts of hypertrophic scar

  5. 目的检测与血管内皮细胞激活及增生相关的血管内皮生长因子(VEGF)、细胞间粘附分子1(ICAM1)、以及CFos原癌基因在肥厚性瘢痕组织中的表达。

    Objective To determine the expression of ICAM 1 , VEGF , and c fos proteins in hypertrophic scars .

  6. 结论一定能量密度(1000J/cm2)脉冲Nd∶YAG激光对体外培养肥厚性瘢痕成纤维细胞胶原合成具有选择性抑制作用。

    Conclusion Pulsed Nd : YAG laser at energy density of 1000J / cm 2 can selectively suppress collagen synthesis of cultured fibroblasts in HS .

  7. 目的通过体外机械性压力导致前列腺素E2(PGE2)释放,探讨肥厚性瘢痕松解过程中产生PGE2的规律。

    Objective To investigate the role of PGE2 in the process of hypertrophy remission included by mechanical compression in vitro .

  8. 结论机械性压力作用于肥厚性瘢痕可导致PGE2释放,并有助于瘢痕松解。

    Conclusion Mechanical compression induced the release of PGE2 in HS , and it helps the remission of HS .

  9. 结果肥厚性瘢痕与正常皮肤成纤维细胞胶原合成、Ⅰ型前胶原mRNA水平在500J/cm2照射后无变化,1500J/cm2、2000J/cm2照射后显著降低(P<0.001);

    Results Collagen synthesis and type I procollagen mRNA level in HS and normal dermal fibroblasts remained unchanged at energy level of 500J / cm 2 , and were significantly decreased at energy densities of 1500 and 200J / cm 2 ( P < 0.001 ) .

  10. 结果肥厚性瘢痕(HS)中PGE2的基本水平明显低于普通性瘢痕(NS)。压力可导致肥厚性瘢痕中PGE2释放的明显增加。

    Results PGE2 basal levels in hypertrophic ( HS ) were significantly lower than those present in normotrophic ( NS ), and compression induced a significant increase in the release of PGE2 in HS .

  11. 肥厚性瘢痕移植至裸鼠后的病理学观察

    Pathological observations on the hypertrophic scars transplanted to the nude mouse

  12. 61例烧伤肥厚性瘢痕形态学观察与细胞增殖活性的研究

    Study on the morphology and proliferating activity of hypertrophic scars

  13. 肥厚性瘢痕胶原降解代谢的初步探讨

    A preliminary discussion on collagenic degradation of hypertrophic scar

  14. 桃仁涂膜剂抗人源移植裸鼠肥厚性瘢痕的靶点研究

    Peach Kernel Source Plaster Anti-human Hypertrophic Scar in Nude Mice Transplanted Target Research

  15. 肥厚性瘢痕组织形态与胶原降解关系的实验研究

    An Experimental Study on the Relationship Between Histomorphology and Collagen Degradation in Hypertrophic Scar

  16. 盐酸维拉帕米治疗肥厚性瘢痕作用机制的实验研究

    The experimental study on effect mechanism of treatment of verapamil hydrochoride to hypertrophic scar

  17. 肥厚性瘢痕细胞凋亡检测及其相关调控因素的研究

    A study on the detection of apoptosis of hypertrophic scar and its related modulating factors

  18. 肥厚性瘢痕中TGF-β基因表达和蛋白产物的定量研究

    Quantitative study on gene expression and protein of transforming growth factor β in hypertrophic scar

  19. 肥厚性瘢痕的基因表达

    The gene expression in hypertrophic scar

  20. 瘢痕疙瘩及肥厚性瘢痕临床治疗试验:10年文献评价

    Clinical trials for keloids and hypertrophic scars : evaluation of Chinese medical literatures in the past 10 years

  21. 目的探讨肥厚性瘢痕的形态学特点及成纤维细胞增殖活性与其发生的关系。

    Objective To explore the relationship between proliferating activity of fibroblast and occurrence of hypertrophic scars ( HS ) .

  22. 本文观察了肥厚性瘢痕的组织形态,探讨了它们与胶原降解的关系,结果发现肥厚性瘢痕组织中胶原纤维排列紊乱,形成胶原结节。

    In order to explore the relationship between the histomorphology and collagen degradation in hypertrophic scar , its histomorphology was observed .

  23. 背景:肥厚性瘢痕是是烧伤和创伤后局部胶原合成与降解平衡失调,胶原异常聚集的结果。

    BACKGROUND : Hypertrophic scar results from imbalance between local collagen synthesis and degradation and abnormal aggregation of collagen after burn and trauma .

  24. 方法对1993/2002发表在国内116种医学杂志上的瘢痕疙瘩及肥厚性瘢痕临床治疗试验文献共261篇进行调查和分析。

    METHODS : Totally 261 clinical trials for keloids and hypertrophic scars published in 116 domestic medical journals during then years of 1993-2002 were investigated and analyzed .

  25. 目的探讨肥厚性瘢痕的发生与成纤维细胞和血管内皮细胞凋亡的关系,以及有关调控因素的影响。

    Objective To investigate the relationships between the development of hypertrophic scar ( HS ) and apoptosis of fibroblast and endothelial cell , and to elucidate the influence of related modulating factors .