第一篇：Au Yeung, C. L., et al. (2016). "Exosomal transfer of stroma-derived miR21 confers paclitaxel resistance in ovarian cancer cells through targeting APAF1." Nat Commun 7: 11150.
摘要解析：
Advanced ovarian cancer usually spreads to the visceral adipose tissue（内脏脂肪组织） of the omentum（网膜）.--- 第一句：当前的研究进展
However, the omental stromal cell-derived molecular determinants that modulate ovarian cancer growth have not been characterized. ---第二句：有哪些问题没有解决。
Here, using next-generation sequencing technology, we identify significantly higher levels of microRNA-21 (miR21) isomiRNAs in exosomes and tissue lysates isolated from cancer-associated adipocytes (CAAs) and fibroblasts (CAFs) than in those from ovarian cancer cells. ---第三句：我们用A手段，发现了B东西。
Functional studies reveal that miR21 is transferred from CAAs or CAFs to the cancer cells, where it suppresses ovarian cancer apoptosis and confers chemo-resistance by binding to its direct novel target, APAF1. ---第四句：B东西的功能验证以及机制研究。
These data suggest that the malignant phenotype of metastatic ovarian cancer cells can be altered by miR21 delivered by exosomes derived from neighbouring stromal cells in the omental tumour microenvironment, and that inhibiting the transfer of stromal-derived miR21 is an alternative modality in the treatment of metastatic and recurrent ovarian cancer.---第五句话：对B东西的功能进行为分析，有哪些意义云云。
总结：①当前研究内容以及有哪些问题没有解决。②作者的研究内容。③结论。

第二篇：Byles, V., et al. (2013). "The TSC-mTOR pathway regulates macrophage polarization." Nat Commun 4: 2834.
Macrophages are able to polarize to proinflammatory M1 or alternative M2 states with distinct phenotypes and physiological functions. 第一句：巨噬细胞极化的背景介绍。
How metabolic status regulates macrophage polarization remains not well understood, and here we examine the role of mTOR (mechanistic target of rapamycin), a central metabolic pathway that couples nutrient sensing to regulation of metabolic processes. 第二句：需要解决的问题：代谢状态解是如何调控巨噬细胞极化的，仍未研究，并列出了作者的研究内容，即mTOR这个代谢通路在巨噬细胞活化方面的作用。
Using a mouse model in which myeloid lineage-specific deletion of Tsc1 (Tsc1(Delta/Delta)) leads to constitutive mTOR complex 1 (mTORC1) activation, we find that Tsc1(Delta/Delta) macrophages are refractory to IL-4-induced M2 polarization, but produce increased inflammatory responses to proinflammatory stimuli. 第三句：具体的研究内容，使用了条敲小鼠作为研究手段，发现了Tsc1巨噬细胞能够对抗IL-4诱导的M2极化，其能够增强促炎症刺激的炎症应答。
Moreover, mTORC1-mediated downregulation of Akt signalling critically contributes to defective polarization. 第四句话：mTORC-1能够下调Akt信号通路，削弱了巨噬细胞的极化。
These findings highlight a key role for the mTOR pathway in regulating macrophage polarization, and suggest how nutrient sensing and metabolic status could be 'hard-wired' to control of macrophage function, with broad implications for regulation of type 2 immunity, inflammation and allergy.第五句话：总结，mTOR通路在调节巨噬细胞方面有着重要作用，以及营养感知与代谢状态是如何影响巨噬细胞功能的。

第三篇：Czimmerer, Z., et al. (2018). "The Transcription Factor STAT6 Mediates Direct Repression of Inflammatory Enhancers and Limits Activation of Alternatively Polarized Macrophages." Immunity 48(1): 75-90 e76.
摘要解析：
The molecular basis of signal-dependent transcriptional activation has been extensively studied in macrophage polarization, but our understanding remains limited regarding the molecular determinants of repression.---第一句话：当前的研究背景与未解决的问题。即某信号通路的活化在巨噬细胞活化过程中被研究得很广泛，但是影响其抑制巨噬细胞活化的机制还未解决。
Here we show that IL-4-activated STAT6 transcription factor is required for the direct transcriptional repression of a large number of genes during in vitro and in vivo alternative macrophage polarization.---第二句话：作者的研究内容。即IL-4活化的STAT6转录因子能够直接参与巨噬细胞体内与体外活化的大量抑制性基因，这一步相当于表型分析了。
Repression results in decreased lineage-determining transcription factor, p300, and RNA polymerase II binding followed by reduced enhancer RNA expression, H3K27 acetylation, and chromatin accessibility.---第三句话：研究内容：抑制会导致p3000，RNA聚合酶II的下降，接头会导致RNA表达，H3K27乙酰化，染色体组装的减弱。
The repressor function of STAT6 is HDAC3 dependent on a subset of IL-4-repressed genes. ---第四句话：研究内容：STAT6的抑制功能依赖于HDAC3，这一个是IL-4抑制基因集的某个亚群。
In addition, STAT6-repressed enhancers show extensive overlap with the NF-kappaB p65 cistrome and exhibit decreased responsiveness to lipopolysaccharide after IL-4 stimulus on a subset of genes.---第五句话：研究内容：此外，STAT6抑制的增强子显示，NF-kappaB p65顺反组与IL-4刺激后，对LPS诱导的下降的基因集有大量的重叠。
As a consequence, macrophages exhibit diminished inflammasome activation, decreased IL-1beta production, and pyroptosis. ----第六句话：研究内容：巨噬细胞表现出炎性小体活化的减弱，IL-1beta生成的减少。
Thus, the IL-4-STAT6 signaling pathway establishes an alternative polarization-specific epigenenomic signature resulting in dampened macrophage responsiveness to inflammatory stimuli.---第七句话：结论：IL-4 STAT6信号转导通路参与了替代型巨噬细胞的活化，导致了巨噬细胞对炎性刺激的降低。
总结：①引出研究背景，当前存在哪些问题。②研究内容。③结论。

第四篇：Cai, L., et al. (2018). "MicroRNA-329 inhibits cell proliferation and tumor growth while facilitates apoptosis via negative regulation of KDM1A in gastric cancer." J Cell Biochem 119(4): 3338-3351.
摘要剖析：Altered expression of microRNA (miRNA) is strongly implicated in gastric cancer (GC). ---第一句话：研究背景。
Here, we demonstrated a decreased expression of miRNA-329 in GC. ---第二句话：研究内容。首选是表型，即miRNA-329在GC中下降。
Then we explored the regulatory mechanisms responsible for its effect on GC cells. ---第三句话：研究miRNAA-329对GC细胞的调控功能。
GC tissues and their adjacent non-tumor tissues were collected. Complete follow-up was updated. A series of inhibitors, mimics, and siRNA against KDM1A were introduced to validate regulatory mechanisms for miR-497 and KDM1A in BGC-823 cells. ---第四到第六句话：具体的研究内容，表型内容。
Quantitative real-time polymerase chain reaction (qRT-PCR) and western blot assay were employed for evaluating the expressions of miRNA-329, KDM1A, H3K4me1, and H3K4me2.---第七句话：qPCR与WB来研究了miRNA以及相应靶基因的变化。
Cell proliferation, cycle progression, and apoptosis were assessed by means of an MTT assay and flow cytometry. 第八句话：研究内容，细胞表型分析。
Cell colony formation was assessed. uman gastric cancer xenotransplanted into nude mice was studied. ---第九句话：研究内容，动物实验。
As opposed to adjacent tissues and gastritis tissues, miRNA-329 was highly expressed and KDM1A was low expressed in GC tissues.---第九句话：数据结果。
The patients with high miRNA-329 expression or low KDM1A expression had longer survival periods. ---第十句话：患者数据结果。
The miRNA-329 mimics and siRNA against KDM1A decreased KDM1A expression and increased H3K4me1 and H3K4me2 expressions. 第十一句话：细胞数据结果。
Forced expression of miRNA-329 in gastric cancer cells significantly promotes their capacity of apoptosis but reduces proliferation, migration, and invasion. 第十一句话，细胞表型结果。
KDM1A is a direct downstream target for miRNA-329. 第十二句话：miRNA的靶基因。
In a nude mouse subcutaneous tumor system, in vivo tumor growth of BGC-823 was significantly inhibited after treatment of miRNA-329 mimics or siRNA against KDM1A.第十三句话：动物实验结果。
We conclude that miRNA-329 functions as a tumor suppressor in GC, which could be achieved via transcriptional suppression of KDM1A.第十四句话：结论。
结论：这篇摘要比较长。大概也能分为三部分：①研究背景；②研究内容，这一部分比较多，先是提出了要研究哪些东西，后面就接着写了数据的结果；③文章结论。

第五篇：Eshleman, E. M., et al. (2017). "Down regulation of macrophage IFNGR1 exacerbates systemic L. monocytogenes infection." PLoS Pathog 13(5): e1006388.
摘要剖析：Interferons (IFNs) target macrophages to regulate inflammation and resistance to microbial infections. The type II IFN (IFNgamma) acts on a cell surface receptor (IFNGR) to promote gene expression that enhance macrophage inflammatory and anti-microbial activity.Type I IFNs can dampen macrophage responsiveness to IFN-gamma and are associated with increased susceptibility to numerous bacterial infections.----第1到3句话：研究背景
The precise mechanisms responsible for these effects remain unclear. ---第4句话：未解决的问题。
Type I IFNs silence macrophage ifngr1 transcription and thus reduce cell surface expression of IFNGR1. -------第5句话：研究背景。
To test how these events might impact macrophage activation and host resistance during bacterial infection, we developed transgenic mice that express a functional FLAG-tagged IFNGR1 (fGR1) driven by a macrophage-specific promoter. ----第6句话：本文的研究内容。
Macrophages from fGR1 mice expressed physiologic levels of cell surface IFNGR1 at steady state and responded equivalently to WT C57Bl/6 macrophages when treated with IFNgamma alone. ----第7句话：表型分析。
However, fGR1 macrophages retained cell surface IFNGR1 and showed enhanced responsiveness to IFN-gamma in the presence of type I IFNs. ---第8句话：研究内容：表型分析。
When fGR1 mice were infected with the bacterium Listeria monocytogenes their resistance was significantly increased, despite normal type I and II IFN production. Enhanced resistance was dependent on IFNgamma and associated with increased macrophage activation and antimicrobial function. ---第9句话：表型分析。
These results argue that down regulation of myeloid cell IFNGR1 is an important mechanism by which type I IFNs suppress inflammatory and anti-bacterial functions of macrophages.---第10句话：研究结论
结论：这个摘要也比较长，大致结构属于①研究背景；②研究问题；③研究内容；④研究结论。

从这五文献我们可以知道，摘要的结构就是四个内容：①研究背景；②研究问题（①和②有的文章是合并起来的），③本文的研究内容；④研究得到的结论。另外，写摘要的时候，用的时态都是一般现在时，这点要注意。