Macrophage最新文献

Autophagy in inflammation: the p38α MAPK-ULK1 axis 炎症中的自噬：p38αMAPK-ULK1轴

Macrophage

Pub Date : 2018-03-09 DOI: 10.14800/MACROPHAGE.1629

H. She, Yingli He, Ying‐ren Zhao, Zixu Mao

Autophagy and inflammation are two processes vital for immune cells to perform their functions. Their proper interplay upon signal is pivotal for proper response to stress. The stress kinase p38α MAPK in microglia senses inflammatory cue LPS, directly phosphorylates ULK1, relieves the autophagic inhibition on the inflammatory machinery, and thus allows for a full immune response.

自噬和炎症是免疫细胞发挥其功能的两个重要过程。它们在信号上的适当相互作用是对压力作出适当反应的关键。小胶质细胞中的应激激酶p38α MAPK感知炎症线索LPS，直接磷酸化ULK1，减轻对炎症机制的自噬抑制，从而允许充分的免疫反应。

引用次数: 4

Autophagy in inflammation: the p38α MAPK-ULK1 axis. 炎症中的自噬：p38α MAPK-ULK1 轴。

Macrophage

Pub Date : 2018-01-01 Epub Date: 2018-03-09

Hua She, Yingli He, Yingren Zhao, Zixu Mao

Autophagy and inflammation are two processes vital for immune cells to perform their functions. Their proper interplay upon signal is pivotal for proper response to stress. The stress kinase p38α MAPK in microglia senses inflammatory cue LPS, directly phosphorylates ULK1, relieves the autophagic inhibition on the inflammatory machinery, and thus allows for a full immune response.

自噬和炎症是免疫细胞发挥其功能的两个重要过程。自噬和炎症是免疫细胞发挥其功能的两个重要过程，它们在发出信号后的适当相互作用是对应激做出适当反应的关键。小胶质细胞中的应激激酶 p38α MAPK 感受到炎症线索 LPS 后，直接使 ULK1 磷酸化，解除自噬对炎症机制的抑制，从而使免疫反应得以全面展开。

引用次数: 0

Myeloid cell neuropilin 1 ameliorates high-fat diet-induced insulin resistance via suppression of Nlrp3 inflammasome. 髓系细胞neuropilin 1通过抑制Nlrp3炎性体改善高脂肪饮食诱导的胰岛素抵抗。

Macrophage

Pub Date : 2017-09-18 DOI: 10.14800/MACROPHAGE.1594

X. Dai, I. Okon, M. Zou

The history of neuropilin 1 (Nrp1) research is checkered with many unexpected and exciting findings. Nrp1 functions as a co-receptor for class 3 semaphorins, and several canonical growth factors, including vascular endothelial growth factor (VEGF) and hepatocyte growth factor (HGF). It has been implicated in the development of central nervous system, angiogenesis, and migration. Accumulating evidence demonstrates that Nrp1 is also highly expressed in immune cells, including macrophages and dendritic cells. Until now, the functions of Nrp1 within these cells remained poorly studied and elusive. Here, we provide exciting insights on a novel role for myeloid cell Nrp1 in the mitigation of dietary insulin resistance through inhibiting Nlrp3 inflammasome.

神经匹林1 (Nrp1)的研究历史充满了许多意想不到和令人兴奋的发现。Nrp1是3类信号素和几种典型生长因子的共同受体，包括血管内皮生长因子(VEGF)和肝细胞生长因子(HGF)。它与中枢神经系统的发育、血管生成和迁移有关。越来越多的证据表明Nrp1也在免疫细胞中高表达，包括巨噬细胞和树突状细胞。到目前为止，Nrp1在这些细胞中的功能研究仍然很少，难以捉摸。在这里，我们提供了髓样细胞Nrp1通过抑制Nlrp3炎性体在减轻饮食胰岛素抵抗中的新作用的令人兴奋的见解。

引用次数: 2

Myeloid cell neuropilin 1 ameliorates high-fat diet-induced insulin resistance via suppression of Nlrp3 inflammasome. 髓系细胞neuropilin 1通过抑制Nlrp3炎性体改善高脂肪饮食诱导的胰岛素抵抗。

Macrophage

Pub Date : 2017-01-01 Epub Date: 2017-09-19

Xiaoyan Dai, Imoh Okon, Ming-Hui Zou

The history of neuropilin 1 (Nrp1) research is checkered with many unexpected and exciting findings. Nrp1 functions as a co-receptor for class 3 semaphorins, and several canonical growth factors, including vascular endothelial growth factor (VEGF) and hepatocyte growth factor (HGF). It has been implicated in the development of central nervous system, angiogenesis, and migration. Accumulating evidence demonstrates that Nrp1 is also highly expressed in immune cells, including macrophages and dendritic cells. Until now, the functions of Nrp1 within these cells remained poorly studied and elusive. Here, we provide exciting insights on a novel role for myeloid cell Nrp1 in the mitigation of dietary insulin resistance through inhibiting Nlrp3 inflammasome.

神经匹林1 (Nrp1)的研究历史充满了许多意想不到和令人兴奋的发现。Nrp1是3类信号素和几种典型生长因子的共同受体，包括血管内皮生长因子(VEGF)和肝细胞生长因子(HGF)。它与中枢神经系统的发育、血管生成和迁移有关。越来越多的证据表明Nrp1也在免疫细胞中高表达，包括巨噬细胞和树突状细胞。到目前为止，Nrp1在这些细胞中的功能研究仍然很少，难以捉摸。在这里，我们提供了髓样细胞Nrp1通过抑制Nlrp3炎性体在减轻饮食胰岛素抵抗中的新作用的令人兴奋的见解。

引用次数: 0

Mammary epithelial polarity and macrophage infiltration. 乳腺上皮极性与巨噬细胞浸润。

Macrophage

Pub Date : 2017-01-01 Epub Date: 2017-03-13 DOI: 10.14800/Macrophage.1521

Ren Xu

Loss of epithelial cell polarity and inflammation are hallmarks of breast cancer development. Although the association between the disruption of tissue polarity and inflammation has been demonstrated, we know little about how these two events are coupled. Using the 3D co-culture model of mammary epithelial cells and monocytes, a recent study reveals a link between disruption of epithelial polarity and monocytes infiltration.

上皮细胞极性的丧失和炎症是乳腺癌发展的标志。虽然组织极性破坏和炎症之间的关联已被证实，但我们对这两个事件是如何耦合的知之甚少。利用乳腺上皮细胞和单核细胞的3D共培养模型，最近的一项研究揭示了上皮极性破坏与单核细胞浸润之间的联系。

引用次数: 1

The role of Siglec-1 in HIV-1/macrophage interaction. siglec1在HIV-1/巨噬细胞相互作用中的作用。

Macrophage

Pub Date : 2016-10-17 DOI: 10.14800/MACROPHAGE.1435

O. Jobe, Jiae Kim, M. Rao

Although CD4 T-cells are a major target for HIV, recent work has demonstrated the ability of macrophages despite expressing relatively low levels of CD4, to be a target of the virus. Our recent study has found that the presence of growth factors not only play a role in the phenotype of these monocyte-derived-macrophages, but also are an important aspect of the permissiveness of these cells to infection. The work utilized cellular and biophysical methods to examine Siglec-1 on macrophages as a primary receptor in HIV-1 infection. These findings support the notion that Siglec-1 and macrophages and their interactions with the HIV-1 envelope should be considered in HIV-1 vaccine development.

尽管CD4 t细胞是HIV的主要靶标，但最近的研究表明，尽管巨噬细胞表达相对较低的CD4水平，但巨噬细胞仍有能力成为HIV的靶标。我们最近的研究发现，生长因子的存在不仅在这些单核细胞衍生的巨噬细胞的表型中起作用，而且是这些细胞对感染的容受性的一个重要方面。这项工作利用细胞和生物物理方法来检测巨噬细胞上的siglec1作为HIV-1感染的主要受体。这些发现支持了在HIV-1疫苗开发中应考虑siglec1和巨噬细胞及其与HIV-1包膜的相互作用的观点。

引用次数: 7

Coordinated expression of tyro3, axl, and mer receptors in macrophage ontogeny 巨噬细胞个体发生中tyro3、axl和mer受体的协调表达

Macrophage

Pub Date : 2016-04-22 DOI: 10.14800/MACROPHAGE.1261

Anna Malawista, Xiaomei Wang, M. Trentalange, H. Allore, Ruth R. Montgomery

The TAM receptors (Tyro3, Axl, and Mer) are a family of homologous receptor-tyrosine kinases that inhibit Toll-like receptor signaling to regulate downstream pathways and restore homeostasis. TAM triple mutant mice (Tyro3−/−, Axl−/−, Mer−/−) have elevated levels of pro-inflammatory cytokines and are prone to developing lymphoproliferative disorders and autoimmunity. Understanding differential expression of TAM receptors among human subjects is critical to harnessing this pathway for therapeutic interventions. We have quantified changes in TAM expression during the ontogeny of human macrophages using paired samples of monocytes and macrophages to take advantage of characteristic expression within an individual. No significant differences in levels of Tyro3 were found between monocytes and macrophages (flow cytometry: p=0.652, immunoblot: p=0.231, qPCR: p=0.389). Protein levels of Axl were reduced (flow cytometry: p=0.049, immunoblot: p<0.001) when monocytes matured to macrophages. No significant differences in the levels of Axl mRNA transcripts were found (qPCR: p=0.082), however, Tyro3 and Axl were proportionate. The most striking difference was upregulation of expression of Mer with both protein and mRNA being significantly increased when monocytes developed into macrophages (flow cytometry: p<0.001, immunoblot: p<0.001, qPCR: p=0.004). A fuller characterization of TAM receptor expression in macrophage ontogeny informs our understanding of their function and potential therapeutic interventions.

TAM受体(Tyro3、Axl和Mer)是一类同源受体酪氨酸激酶，可抑制toll样受体信号传导，调节下游通路，恢复体内平衡。TAM三重突变小鼠(Tyro3−/−，Axl−/−，Mer−/−)的促炎细胞因子水平升高，容易发生淋巴增生性疾病和自身免疫。了解人类受试者之间TAM受体的差异表达对于利用这一途径进行治疗干预至关重要。我们利用单核细胞和巨噬细胞的配对样本，利用个体内的特征表达，量化了人巨噬细胞个体发生过程中TAM表达的变化。单核细胞与巨噬细胞间Tyro3表达水平无显著差异(流式细胞术:p=0.652，免疫印迹:p=0.231, qPCR: p=0.389)。当单核细胞成熟为巨噬细胞时，Axl蛋白水平降低(流式细胞术:p=0.049，免疫印迹:p<0.001)。Axl mRNA转录本水平差异无统计学意义(qPCR: p=0.082)，但Tyro3与Axl成正比。最显著的差异是单核细胞向巨噬细胞发展时，Mer表达上调，蛋白和mRNA均显著升高(流式细胞术:p<0.001，免疫印迹:p<0.001, qPCR: p=0.004)。巨噬细胞个体发育中TAM受体表达的更全面表征有助于我们了解其功能和潜在的治疗干预措施。

{"title":"Coordinated expression of tyro3, axl, and mer receptors in macrophage ontogeny","authors":"Anna Malawista, Xiaomei Wang, M. Trentalange, H. Allore, Ruth R. Montgomery","doi":"10.14800/MACROPHAGE.1261","DOIUrl":"https://doi.org/10.14800/MACROPHAGE.1261","url":null,"abstract":"The TAM receptors (Tyro3, Axl, and Mer) are a family of homologous receptor-tyrosine kinases that inhibit Toll-like receptor signaling to regulate downstream pathways and restore homeostasis. TAM triple mutant mice (Tyro3−/−, Axl−/−, Mer−/−) have elevated levels of pro-inflammatory cytokines and are prone to developing lymphoproliferative disorders and autoimmunity. Understanding differential expression of TAM receptors among human subjects is critical to harnessing this pathway for therapeutic interventions. We have quantified changes in TAM expression during the ontogeny of human macrophages using paired samples of monocytes and macrophages to take advantage of characteristic expression within an individual. No significant differences in levels of Tyro3 were found between monocytes and macrophages (flow cytometry: p=0.652, immunoblot: p=0.231, qPCR: p=0.389). Protein levels of Axl were reduced (flow cytometry: p=0.049, immunoblot: p<0.001) when monocytes matured to macrophages. No significant differences in the levels of Axl mRNA transcripts were found (qPCR: p=0.082), however, Tyro3 and Axl were proportionate. The most striking difference was upregulation of expression of Mer with both protein and mRNA being significantly increased when monocytes developed into macrophages (flow cytometry: p<0.001, immunoblot: p<0.001, qPCR: p=0.004). A fuller characterization of TAM receptor expression in macrophage ontogeny informs our understanding of their function and potential therapeutic interventions.","PeriodicalId":90918,"journal":{"name":"Macrophage","volume":"3 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2016-04-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"66657062","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 10

MK2: an unrecognized regulator of tumor promoting macrophages in colorectal cancer? MK2:结直肠癌中促瘤巨噬细胞未被识别的调节因子?

Macrophage

Pub Date : 2016-02-01 DOI: 10.14800/macrophage.1166

Eliseo F. Castillo, A. Ray, E. Beswick

Colorectal cancer (CRC) is one of the most common malignancies and is associated closely with inflammation before and after development. Macrophages promote colitis and colitis-associated CRC. M1 macrophages contribute to colitis directly through the production of proinflammatory cytokines and through activation of proinflammatory immune cell phenotypes. In cancer, both M1 and M2 macrophages participate in tumor development and progression through cytokine production, changes in cell signaling and activation of T cells. We have identified the mitogen-activated protein kinase-activated protein kinase 2 (MK2) as a regulator of macrophages during colitis-associated CRC (CAC). MK2 is a proinflammatory kinase that promotes production of IL-1α, IL-1β, IL-6 and TNF-α. MK2−/− mice have decreases in macrophages, macrophage-associated chemokines, and proinflammatory cytokines. Most significantly, MK2−/− mice do not develop neoplasms in an inflammatory model of CRC. However, addition of MK2+/+ macrophages to MK2−/− mice increases production of proinflammatory cytokines. In wild type mice, both cytokines and tumor burdens increase upon addition of additional macrophages. These data support the importance of MK2 in macrophage regulation during inflammation-associated CRC.

结直肠癌(CRC)是最常见的恶性肿瘤之一，其发病前后与炎症密切相关。巨噬细胞促进结肠炎和结肠炎相关的结直肠癌。M1巨噬细胞通过产生促炎细胞因子和激活促炎免疫细胞表型直接促进结肠炎。在癌症中，M1和M2巨噬细胞都通过细胞因子的产生、细胞信号的改变和T细胞的激活参与肿瘤的发生和进展。我们已经确定丝裂原活化蛋白激酶活化蛋白激酶2 (MK2)在结肠炎相关CRC (CAC)中作为巨噬细胞的调节因子。MK2是一种促炎激酶，可促进IL-1α、IL-1β、IL-6和TNF-α的产生。MK2−/−小鼠巨噬细胞、巨噬细胞相关趋化因子和促炎细胞因子减少。最重要的是，MK2−/−小鼠在CRC炎症模型中不会发生肿瘤。然而，在MK2−/−小鼠中添加MK2+/+巨噬细胞会增加促炎细胞因子的产生。在野生型小鼠中，细胞因子和肿瘤负荷随着巨噬细胞的增加而增加。这些数据支持了MK2在炎症相关性CRC中巨噬细胞调节中的重要性。

{"title":"MK2: an unrecognized regulator of tumor promoting macrophages in colorectal cancer?","authors":"Eliseo F. Castillo, A. Ray, E. Beswick","doi":"10.14800/macrophage.1166","DOIUrl":"https://doi.org/10.14800/macrophage.1166","url":null,"abstract":"Colorectal cancer (CRC) is one of the most common malignancies and is associated closely with inflammation before and after development. Macrophages promote colitis and colitis-associated CRC. M1 macrophages contribute to colitis directly through the production of proinflammatory cytokines and through activation of proinflammatory immune cell phenotypes. In cancer, both M1 and M2 macrophages participate in tumor development and progression through cytokine production, changes in cell signaling and activation of T cells. We have identified the mitogen-activated protein kinase-activated protein kinase 2 (MK2) as a regulator of macrophages during colitis-associated CRC (CAC). MK2 is a proinflammatory kinase that promotes production of IL-1α, IL-1β, IL-6 and TNF-α. MK2−/− mice have decreases in macrophages, macrophage-associated chemokines, and proinflammatory cytokines. Most significantly, MK2−/− mice do not develop neoplasms in an inflammatory model of CRC. However, addition of MK2+/+ macrophages to MK2−/− mice increases production of proinflammatory cytokines. In wild type mice, both cytokines and tumor burdens increase upon addition of additional macrophages. These data support the importance of MK2 in macrophage regulation during inflammation-associated CRC.","PeriodicalId":90918,"journal":{"name":"Macrophage","volume":"3 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2016-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"66657043","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 3

The role of Siglec-1 in HIV-1/macrophage interaction. siglec1在HIV-1/巨噬细胞相互作用中的作用。

Macrophage

Pub Date : 2016-01-01 Epub Date: 2016-09-17

Ousman Jobe, Jiae Kim, Mangala Rao

Although CD4 T-cells are a major target for HIV, recent work has demonstrated the ability of macrophages despite expressing relatively low levels of CD4, to be a target of the virus. Our recent study has found that the presence of growth factors not only play a role in the phenotype of these monocyte-derived-macrophages, but also are an important aspect of the permissiveness of these cells to infection. The work utilized cellular and biophysical methods to examine Siglec-1 on macrophages as a primary receptor in HIV-1 infection. These findings support the notion that Siglec-1 and macrophages and their interactions with the HIV-1 envelope should be considered in HIV-1 vaccine development.

尽管CD4 t细胞是HIV的主要靶标，但最近的研究表明，尽管巨噬细胞表达相对较低的CD4水平，但巨噬细胞仍有能力成为HIV的靶标。我们最近的研究发现，生长因子的存在不仅在这些单核细胞衍生的巨噬细胞的表型中起作用，而且是这些细胞对感染的容受性的一个重要方面。这项工作利用细胞和生物物理方法来检测巨噬细胞上的siglec1作为HIV-1感染的主要受体。这些发现支持了在HIV-1疫苗开发中应考虑siglec1和巨噬细胞及其与HIV-1包膜的相互作用的观点。

引用次数: 0

TRAF3: a novel tumor suppressor gene in macrophages. 巨噬细胞中一种新的肿瘤抑制基因TRAF3。

Macrophage

Pub Date : 2015-09-30 DOI: 10.14800/MACROPHAGE.1009

Almin I. Lalani, Chang Luo, Yeming Han, P. Xie

Tumor necrosis factor receptor-associated factor 3 (TRAF3), a member of the TRAF family of cytoplasmic adaptor proteins with E3 ligase activity, is ubiquitously expressed in various cell types of the immune system. It is shared for signaling by a variety of adaptive and innate immune receptors as well as cytokine receptors. Previous studies examining conditional TRAF3-deficient mouse models that have the Traf3 gene specifically deleted in B lymphocytes or T lymphocytes have revealed the diverse and critical in vivo functions of TRAF3 in adaptive immunity. Although in vitro evidence points to a pivotal and indispensable role for TRAF3 in type I interferon production induced by pattern recognition receptors in macrophages and dendritic cells, the in vivo functions of TRAF3 in the innate immune system had long remained unclear. Three laboratories have recently addressed this gap in knowledge by investigating myeloid cell-specific TRAF3-deficient (genotype: TRAF3flox/floxLysM+/Cre) mice. The new evidence together demonstrates that specific ablation of TRAF3 in myeloid cells leads to inflammatory diseases, altered progression of diabetes, and spontaneous development of different types of tumors and infections in mice. These new findings indicate that TRAF3 acts as an anti-inflammatory factor and is required for optimal innate immunity in myeloid cells. Strikingly, the new evidence also identifies TRAF3 as a novel tumor suppressor gene in macrophages and other myeloid cells. In this review, we discuss and summarize the new findings and current knowledge about the multi-faceted regulatory roles and complex signaling mechanisms of myeloid cell TRAF3 in inflammation, innate immunity, and tumor development.

肿瘤坏死因子受体相关因子3 (Tumor necrosis factor receptor-associated factor 3, TRAF3)是具有E3连接酶活性的细胞质衔接蛋白traf家族的一员，在免疫系统的各种细胞类型中普遍表达。它是多种适应性和先天免疫受体以及细胞因子受体共享的信号转导。先前的研究检测了在B淋巴细胞或T淋巴细胞中特异性缺失Traf3基因的条件Traf3缺陷小鼠模型，揭示了Traf3在体内适应性免疫中的多种关键功能。尽管体外证据表明TRAF3在巨噬细胞和树突状细胞模式识别受体诱导的I型干扰素产生中起着关键和不可或缺的作用，但在体内，TRAF3在先天免疫系统中的功能一直不清楚。三个实验室最近通过研究骨髓细胞特异性traf3缺陷(基因型:TRAF3flox/floxLysM+/Cre)小鼠来解决这一知识空白。这些新证据共同表明，骨髓细胞中TRAF3的特异性消融可导致小鼠炎症性疾病、糖尿病的改变进展以及不同类型肿瘤和感染的自发发展。这些新发现表明，TRAF3作为一种抗炎因子，是骨髓细胞最佳先天免疫所必需的。引人注目的是，新的证据还确定了TRAF3是巨噬细胞和其他髓细胞中的一种新的肿瘤抑制基因。在这篇综述中，我们讨论和总结了髓细胞TRAF3在炎症、先天免疫和肿瘤发展中的多方面调节作用和复杂信号机制的新发现和现有知识。

{"title":"TRAF3: a novel tumor suppressor gene in macrophages.","authors":"Almin I. Lalani, Chang Luo, Yeming Han, P. Xie","doi":"10.14800/MACROPHAGE.1009","DOIUrl":"https://doi.org/10.14800/MACROPHAGE.1009","url":null,"abstract":"Tumor necrosis factor receptor-associated factor 3 (TRAF3), a member of the TRAF family of cytoplasmic adaptor proteins with E3 ligase activity, is ubiquitously expressed in various cell types of the immune system. It is shared for signaling by a variety of adaptive and innate immune receptors as well as cytokine receptors. Previous studies examining conditional TRAF3-deficient mouse models that have the Traf3 gene specifically deleted in B lymphocytes or T lymphocytes have revealed the diverse and critical in vivo functions of TRAF3 in adaptive immunity. Although in vitro evidence points to a pivotal and indispensable role for TRAF3 in type I interferon production induced by pattern recognition receptors in macrophages and dendritic cells, the in vivo functions of TRAF3 in the innate immune system had long remained unclear. Three laboratories have recently addressed this gap in knowledge by investigating myeloid cell-specific TRAF3-deficient (genotype: TRAF3flox/floxLysM+/Cre) mice. The new evidence together demonstrates that specific ablation of TRAF3 in myeloid cells leads to inflammatory diseases, altered progression of diabetes, and spontaneous development of different types of tumors and infections in mice. These new findings indicate that TRAF3 acts as an anti-inflammatory factor and is required for optimal innate immunity in myeloid cells. Strikingly, the new evidence also identifies TRAF3 as a novel tumor suppressor gene in macrophages and other myeloid cells. In this review, we discuss and summarize the new findings and current knowledge about the multi-faceted regulatory roles and complex signaling mechanisms of myeloid cell TRAF3 in inflammation, innate immunity, and tumor development.","PeriodicalId":90918,"journal":{"name":"Macrophage","volume":"2 1","pages":"e1009"},"PeriodicalIF":0.0,"publicationDate":"2015-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"66656983","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 25