http://chineseinput.net/에서 pinyin(병음)방식으로 중국어를 변환할 수 있습니다.
변환된 중국어를 복사하여 사용하시면 됩니다.
김만권(Man Kwon Kim) 한국철학회 2021 철학 Vol.- No.147
이 논문의 목적은 21세기에 등장한 ‘탈진실’ 시대의 정치가 어떻게 민주주의 사회에서 구축될 수 있었는지 정치철학적 입장에서 밝히는 것이다. 이를 위해 첫째, 적용 가능한 민주주의 모델을 정치철학적 견지에서 점검한다. 둘째, 탈진실화와 연관성이 깊은 모델로서 샹탈 무페의 논쟁적 민주주의를 점검한다. 셋째, 논쟁적 민주주의 모델이 강조하는 헤게모니 투쟁이 탈진실화와 갖는 친화력을 보여주는 정치현상으로서 21세기 포퓰리즘을 살펴본다. 넷째, 우리사회에서 일어나고 있는 탈진실화의 이데올로기적 요소로서 ‘분단모순’과 ‘신자유주의’를 분석한다. 이를 바탕으로 우리사회에서 ‘탈진실’ 정치가 구축되는 과정에서, 특히 이데올로기가 동원의 정치와 연관하여 어떤 영향을 미쳤는지 밝힌다. 마지막으로 탈진실의 시대에 무페의 논쟁적 민주주의 모델이 지닌 정치철학적 의미를 평가한다. Taking the perspective of political philosophy, this paper delves into the question of how the politics of post-truth emerged in the early 21st century has become prevailed in the contemporary democracies. To answer this question, it develops a five fold discussion: first, it examines four models of democracy provided in the field of political philosophy; second, it specifically explores the agonistic model of democracy provided by Chantal Mouffe as a theory which is able to explain the politics of post-truth; third, as the significant element of post-truth it critically discusses the affinity between the struggle for hegemony, which Mouffe emphasizes, and populism, which is globally prevailed in the 21st century; fourth, it investigates anti-communism and neo-liberalism as the ideological elements provoking the politics of post-truth in South Korea; finally, it evaluates political and philosophical implications of agonistic model of democracy in the age of post-truth.
Li, H.,Kilpelä,inen, T. O.,Liu, C.,Zhu, J.,Liu, Y.,Hu, C.,Yang, Z.,Zhang, W.,Bao, W.,Cha, S.,Wu, Y.,Yang, T.,Sekine, A.,Choi, B. Y.,Yajnik, C. S.,Zhou, D.,Takeuchi, F.,Yamamoto, K.,Chan, J. C.,Man Springer-Verlag 2012 Diabetologia Vol.55 No.4
<P><B>Aims/hypothesis</B></P><P><I>FTO</I> harbours the strongest known obesity-susceptibility locus in Europeans. While there is growing evidence for a role for <I>FTO</I> in obesity risk in Asians, its association with type 2 diabetes, independently of BMI, remains inconsistent. To test whether there is an association of the <I>FTO</I> locus with obesity and type 2 diabetes, we conducted a meta-analysis of 32 populations including 96,551 East and South Asians.</P><P><B>Methods</B></P><P>All studies published on the association between <I>FTO</I>-rs9939609 (or proxy [<I>r</I><SUP>2</SUP> > 0.98]) and BMI, obesity or type 2 diabetes in East or South Asians were invited. Each study group analysed their data according to a standardised analysis plan. Association with type 2 diabetes was also adjusted for BMI. Random-effects meta-analyses were performed to pool all effect sizes.</P><P><B>Results</B></P><P>The <I>FTO</I>-rs9939609 minor allele increased risk of obesity by 1.25-fold/allele (<I>p</I> = 9.0 × 10<SUP>−19</SUP>), overweight by 1.13-fold/allele (<I>p</I> = 1.0 × 10<SUP>−11</SUP>) and type 2 diabetes by 1.15-fold/allele (<I>p</I> = 5.5 × 10<SUP>−8</SUP>). The association with type 2 diabetes was attenuated after adjustment for BMI (OR 1.10-fold/allele, <I>p</I> = 6.6 × 10<SUP>−5</SUP>). The <I>FTO</I>-rs9939609 minor allele increased BMI by 0.26 kg/m<SUP>2</SUP> per allele (<I>p</I> = 2.8 × 10<SUP>−17</SUP>), WHR by 0.003/allele (<I>p</I> = 1.2 × 10<SUP>−6</SUP>), and body fat percentage by 0.31%/allele (<I>p</I> = 0.0005). Associations were similar using dominant models. While the minor allele is less common in East Asians (12–20%) than South Asians (30–33%), the effect of <I>FTO</I> variation on obesity-related traits and type 2 diabetes was similar in the two populations.</P><P><B>Conclusions/interpretation</B></P><P><I>FTO</I> is associated with increased risk of obesity and type 2 diabetes, with effect sizes similar in East and South Asians and similar to those observed in Europeans. Furthermore, <I>FTO</I> is also associated with type 2 diabetes independently of BMI.</P><P><B>Electronic supplementary material</B></P><P>The online version of this article (doi:10.1007/s00125-011-2370-7) contains peer-reviewed but unedited supplementary material, which is available to authorised users.</P>
Informing direct neutron capture on tin isotopes near the N=82 shell closure
Manning, B.,Arbanas, G.,Cizewski, J. A.,Kozub, R. L.,Ahn, S.,Allmond, J. M.,Bardayan, D. W.,Chae, K. Y.,Chipps, K. A.,Howard, M. E.,Jones, K. L.,Liang, J. F.,Matos, M.,Nesaraja, C. D.,Nunes, F. M.,O'M American Physical Society 2019 Physical Review C Vol.99 No.4
Ab initiostudy of the oxidation on vicinal Si(001) surfaces: The step-selective oxidation
Yeo, Jin-Nam,Jee, Gang Man,Yu, B. D.,Kim, Hanchul,Chung, C.-H.,Yeom, H. W.,Lyo, I.-W.,Kong, Ki-jeong,Miyamoto, Y.,Sugino, O.,Ohno, T. American Physical Society 2007 Physical review. B, Condensed matter and materials Vol.76 No.11
Ebolavirus VP35 suppresses IFN production from conventional but not plasmacytoid dendritic cells
Leung, Lawrence W,Park, Man‐,Seong,Martinez, Osvaldo,Valmas, Charalampos,Ló,pez, Carolina B,Basler, Christopher F Nature Publishing Group 2011 Immunology and cell biology Vol.89 No.7
<P>Ebolaviruses naturally infect a wide variety of cells including macrophages and dendritic cells (DCs), and the resulting cytokine and interferon‐α/β (IFN) responses of infected cells are thought to influence viral pathogenesis. The VP35 protein impairs RIG‐I‐like receptor‐dependent signaling to inhibit IFN production, and this function has been suggested to promote the ineffective host immune response characteristic of ebolavirus infection. To assess the impact of VP35 on innate immunity in biologically relevant primary cells, we used a recombinant Newcastle disease virus encoding VP35 (NDV/VP35) to infect macrophages and conventional DCs, which primarily respond to RNA virus infection via RIG‐I‐like pathways. VP35 suppressed not only IFN but also tumor necrosis factor (TNF)‐α secretion, which are normally produced from these cells upon NDV infection. Additionally, in cells susceptible to the activity of VP35, IRF7 activation is impaired. In contrast, NDV/VP35 infection of plasmacytoid DCs, which activate IRF7 and produce IFN through TLR‐dependent signaling, leads to robust IFN production. When plasmacytoid DCs deficient for TLR signaling were infected, NDV/VP35 was able to inhibit IFN production. Consistent with this, VP35 was less able to inhibit TLR‐dependent versus RIG‐I‐dependent signaling <I>in vitro</I>. These data demonstrate that ebolavirus VP35 suppresses both IFN and cytokine production in multiple primary human cell types. However, cells that utilize the TLR pathway can circumvent this inhibition, suggesting that the presence of multiple viral sensors enables the host to overcome viral immune evasion mechanisms.</P>