原始的英文摘要 TNF-α plays a pivotal role in the pathogenesis of multiple organ dysfunction syndrome (MODS). To investigate the effect of ERK1/2 MAPK on the production of TNF-α in MODS, a model of MODS was established in SD rats. The expression level of ERK1/2mRNA in PBMCs was detected by means of real time quantitative RT-PCR. The ERK1/2 MAPK activity in PBMCs was detected by Western blotting. PBMCs were cultured with various concentrations of ERK1/2 MAPK inhibitor PD98059 or without the treatment, and then TNF-α levels of the supernatant were determined by using sandwich ELISA. The results showed that mRNA expression and activity of ERK1/2 MAPK in PBMCs were significantly higher in MODS rats than in control rats (P<0.05). The ERK1/2 MAPK inhibitor PD98059 decreased the production of TNF-α in a dose-dependent manner. It is concluded that ERK1/2 MAPK plays an important role in the pathogenesis of MODS which is associated with cytokine TNF-α release.
所举例子存在的问题及修改建议:
a) 第一句话点明了本实验要检测TNF-α的的重要临床意义,这很好。但不足的是没有指出现存的问题。
b) 从内容来看,实际的实验设计及检测指标与文章的目的在逻辑上出现了严重的脱节。原摘要的第二句话清楚地说明本研究的主要目的是用一大鼠模型来探讨在多器官功能衰变的发病过程中ERK1/2是如何来大单核细胞TNF-α分泌的, 但从实验设计及方法来看,作者不但没有做任何通过改变ERK1/2 的表达来看ERK1/2对血液中TNF-α浓度影响的体内实验, 就连对本文最关键的指标(即TNF-α浓度变化)的分析也只是在体外实验中完成的。
c) 从表达方式上看: 一是内容结构有些混淆,原作者将正常合理的结构顺序(即诱导动物产生多器官功能衰变→ 分离细胞 → 培养细胞→ 回收培养液、检测TNF-α浓度→ 回收细胞蛋白并做 Western blotting、回收细胞 RNA并做 real time PCR)进行了不合理的倒置; 二是英文用词及表达方式有些欠妥当(detect, determine, examine 中文都可以翻成 “测定” 或 “检测” , 但detect 这个词被用着被动语态时则更侧重于”测定” 或 “检测”后的结果, 而严格地说 mRNA expression 则是包括美国人在内也常误用的非专业的表达方式) 。
根据上面的分析,我建议将原摘要改写为(仅为示范而已):
Tumor necrosis factor-alpha (TNF-α) plays a pivotal role in the pathogenesis of multiple organ dysfunction syndrome (MODS), but the regulation of TNF-α expression in MODS is not fully understood. The present study was therefore conducted to investigate the effect of mitogen-activated protein kinase (MAPK) ERK1/2 on the production of TNF-α in a rat model of MODS. SD rats were induced to develop MODS with xxxxx. Peripheral blood mononuclear cells (PBMCs) were isolated from the xxxxx-challenged animals. After culture of the cells in the absence or presence of various concentrations of ERK signaling-specific inhibitor PD98059 for yyyyyy h, the culture supernatant was collected and analyzed for TNF-α concentration while the cells were subject respectively to total RNA extraction and real time quantitative RT-PCR analysis of ERK1/2 mRNA abundance and to whole cell lysate preparation and Western blotting analysis of ERK1/2 protein contents. The results showed that both ERK1/2 mRNA abundance and protein contents were significantly higher in the PBMCs isolated from the rats with induced MODS than those from the control rats (P<0.05). PD98059 decreased the production of TNF-α in a dose-dependent manner. It can be concluded that ERK1/2 may play an important role in the pathologic production/release of TNF-α and thereby may offer a novel therapeutic target for MODS.