Journal of endotoxin research最新文献

筛选
英文 中文
IEIIS Meeting minireview: Bordetella evolution: lipid A and Toll-like receptor 4. 博德氏菌进化:脂质A和toll样受体4。
Journal of endotoxin research Pub Date : 2007-01-01 DOI: 10.1177/0968051907082609
Iain MacArthur, Paul B Mann, Eric T Harvill, Andrew Preston
{"title":"IEIIS Meeting minireview: Bordetella evolution: lipid A and Toll-like receptor 4.","authors":"Iain MacArthur, Paul B Mann, Eric T Harvill, Andrew Preston","doi":"10.1177/0968051907082609","DOIUrl":"10.1177/0968051907082609","url":null,"abstract":"<p><p>The evolution of Bordetella pertussis and Bordetella parapertussis from Bordetella bronchiseptica involved changes in host range and pathogenicity. Recent data suggest that the human-adapted Bordetella modified their interaction with host immune systems to effect these changes and that decreased stimulation of Toll-like receptor 4 (TLR4) by lipid A is central to this. We discuss Bordetella lipid A structure and genetics within the context of evolution and host immunity.</p>","PeriodicalId":80292,"journal":{"name":"Journal of endotoxin research","volume":"13 4","pages":"243-7"},"PeriodicalIF":0.0,"publicationDate":"2007-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"27065276","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: 0
Review: variability of host-pathogen interaction. 综述:宿主-病原体相互作用的可变性。
Journal of endotoxin research Pub Date : 2007-01-01 DOI: 10.1177/0968051907082605
Corinna Hermann
{"title":"Review: variability of host-pathogen interaction.","authors":"Corinna Hermann","doi":"10.1177/0968051907082605","DOIUrl":"https://doi.org/10.1177/0968051907082605","url":null,"abstract":"<p><p>The course of every infection is different. The same pathogen can lead to subclinical, mild, severe or lethal infections in individuals. But is this just chance or determined by individual differences--on the side of the host as well as on the side of the pathogen? If so, we might need to consider these variations for treatment decisions. Indeed, we now understand that genetic polymorphisms and health status represent inborn and acquired risk factors. Similarly, pathogens impress with an increasing number of already identified virulence factors and host response modifiers. The emerging, more complex, view of the factors determining course and outcome of infections promises to enable more tailored and thus, hopefully, more effective treatment decisions.</p>","PeriodicalId":80292,"journal":{"name":"Journal of endotoxin research","volume":"13 4","pages":"199-218"},"PeriodicalIF":0.0,"publicationDate":"2007-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/0968051907082605","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"27065272","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: 16
Transcriptional activation of MMP-13 by periodontal pathogenic LPS requires p38 MAP kinase. 牙周致病性LPS对MMP-13的转录激活需要p38 MAP激酶。
Journal of endotoxin research Pub Date : 2007-01-01 DOI: 10.1177/0968051907079118
Carlos Rossa, Min Liu, Paul Bronson, Keith L Kirkwood
{"title":"Transcriptional activation of MMP-13 by periodontal pathogenic LPS requires p38 MAP kinase.","authors":"Carlos Rossa,&nbsp;Min Liu,&nbsp;Paul Bronson,&nbsp;Keith L Kirkwood","doi":"10.1177/0968051907079118","DOIUrl":"https://doi.org/10.1177/0968051907079118","url":null,"abstract":"<p><p>Matrix metalloprotease-13 (MMP-13) is induced by pro-inflammatory cytokines and increased expression is associated with a number of pathological conditions such as tumor metastasis, osteoarthritis, rheumatoid arthritis and periodontal diseases. MMP-13 gene regulation and the signal transduction pathways activated in response to bacterial LPS are largely unknown. In these studies, the role of the mitogen-activated protein kinase (MAPK) pathways in the regulation of MMP-13 induced by lipopolysaccharide was investigated. Lipopolysaccharide from Escherichia coli and Actinobacillus actinomycetemcomitans significantly (P < 0.05) increased MMP-13 steady-state mRNA (average of 27% and 46% increase, respectively) in murine periodontal ligament fibroblasts. MMP-13 mRNA induction was significantly reduced by inhibition of p38 MAP kinase. Immunoblot analysis indicated that p38 signaling was required for LPS-induced MMP-13 expression. Lipopolysaccharide induced proximal promoter reporter (-660/+32 mMMP-13) gene activity required p38 signaling. Collectively, these results indicate that lipopolysaccharide-induced murine MMP-13 is regulated by p38 signaling through a transcriptional mechanism.</p>","PeriodicalId":80292,"journal":{"name":"Journal of endotoxin research","volume":"13 2","pages":"85-93"},"PeriodicalIF":0.0,"publicationDate":"2007-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/0968051907079118","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26822626","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: 31
Decreased beating rate variability of spontaneously contracting cardiomyocytes after co-incubation with endotoxin. 与内毒素共孵育后自发性收缩心肌细胞的搏动速率变异性降低。
Journal of endotoxin research Pub Date : 2007-01-01 DOI: 10.1177/0968051907086233
Hendrik Schmidt, Jana Saworski, Karl Werdan, Ursula Müller-Werdan
{"title":"Decreased beating rate variability of spontaneously contracting cardiomyocytes after co-incubation with endotoxin.","authors":"Hendrik Schmidt,&nbsp;Jana Saworski,&nbsp;Karl Werdan,&nbsp;Ursula Müller-Werdan","doi":"10.1177/0968051907086233","DOIUrl":"https://doi.org/10.1177/0968051907086233","url":null,"abstract":"<p><p>Decreased heart rate variability (HRV) in critically ill patients indicates a poor prognosis. In heart failure patients, there is an elevated sympathetic tone, reflected by a dominance of sympathetic parameters in HRV, whereas in critically ill patients sympathetic and parasympathetic modulation of heart rate is attenuated despite increased catecholamine blood levels. Thus, autonomic dysfunction in the critically ill cannot be causally related to an impairment at the level of neural transmission, but may be due to a derangement of signal transduction at the effector cell level. On the basis of our working hypothesis that endotoxin may be involved in this blunting of effector cell response to nerval input, we studied the spontaneous beating of cardiomyocytes under the influence of endotoxin. Applying the clinically established indices of HRV to the analysis of beating rate variability (BRV) of neonatal rat cardiomyocytes in serum-free medium, a narrowing of their BRV by endotoxin is demonstrated. We propose that the narrowing of HRV in critically ill patients does not only reflect the altered input from the central or peripheral neurons, but rather a remodeling of the cardiac pacemaker cells by endotoxin and inflammatory mediators.</p>","PeriodicalId":80292,"journal":{"name":"Journal of endotoxin research","volume":"13 6","pages":"339-42"},"PeriodicalIF":0.0,"publicationDate":"2007-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/0968051907086233","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"27212429","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: 30
The role of innate immunity in the pathogenesis of asthma: evidence for the involvement of Toll-like receptor signaling. 先天免疫在哮喘发病机制中的作用:toll样受体信号参与的证据。
Journal of endotoxin research Pub Date : 2007-01-01 DOI: 10.1177/0968051907084652
Nicolas W J Schröder, Moshe Arditi
{"title":"The role of innate immunity in the pathogenesis of asthma: evidence for the involvement of Toll-like receptor signaling.","authors":"Nicolas W J Schröder,&nbsp;Moshe Arditi","doi":"10.1177/0968051907084652","DOIUrl":"https://doi.org/10.1177/0968051907084652","url":null,"abstract":"<p><p>Infectious diseases have a major impact on both the development and the severity of asthma. The rise in incidence of asthma in industrialized countries over the last decades has been attributed to increased hygiene standards as well as the concomitant usage of antibiotics, which together lower the incidence of infections. Although this point of view is supported by both clinical studies and experimental approaches in mice, an increasing body of evidence suggests that certain infectious diseases may predispose for the development of asthma, thus challenging the ;hygiene hypothesis' in its classical form. Toll-like receptors (TLRs) are centrally involved in orchestrating immune responses towards various micro-organisms. Because of this, it is tempting to speculate that signaling through TLRs may be involved in mechanisms provoking Th1- or Th2-biased immune responses and may, therefore, be an important factor in either preventing or promoting allergic airway disease. This review summarizes clinical and experimental data from mouse models focused on the impact of TLR-signaling on allergic asthma.</p>","PeriodicalId":80292,"journal":{"name":"Journal of endotoxin research","volume":"13 5","pages":"305-12"},"PeriodicalIF":0.0,"publicationDate":"2007-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/0968051907084652","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41018230","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: 31
Hematological indices, inflammatory markers and neutrophil CD64 expression: comparative trends during experimental human endotoxemia. 血液学指标、炎症标志物和中性粒细胞CD64表达:实验性人内毒素血症的比较趋势。
Journal of endotoxin research Pub Date : 2007-01-01 DOI: 10.1177/0968051907079101
Wim van der Meer, Peter Pickkers, Colin S Scott, Johannes G van der Hoeven, Jacqueline Klein Gunnewiek
{"title":"Hematological indices, inflammatory markers and neutrophil CD64 expression: comparative trends during experimental human endotoxemia.","authors":"Wim van der Meer,&nbsp;Peter Pickkers,&nbsp;Colin S Scott,&nbsp;Johannes G van der Hoeven,&nbsp;Jacqueline Klein Gunnewiek","doi":"10.1177/0968051907079101","DOIUrl":"https://doi.org/10.1177/0968051907079101","url":null,"abstract":"<p><p>CD64 is a high-affinity Fc(gamma)RI receptor expressed by activated neutrophils that has been recently evaluated as a potential sepsis parameter. In the present study, the kinetics of neutrophil membrane CD64 expression were examined during a standardized inflammatory response, using a human endotoxemia model, and compared with hematological indices, CRP, cytokines and interleukins. Ten healthy subjects received 2 ng/kg intravenous Escherichia coli lipopolysaccharide (LPS). After administration of LPS, neutrophil CD64 showed a biphasic response, characterized by a first increase from 108.5 +/- 7.5 to 133 +/- 6 AFU after 1 h (P = 0.047) and a second increase that started at 6 h and reached its maximum of 167 +/- 13 AFU at 22 h (P < 0.0001). CRP concentrations increased to 40 +/- 5 mg/dl 22 h after the administration of LPS. The cytokines and interleukins reached their maximum response within 1-2 h. The maximum values of pro-inflammatory cytokines (TNF-alpha, IFN-gamma and IL-6) correlated with the CD64 expression at 22 h after LPS administration (r(2) = 0.76, r(2) = 0.78, r(2) = 0.81, respectively, all P < 0.05), whereas this correlation was not found for the anti-inflammatory IL-10 (r(2) = 0.058, P = 0.54), suggesting that neutrophil CD64 expression might be a quantitative marker for innate immunity that could easily be used in the clinical setting.</p>","PeriodicalId":80292,"journal":{"name":"Journal of endotoxin research","volume":"13 2","pages":"94-100"},"PeriodicalIF":0.0,"publicationDate":"2007-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/0968051907079101","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26820768","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: 67
Investigation of the chemical structure and biological activity of oligosaccharides isolated from rough-type Xanthomonas campestris pv. campestris B100 lipopolysaccharide. 从粗糙型野油菜黄单胞菌 B100 脂多糖中分离的低聚糖的化学结构和生物活性研究。
Journal of endotoxin research Pub Date : 2007-01-01 DOI: 10.1177/0968051907079121
Zbigniew Kaczyński, Sebastian Braun, Buko Lindner, Karsten Niehaus, Otto Holst
{"title":"Investigation of the chemical structure and biological activity of oligosaccharides isolated from rough-type Xanthomonas campestris pv. campestris B100 lipopolysaccharide.","authors":"Zbigniew Kaczyński, Sebastian Braun, Buko Lindner, Karsten Niehaus, Otto Holst","doi":"10.1177/0968051907079121","DOIUrl":"10.1177/0968051907079121","url":null,"abstract":"<p><p>The rough-type lipopolysaccharide (LPS) of the phytopathogenic bacterium Xanthomonas campestris pv. campestris B 100 was isolated utilizing the hot phenol-water method and successively de-acylated by treatment with hydrazine and hot potassium hydroxide. Four compounds were separated by preparative high-performance anion-exchange chromatography and studied by sugar analysis and by 1D and 2D homonuclear and heteronuclear (1)H-, (13)C- and (31)P-NMR spectroscopy as well as ESI FT-MS. The two main products were a heptasaccharide and a pentasaccharide of the structures alpha-D-Manp-(1-->3)-alpha-D-Man p-(1-->4)-beta-D-Glcp-(1-->4)-alpha-D-Manp-3P -(1-->5)-alpha-Kdo-(2-->6)-beta-D-GlcpN-4P-(1-->6)-alpha-D-Glc pN-1P (1) and beta-D-Glcp-(1-->4)-alpha-D-Man p-3P-(1-->5)-alpha-Kdo-(2-->6)-beta-D-GlcpN-4 P-(1-->6)-alpha-D-GlcpN-1P (2), respectively. The products in smaller amounts were a heptasaccharide and pentasaccharide possessing the above structures plus a phosphate group at C-4 of the Kdo residue (compounds 3 and 4). Both, heptasaccharide 1 and pentasaccharide 2 were able to induce an oxidative burst in cell cultures of the non-host plant tobacco.</p>","PeriodicalId":80292,"journal":{"name":"Journal of endotoxin research","volume":"13 2","pages":"101-8"},"PeriodicalIF":0.0,"publicationDate":"2007-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/0968051907079121","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26820769","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: 15
Recombinant factor C competes against LBP to bind lipopolysaccharide and neutralizes the endotoxicity. 重组因子C与LBP竞争结合脂多糖,中和其内毒作用。
Journal of endotoxin research Pub Date : 2007-01-01 DOI: 10.1177/0968051907079573
Peng Li, Bow Ho, Jeak Ling Ding
{"title":"Recombinant factor C competes against LBP to bind lipopolysaccharide and neutralizes the endotoxicity.","authors":"Peng Li,&nbsp;Bow Ho,&nbsp;Jeak Ling Ding","doi":"10.1177/0968051907079573","DOIUrl":"https://doi.org/10.1177/0968051907079573","url":null,"abstract":"<p><p>Endotoxin-mediated inflammation and septic shock remains a grave challenge to human healthcare management. It is, therefore, a worthwhile effort to develop anti-lipopolysaccharide (LPS) strategies to prevent downstream effects. Here, we demonstrate that purified recombinant Factor C (rFC) cloned from the horseshoe crab, binds LPS with high affinity, preventing it from binding a peptide derived from the human LPS-binding protein (LBP). Factor C is an innate immune defense protein present in the horseshoe crab hemocytes. The full-length rFC was found to be more efficacious in blocking LBP-mediated downstream effects than either of the individual LPS-binding peptides (Sushi 1 and Sushi 3) derived from rFC. When added to human macrophage culture, rFC blocks the LPS-induced phosphorylation of p38, which, in turn, inhibits the consequential overexpression of TNF-alpha and IL-8. The tandem arrangement of the LPS-binding Sushi domains in the Factor C molecule appears to be required for the synergy and amplification of LPS-binding in vivo to achieve such high affinity for LPS. Thus, rFC binds and neutralizes LPS to arrest signal transduction via the p38 pathway. The rFC does not show acute cytotoxicity and could be a potential lead for further development into an endotoxin-antagonist to inhibit inflammation and septic shock.</p>","PeriodicalId":80292,"journal":{"name":"Journal of endotoxin research","volume":"13 3","pages":"150-7"},"PeriodicalIF":0.0,"publicationDate":"2007-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/0968051907079573","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26820775","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: 9
Pretreatment of curcumin attenuates coagulopathy and renal injury in LPS-induced endotoxemia. 姜黄素预处理可减轻脂多糖诱导的内毒素血症的凝血功能和肾损伤。
Journal of endotoxin research Pub Date : 2007-01-01 DOI: 10.1177/0968051907078605
Hsiang-Wen Chen, Hung-Tien Kuo, Chee-Yin Chai, Jian-Liang Ou, Rei-Cheng Yang
{"title":"Pretreatment of curcumin attenuates coagulopathy and renal injury in LPS-induced endotoxemia.","authors":"Hsiang-Wen Chen,&nbsp;Hung-Tien Kuo,&nbsp;Chee-Yin Chai,&nbsp;Jian-Liang Ou,&nbsp;Rei-Cheng Yang","doi":"10.1177/0968051907078605","DOIUrl":"https://doi.org/10.1177/0968051907078605","url":null,"abstract":"<p><p>Disseminated intravascular coagulation (DIC) is a lethal situation in severe infections, characterized by the systemic formation of microthrombi complicated with bleeding tendency and organ dysfunction. Current clinical trials are not promising. In this study, we investigated the protective effect of curcumin in a lipopolysaccharide (LPS)-induced DIC model in rats. Experimental DIC was induced by sustained infusion of LPS (10 mg/kg body weight) for 4 h through the tail vein. Curcumin (60 mg/kg body weight) was given intraperitoneally 3 h before LPS infusion. Results showed that, in vivo, curcumin reduced the mortality rate of LPS-infused rats by decreasing the circulating TNF-alpha levels and the consumption of peripheral platelets and plasma fibrinogen. Furthermore, in vivo curcumin also has the effect of preventing the formation of fibrin deposition in the glomeruli of kidney. These results reveal the therapeutic potential of curcumin in infection-related coagulopathy of DIC.</p>","PeriodicalId":80292,"journal":{"name":"Journal of endotoxin research","volume":"13 1","pages":"15-23"},"PeriodicalIF":0.0,"publicationDate":"2007-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/0968051907078605","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"26822619","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: 43
DNA and RNA autoantigens as autoadjuvants DNA和RNA自身抗原作为自身佐剂
Journal of endotoxin research Pub Date : 2006-12-01 DOI: 10.1177/09680519060120060901
L. Busconi, Christina M. Lau, Abigail S. Tabor, Melissa B. Uccellini, Zachary C Ruhe, S. Akira, G. Viglianti, I. Rifkin, A. Marshak‐Rothstein
{"title":"DNA and RNA autoantigens as autoadjuvants","authors":"L. Busconi, Christina M. Lau, Abigail S. Tabor, Melissa B. Uccellini, Zachary C Ruhe, S. Akira, G. Viglianti, I. Rifkin, A. Marshak‐Rothstein","doi":"10.1177/09680519060120060901","DOIUrl":"https://doi.org/10.1177/09680519060120060901","url":null,"abstract":"AM14 B cells are a prototype for those low affinity autoreactive B cells that routinely mature as naïve cells in peripheral lymphoid tissues. These cells express a transgene-encoded receptor specific for IgG2a and can be effectively activated by immune complexes that incorporate either mammalian DNA or mammalian RNA that has been released from dead or dying cells. Activation depends on the ability of the B-cell receptor to deliver antigen to an internal vesicular compartment containing either Toll-like receptor-9 (TLR9) or TLR7. Since TLR9 and TLR7 are thought to recognize microbial DNA and RNA preferentially, it is important to determine under what conditions mammalian DNA and RNA become effective TLR ligands, and whether the determining factor is delivery or structure. This issue has been addressed by using IgG2a mAbs to deliver immune complexes preloaded with defined fragments of DNA or RNA, or by using modified ODNs/ORNs. The data demonstrate that only certain nucleic acid sequences or structures can induce autoreactive B-cell proliferation, even when delivery to the appropriate TLR compartment is facilitated by uptake through the B-cell receptor (BCR).","PeriodicalId":80292,"journal":{"name":"Journal of endotoxin research","volume":"12 1","pages":"379 - 384"},"PeriodicalIF":0.0,"publicationDate":"2006-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1177/09680519060120060901","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"65208874","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: 23
0
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
相关产品
×
本文献相关产品
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:604180095
Book学术官方微信
小红书