长期运动对十二指肠黏膜一氧化氮合成和铁贮存的调控效应

目的:观察长期运动对十二指肠黏膜一氧化氮合成和铁贮存的影响及一氧化氮对铁贮存的调节作用。方法:实验于2004-04/09在江苏大学医学院铁代谢研究室完成。①健康雌性SD大鼠40只,随机分为静息组、静息并应用一氧化氮抑制剂组、运动组、运动并应用一氧化氮抑制剂组,每组10只。②静息并应用一氧化氮抑制剂组和运动并应用一氧化氮抑制剂组饮用水中含有一氧化氮抑制剂(1g/L),运动组和运动并应用一氧化氮抑制剂组的大鼠游泳3个月。③3个月后分析各组大鼠血浆铁饱和度,一氧化氮浓度以及十二指肠黏膜一氧化氮含量和非血红素铁含量。结果:实验过程中死亡11只,进入结果分析29只(静息组8只、静息并应用一氧化氮抑制剂组5只、运动组8只、运动并应用一氧化氮抑制剂组8只)。①运动及一氧化氮抑制剂对大鼠血浆铁饱和度和一氧化氮浓度的影响:运动组的血浆铁饱和度低于静息组(P<0.01);运动并应用一氧化氮抑制剂组的血浆铁饱和度低于静息并应用一氧化氮抑制剂组(P<0.05),并且高于运动组(P<0.05)。运动组血浆一氧化氮浓度显著高于静息组(P<0.01);运动并应用一氧化氮抑制剂组的血浆一氧化氮浓度低于运动组(P<0.01),与静息并应用一氧化氮抑制剂组差别不显著(P>0.05)。②运动及一氧化氮抑制剂对大鼠十二指肠黏膜一氧化氮和非血红素铁含量的影响:运动组的十二指肠一氧化氮含量高于静息组(P<0.01);静息并应用一氧化氮抑制剂组的一氧化氮含量低于静息组(P<0.01);运动并应用一氧化氮抑制剂组的一氧化氮含量低于运动组(P<0.01),但高于静息并应用一氧化氮抑制剂组(P<0.01),与静息组差别不显著。与静息组比较,运动组和静息并应用一氧化氮抑制剂组的十二指肠黏膜非血红素铁含量均降低(P<0.05)。结论:静息状态下十二指肠黏膜细胞一氧化氮合成具有较高的紧张性,可能参与维持非血红素铁含量。长期运动可刺激十二指肠黏膜一氧化氮合成,降低铁贮存。但其机制是否涉及运动诱导的一氧化氮的直接作用以及是否参与铁吸收的调节有待于进一步研究。     

IPS Empress 2全瓷修复的临床特点

全瓷材料可以提高前牙修复体的自然、逼真效果,它克服了金瓷修复体不透光、颈缘效果差的缺点。但全瓷材料的挠曲性能低,且不能承受过大的抬力,因此仅限于一个单位的修复。最近一种新的全瓷材料(IPS Empress2)由于强度高,可用于前牙多个单位桥的修复,它具有极好的美观性能,高度半透明,边缘完整,它的可蚀刻性增加了与牙齿的粘接,     

Activation of apoptosis associated with enforced myc expression in myeloid progenitor cells is dominant to the suppression of apoptosis by interleukin-3 or erythropoietin

The inappropriate expression of c-myc in cells deprived of growth factors has recently been implicated in the activation of programmed cell death (apoptosis). The studies described here examine the ability of interleukin-3 (IL-3) or erythropoietin (Epo) to suppress apoptosis that occurs in association with enforced myc expression during cell cycle arrest of a murine IL-3-dependent myeloid progenitor cell line, 32D. G1 arrest was observed when culturing 32D cells to high density in medium supplemented with IL-3, or at subconfluent densities in medium supplemented with Epo. Under both conditions, endogenous c-myc expression was downregulated and viability was maintained. In clones of cells in which c-myc is constitutively expressed from a retroviral vector, enforced c-myc expression was associated with the activation of apoptosis at high cell densities. Similarly, enforced c-myc expression was deleterious to cell survival when these cells were cultured in Epo, as apoptosis was evident within 6 hours. The results support the concept that inappropriate c-myc expression activates apoptosis and that neither IL-3 nor Epo can suppress this program under these conditions.