| 1 | SD大鼠长期高盐饮食可导致其高血压并改变肾细胞因子基因表达谱(英文)显示文摘Objective:The present study examines whether a long-term high salt diet causes hypertension and renal injury in normal subjects [Sprague-Dawley(SD) rats] and alters renal cytokine-related gene expression profiles.Methods: Four 10 week old male SD rats received a high salt diet(HS,8%) and the other 4 SD rats received a normal salt diet(NS,0.5 %) for 8 weeks.Mean arterial pressure(MAP) and renal damages such as albuminuria and histological renal injury were determined.The relative mRNA levels of 514 cytokine-related genes(normalized by β-actin) in rat kidneys following NS or HS were determined quantitatively through analysis of 4 sets of gene expression profiles using the mouse cDNA membrane microarrays.Results: We demonstrated that 8 weeks of HS diet increased MAP [(140.0±5.3) vs(112.0±2.2) mmHg;1 mmHg=0.133 kPa,P<0.01],albuminuria [(41.4±3.2) vs(20.1±4.5) mg/d;P<0.01],and caused histological renal injury in SD rats,compared to NS group.Of the 514 genes in the array,there were 27(5.25%) genes with significantly different expression in the kidney of SD rats with HS compared to those of SD rats with NS.Functional clustering analysis indicated the following functional pathways related to high salt diet-induced hypertension:(1) pro-inflammatory response(↑IL-17,CCL28;↓NFκbib);(2) endothelial dysfunction(↓VEGF-A,VEGF-B,endoglin);(3) pro-matrix formation(↑osteopontin,IGFBP-5;↓IFN-γ);and(4) attenuated cell survival and differentiation(↓CNTF,IGF-Ⅱ R,ephrin-B1).Northern blot confirmed that 8 weeks of HS diet significantly decreased renal expression of VEGF mRNA,compared to NS group(P<0.01).ELISA showed that HS diet significantly decreased renal protein levels of VEGF and CCL28.Conclusion: These findings support the hypothesis that hypertension can be induced in normal rats by a long-term high salt diet,which is associated with increased renal injury and marked changes in renal cytokine gene expression profiles that are closely related to the pro-inflammatory response,pro-matrix formation,endothelial dysfunction,and attenuated cell survival and differentiation. | Emily YOUNG Kevan B.TUCKER Megan SHPARAGO Amelia Purser BAILEY | 2009 | 北京大学学报(医学版)2009，41，5： | 2 |
| 2 | 加里福尼亚科林加弱震和强震地面运动反应观测的比较显示文摘0 引言 在估计地震危险性中,局部场地条件对地面运动的效应十分重要。山脊和谷地的放大作用,加重了1985年3月3日发生在智利瓦尔帕莱索市郊的地震破坏。软湖沉积的长周期放大作用,扩大了墨西哥城1985年9月19日地震的震害和生命损失。 近年来,在观测、计算和模拟场地效应方面有了显著进展。Tucker等人论述了场地效应的经验性特征,并利用地质和地球物理数据对这些场地效应进行了模拟。人们还正在试图定量地预测地震时的场地效应,将预测结果体现在土地利用决策中。 | S.JARP C.CRAMER B.TUCKER A.SHAKAL 郑鹄 | 1990 | 山西地震1990，，3： | 0 |
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