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‘코로나19’ 위기대응 공식 채널로서 17개 광역자치단체 홈페이지 비교 연구
송철민 ( Song Chulmin ),이지화 ( Lee Jihwa ),허지수 ( Heo Jisu ),이성미 ( Lee Sungmi ),이서현 ( Lee Seohyeon ) 한국지역언론학회 2021 언론과학연구 Vol.21 No.1
본 연구에서는 ‘코로나19’ 감염병 위기 상황에서 17개 광역자치단체가 위기대응 공식 채널로서 홈페이지를 어떻게 활용하고 있는지 살펴보았다. 분석을 위해 홈페이지 기능을 정보제공, 상호작용, 편의 증진, 기타로 구분하였다. 분석 결과 대부분의 광역자치단체는 발생 동향, 예방수칙, 방역 현황 등 감염병 예방을 위해 필요한 정보들을 신속하고 일관되게 전달하고 있는 것으로 나타났다. 하지만 대부분의 정보가 일방향적으로 제공되고 있어 홈페이지의 장점이라 할 수 있는 지역주민과의 쌍방향 소통 기능은 미흡한 것으로 확인되었다. 편의 증진 부분에서는 카드뉴스, 지도 등 다양한 방법을 활용하여 관련 정보에 대한 이해를 높이기 위해 노력하고 있었다. 하지만 일부 광역자치단체에서는 보도자료를 통해 텍스트 위주의 정보를 제공하는 등 지역주민들의 정보 접근 용이성을 떨어뜨리는 것으로 나타났다. 전체적으로 광역자치단체들은 위기정보 제공은 잘하고 있으나 홈페이지의 상호작용 기능은 충분히 활용하지 못하고 있음을 확인했다. The purpose of this study is to examine how 17 regional governments have used a webpage as an official crisis response channel during COVID-19. For this study, we separated the webpage functions into categories such as information provision, interaction, and convenience enhancement. Our analysis showed that most of the regional governments promptly and consistently delivered information necessary for infection prevention, such as outbreak trends, precautions, and quarantine status. However, the regional governments provided most of the crisis information in one direction; the two-way communication function with residents, which is the advantage of using a webpage, was insufficient. In terms of convenience enhancement, governments tried to increase the residents’ understanding of crisis information by using various methods, such as Card News and maps. However, some regional governments provided text-oriented information through press releases, which have limited accessibility. Overall, we found that most of the regional governments primarily focused on providing crisis information and did not actively utilize the interactive functions of the webpage.
Lee, Ji Yoon,Chung, Jihwa,Kim, Kyoung Hwa,An, Shung Hyun,Kim, Minsuk,Park, Junbeom,Kwon, Kihwan Elsevier 2018 Atherosclerosis Vol.270 No.-
<P><B>Abstract</B></P> <P><B>Background and aims</B></P> <P>Vascular endothelial cells (ECs) are exposed to fluid shear stress (FSS), which modulates vascular pathophysiology. Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) is crucial in endothelial dysfunction and atherosclerosis. We elucidated the mechanism regulating LOX-1 expression in ECs by FSS.</P> <P><B>Methods</B></P> <P>Human umbilical vein endothelial cells were exposed to laminar shear stress (LSS) of indicated intensities using a unidirectional steady flow, or to oscillatory shear stress (OSS) using a bidirectional disturbed flow. <I>In vivo</I> studies were performed in a mouse model of partial carotid ligation and human pulmonary artery sections.</P> <P><B>Results</B></P> <P>Within ECs, OSS upregulated LOX-1 expression, while LSS (20 dyne/cm<SUP>2</SUP>) downregulated it. We confirmed that OSS-induced LOX-1 expression was suppressed when the mechanotransduction was inhibited by knockdown of the mechanosensory complex. In addition, we demonstrated that Kruppel-like factor 2 (KLF2) has an inhibitory role on OSS-induced LOX-1 expression. Next, we determined that activator protein-1 (AP-1) was the key transcription factor inducing LOX-1 expression by OSS, which was inhibited by KLF2 overexpression. To explore whether the intensity of LSS affects LOX-1 expression, we tested three different intensities (20, 60, and 120 dyne/cm<SUP>2</SUP>) of LSS. We observed higher LOX-1 expression with high shear stresses of 120 dyne/cm<SUP>2</SUP> compared to 20 and 60 dyne/cm<SUP>2</SUP>, with OSS-like KLF2-AP-1 signaling patterns. Furthermore, ECs within disturbed flow regions showed upregulated LOX-1 expression <I>in vivo</I>.</P> <P><B>Conclusions</B></P> <P>We concluded that LOX-1 expression on ECs is regulated via FSS depending on its intensity as well as pattern. Furthermore, this is mediated through the KLF2-AP1 pathway of mechanotransduction.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Fluid shear stress regulates LOX-1 expression in vascular ECs through mechanosensory complex. </LI> <LI> KLF2-AP-1 pathway is involved in LOX-1 expression in ECs by FSS. </LI> <LI> Pathologically high shear stress exceeding the normal physiological range acts similar to OSS by inducing LOX-1 expression through the KLF2-AP-1 pathway. </LI> <LI> In a mouse model of partial carotid artery ligation, LOX-1 expression in ECs is upregulated in regions of pro-atherogenic disturbed flow. </LI> <LI> In human pulmonary artery sections, disturbed flow regions showed upregulated LOX-1 expression. </LI> </UL> </P>