“누가 이야기하는가?” - 우베 욘존의 『기념일들』의 다성적 서술

이재원 ( Lee¸ Jaewon ) 한국독일어문학회 2021 독일어문학 Vol.94 No.-

이 논문은 우베 욘존의 장편소설 『기념일들』을 특징짓는 복잡한 서술구조를 분석한다. 『기념일들』은 ‘계약’이라는 허구적 설정을 통해 다층적 차원에서의 대화적 구조로 이루어진다. 주인공 게지네와 딸 마리의 계약 차원에서는 게지네가 마리에게 자신의 가족사를 들려주는 과정에 마리가 적극적으로 개입하여 개인적이고 주관적인 기억에 대한 성찰이 이루어진다. 죽은 사람과의 계약의 차원에서는 게지네와 ‘작가 동지’에 의해 죽은 사람들을 둘러싼 독일의 과거가 서술되는 가운데 전후 독일의 집단적 기억에 대한 비판적인 성찰이 시도된다. 마리와 죽은 사람들이 서술에 적극적으로 참여하는 독립적인 ‘목소리’로 등장하기는 하지만 서술자로 보기는 어려운 반면, 게지네와 작가의 계약을 통해 두 사람이 소설 전체를 함께 서술하는 공동서술자로 나타난다. 이러한 독특한 서술상황으로 인해 기존의 서사이론의 틀에서 서술자를 확정하려는 시도는 실패할 수밖에 없다. 이는 ‘다성적 소설’에 관한 바흐친의 이론을 통해 설명할 수 있다. 다성적 소설에서는 인물이 작가의 생각을 전달하는 매체 혹은 도구가 아니라 자신의 목소리를 갖는 능동적 주체로 등장한다. 작가와 인물이 동등한 위치에서 함께 서술한다는 설정은 소설이 전지적 작가에 의해 창조된 완결된 세계가 아니라 욘존이라는 작가 개인의 하나의 견해일 뿐임을 분명히 하며 독자에게 이 대화에 참여할 것을 촉구한다. 『기념일들』은 다층적 구성과 다성적 서술을 통해 독일의 최근 역사를 일방적으로 전달하는 것을 넘어 독자에게 비판적으로 성찰하게 한다. Dieser Aufsatz analysiert das komplizierte Erzählgefüge in Uwe Johnsons Roman Jahrestage. Aus dem Leben von Gesine Cresspahl. Die Geschichten im Roman werden durch die fiktiven „Verträge“ der Hauptfigur Gesine jeweils anders erzählt: in Bezug auf ihre Tochter Marie, in Bezug auf die Toten und den Schriftsteller Johnson. Dadurch ordnet der Roman verschiedene Erzähler ihren jeweiligen Geschichten zu. Auf der Ebene des Vertrags mit Marie erzählt Gesine mündlich die Familiengeschichte Cresspahls und dabei wird das Problem der individuellen subjektiven Erinnerung reflektiert. Auf der Ebene des Vertrags mit den Toten schreiben Gesine und der Schriftsteller die Geschichte der NS-Zeit und der deutschen Teilung und dadurch versuchen sie die deutschen kollektiven Erinnerungen zu reflektieren. Dabei fungiern Marie und die Toten zwar als selbständige Stimmen, aber nicht als Erzähler. Auf der Ebene des Vertrags mit dem Autor Johnson erzählen Gesine und der Schriftsteller zusammen. Dies ist eine polyphone Erzählstruktur, bei der Figuren nicht als ein Medium oder ein Mittel des Autors, sondern als aktive Subjekte mit eigener Stimme auftreten. Durch diese Erzählweise zeigt Johnson, dass der Roman keine vom auktorialen Autor geschriebene geschlossene Welt darstellt, sondern nur ein „Entwurf“ der deutschen Geschichte, d.h. eine Ansicht eines deutschen Autors ist. Nun fordert er die Leser auf, diesen Entwurf mit ihren Meinungen zu vergleichen und aktiv zu seiner Vollendung beizutragen.

Pilot Experiment And Numerical Study Of Drying Sludge Using Superheated Steam And Heated Air

Jaewon Lee(이재원),Sanghoon Lee(이상훈),Cheolho Shin(신철호),Seonho Lee(이선호),Junhyung Park(박준형) 대한환경공학회 2021 대한환경공학회 학술발표논문집 Vol.2021 No.11

Peli3 ablation ameliorates acetaminophen-induced liver injury through inhibition of GSK3β phosphorylation and mitochondrial translocation

Lee Jaewon,Ha Jihoon,Kim Jun-Hyeong,Seo Dongyeob,Kim Minbeom,Lee Yerin,Park Seong Shil,Choi Dahee,Park Jin Seok,Lee Young Jae,Yang Siyoung,Yang Kyung-Min,Jung Su Myung,Hong Suntaek,Koo Seung-Hoi,Bae Y 생화학분자생물학회 2023 Experimental and molecular medicine Vol.55 No.-

The signaling pathways governing acetaminophen (APAP)-induced liver injury have been extensively studied. However, little is known about the ubiquitin-modifying enzymes needed for the regulation of APAP-induced liver injury. Here, we examined whether the Pellino3 protein, which has E3 ligase activity, is needed for APAP-induced liver injury and subsequently explored its molecular mechanism. Whole-body Peli3−/− knockout (KO) and adenovirus-mediated Peli3 knockdown (KD) mice showed reduced levels of centrilobular cell death, infiltration of immune cells, and biomarkers of liver injury, such as alanine aminotransferase (ALT) and aspartate aminotransferase (AST), upon APAP treatment compared to wild-type (WT) mice. Peli3 deficiency in primary hepatocytes decreased mitochondrial and lysosomal damage and reduced the mitochondrial reactive oxygen species (ROS) levels. In addition, the levels of phosphorylation at serine 9 in the cytoplasm and mitochondrial translocation of GSK3β were decreased in primary hepatocytes obtained from Peli3−/− KO mice, and these reductions were accompanied by decreases in JNK phosphorylation and mitochondrial translocation. Pellino3 bound more strongly to GSK3β compared with JNK1 and JNK2 and induced the lysine 63 (K63)-mediated polyubiquitination of GSK3β. In rescue experiments, the ectopic expression of wild-type Pellino3 in Peli3−/− KO hepatocytes restored the mitochondrial translocation of GSK3β, but this restoration was not obtained with expression of a catalytically inactive mutant of Pellino3. These findings are the first to suggest a mechanistic link between Pellino3 and APAP-induced liver injury through the modulation of GSK3β polyubiquitination.

Multimatrix distribution and bioaccumulation of legacy and emerging per- and polyfluoroalkyl substances (PFASs) in the environment of Korea

Jaewon Lee(이재원),Hyun-Kyung Lee(이현경),Yunjae Jo(조윤재),Jae-Eun Lim(임재은),Soyeon Park(박소연),Jae-Woo Lee(이재우),Young-Hee Kim(김영희),Hyo-Bang Moon(문효방) 환경독성보건학회 2019 한국독성학회 심포지움 및 학술발표회 Vol.2019 No.10

Enhanced mass transfer rate of methane in aqueous phase via methyl-functionalized SBA-15

Lee, Jaewon,Kim, Kwangmin,Chang, In Seop,Kim, Myung-Gil,Ha, Kyoung-Su,Lee, Eun Yeol,Lee, Jinwon,Kim, Choongik Elsevier 2016 Journal of molecular liquids Vol.215 No.-

<P><B>Abstract</B></P> <P>Methyl-functionalized mesoporous silica SBA-15, synthesized from tetraethyl-orthosilicate (TEOS) and methyltriethoxysilane (MTES), were employed as additives for the enhancement of volumetric mass transfer coefficient (<I>k</I> <SUB>L</SUB> <I>a</I>) of methane in aqueous solution. The surface functional group, highly ordered structure, and exceptionally high surface area exerted great influence on mass transfer rate of methane in aqueous solution. Especially, the fraction of surface functional groups controlled by adjusting the ratio of TEOS to MTES was found to be a crucial factor. Mesoporous characteristics of synthesized materials were investigated via BET surface area analysis, small angle X-ray diffraction, and FT-IR spectroscopy. At an optimal molar ratio (20:1) of TEOS and MTES, an 88% enhancement of <I>k</I> <SUB>L</SUB> <I>a</I> for methane in water was observed at 30°C.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Methyl-functionalized silica SBA-15 were synthesized and characterized. </LI> <LI> Synthesized materials were employed as additives in aqueous solution. </LI> <LI> Enhanced methane–water volumetric mass transfer coefficient was observed. </LI> <LI> 88% enhancement of <I>k</I> <SUB>L</SUB> <I>a</I> for methane in water was observed. </LI> </UL> </P>

Neuroprotective effects of MHY908, a PPAR α/γ dual agonist, in a MPTP-induced Parkinson’s disease model

Lee, Yujeong,Cho, Jung-Hyun,Lee, Seulah,Lee, Wonjong,Chang, Seung-Cheol,Chung, Hae Young,Moon, Hyung Ryong,Lee, Jaewon Elsevier 2019 Brain Research Vol.1704 No.-

<P><B>Abstract</B></P> <P>Peroxisome proliferator-activated receptors (PPARs) are nuclear receptors and are considered promising therapeutic targets in several neurodegenerative diseases. A number of PPAR agonists have been shown to have neuroprotective properties in the presence of oxidative stress, neuroinflammatory response, and apoptosis in various neurodegenerative disease. MHY908 is a novel PPAR α/γ dual agonist, which has been shown to suppress inflammatory response and attenuate insulin resistance in aged rats and db/db mice. Here, we evaluated the neuroprotective effects of MHY908 in a 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-induced mouse model of PD. Pretreatment with MHY908 attenuated MPTP-induced dopaminergic neuronal loss and motor deficit. MPTP-induced glial activations were mitigated by MHY908 in the nigrostriatal pathway, and MHY908 effectively blocked 1-methyl-4-phenylpyridinium (MPP<SUP>+</SUP>)-induced cell death and ROS production in SH-SY5Y neuroblastoma cells. Further study revealed MHY908 inhibited MPP<SUP>+</SUP>-induced astroglial activation by suppressing NF-κB signaling in primary astrocytes. Taken together, the present study suggests that PPAR α/γ dual agonists be considered potentially useful preventions for PD and other neurodegenerative diseases associated with neuroinflammation.</P> <P><B>Highlight</B></P> <P> <UL> <LI> MHY908 attenuated MPTP-induced motor deficits and dopaminergic neuronal death. </LI> <LI> MHY908 also ameliorated MPTP-induced glial activation in the STR and SN. </LI> <LI> MHY908 pretreatment protected SH-SY5Y neuroblastoma cells against MPP<SUP>+</SUP> toxicity. </LI> <LI> Pretreatment of MHY908 inhibited MPP<SUP>+</SUP>-induced ROS generation. </LI> <LI> MHY908 treatment attenuated MPP<SUP>+</SUP>-induced primary astrocyte activation and nuclear translocation of NF-κB. </LI> </UL> </P>

Hypoxic priming of mESCs accelerates vascular-lineage differentiation through HIF1-mediated inverse regulation of Oct4 and VEGF

Lee, Sae-Won,Jeong, Han-Kyul,Lee, Ji-Young,Yang, Jimin,Lee, Eun Ju,Kim, Su-Yeon,Youn, Seock-Won,Lee, Jaewon,Kim, Woo Jean,Kim, Kyu-Won,Lim, Jeong Mook,Park, Jong-Wan,Park, Young-Bae,Kim, Hyo-Soo WILEY-VCH Verlag 2012 EMBO molecular medicine Vol.4 No.9

<P>Hypoxic microenvironment plays an important role in determining stem cell fates. However, it is controversial to which direction between self-renewal and differentiation the hypoxia drives the stem cells. Here, we investigated whether a short exposure to hypoxia (termed ‘hypoxic-priming’) efficiently directed and promoted mouse embryonic stem cells (mESCs) to differentiate into vascular-lineage. During spontaneous differentiation of embryoid bodies (EBs), hypoxic region was observed inside EB spheroids even under normoxic conditions. Indeed, hypoxia-primed EBs more efficiently differentiated into cells of vascular-lineage, than normoxic EBs did. We found that hypoxia suppressed Oct4 expression via direct binding of HIF-1 to reverse hypoxia-responsive elements (rHREs) in the Oct4 promoter. Furthermore, vascular endothelial growth factor (VEGF) was highly upregulated in hypoxia-primed EBs, which differentiated towards endothelial cells in the absence of exogenous VEGF. Interestingly, this differentiation was abolished by the HIF-1 or VEGF blocking. <I>In vivo</I> transplantation of hypoxia-primed EBs into mice ischemic limb elicited enhanced vessel differentiation. Collectively, our findings identify that hypoxia enhanced ESC differentiation by HIF-1-mediated inverse regulation of Oct4 and VEGF, which is a novel pathway to promote vascular-lineage differentiation.</P>

Learning, memory deficits, and impaired neuronal maturation attributed to acrylamide

Lee, Seulah,Park, Hee Ra,Lee, Joo Yeon,Cho, Jung-Hyun,Song, Hye Min,Kim, Ah Hyun,Lee, Wonjong,Lee, Yujeong,Chang, Seung-Cheol,Kim, Hyung Sik,Lee, Jaewon TAYLOR & FRANCIS 2018 JOURNAL OF TOXICOLOGY AND ENVIRONMENTAL HEALTH PAR Vol.81 No.9

<P>Acrylamide (ACR) is a neurotoxin known to produce neurotoxicity characterized by ataxia, skeletal muscle weakness, cognitive impairment, and numbness of the extremities. Previously, investigators reported that high-dose (50mg/kg) ACR impaired hippocampal neurogenesis and increased neural progenitor cell death; however, the influence of subchronic environmentally relevant low dose-(2, 20, or 200g/kg) ACRs have not been examined in adult neurogenesis or cognitive function in mice. Accordingly, the aim of the present study was to investigate whether low-dose ACR adversely affected mouse hippocampal neurogenesis and neurocognitive functions. Male C57BL/6 mice were orally administered vehicle or ACR at 2, 20, or 200g/kg/day for 4weeks. ACR did not significantly alter the number of newly generated cells or produce neuroinflammation or neuronal loss in hippocampi. However, behavioral studies revealed that 200g/kg ACR produced learning and memory impairment. Furthermore, incubation of ACR with primary cultured neurons during the developmental stage was found to delay neuronal maturation without affecting cell viability indicating the presence of developmental neurotoxicity. These findings indicate that although exposure to in vivo low-dose ACR daily for 4weeks exerted no apparent marked effect on hippocampal neurogenesis, in vitro observations in primary cultured neurons noted adverse effects on learning and memory impairment suggestive of neurotoxic actions.</P>

The Influence of Face Shields on the Quality of Colonoscopy in the Era of the COVID-19 Pandemic

Lee Jin Wook,Lee Hyo Jeong,Kim Dae Sung,Yoon Jiyoung,Hong Seung Wook,Hwang Ha Won,Lee Jong-Soo,Kim Gwang-Un,Lee Sinwon,Choe Jaewon,Park Jin Hwa,Yang Dong-Hoon,Byeon Jeong-Sik 거트앤리버 소화기연관학회협의회 2022 Gut and Liver Vol.16 No.3

Background/Aims: The worldwide coronavirus disease 2019 pandemic has led endoscopists to use personal protective equipment (PPE) for infection prevention. This study aimed to investigate whether wearing a face shield as PPE affects the quality of colonoscopy. Methods: We reviewed the medical records and colonoscopy findings of patients who underwent colonoscopies at Asan Medical Center, Korea from March 10 to May 31, 2020. The colonoscopies in this study were performed by five gastroenterology fellows and four expert endoscopists. We compared colonoscopy quality indicators, such as withdrawal time, adenoma detection rate (ADR), mean number of adenomas per colonoscopy (APC), polypectomy time, and polypectomy adverse events, both before and after face shields were added as PPE on April 13, 2020. Results: Of the 1,344 colonoscopies analyzed, 715 and 629 were performed before and after the introduction of face shields, respectively. The median withdrawal time was similar between the face shield and no-face shield groups (8.72 minutes vs 8.68 minutes, p=0.816), as was the ADR (41.5% vs 39.8%, p=0.605) and APC (0.72 vs 0.77, p=0.510). Polypectomy-associated quality indicators, such as polypectomy time and polypectomy adverse events were also not different between the groups. Quality indicators were not different between the face shield and no-face shield groups of gastroenterology fellows, or of expert endoscopists. Conclusions: Colonoscopy performance was not unfavorably affected by the use of a face shield. PPE, including face shields, can be recommended without a concern about colonoscopy quality deterioration.

Portal vein reconstruction in pediatric liver transplantation using end-to-side jump graft: A case report

Jaewon Lee,Nam-Joon Yi,Jae-Yoon Kim,Hyun Hwa Choi,Jiyoung Kim,Sola Lee,Su young Hong,Ung Sik Jin,Seong-Mi Yang,Jeong-Moo Lee,Suk Kyun Hong,YoungRok Choi,Kwang-Woong Lee,Kyung-Suk Suh 한국간담췌외과학회 2023 Annals of hepato-biliary-pancreatic surgery Vol.27 No.3

Attenuated portal vein (PV) flow is challenging in pediatric liver transplantation (LT) because it is unsuitable for classic end-to-end jump graft reconstruction from a small superior mesenteric vein (SMV). We thus introduce a novel technique of an end-to-side jump graft from SMV during pediatric LT using an adult partial liver graft. We successfully performed two cases of end-to-side retropancreatic jump graft using an iliac vein graft for PV reconstruction. One patient was a 2-year-old boy with hepatoblastoma and a Yerdel grade 3 PV thrombosis who underwent split LT. Another patient was an 8-month-old girl who had biliary atresia and PV hypoplasia with stenosis on the confluence level of the SMV; she underwent retransplantation because of graft failure related to PV thrombosis. After native PV was resected at the SMV confluence level, an end-to-side reconstruction was done from the proximal SMV to an interposition iliac vein. The interposition vein graft through posterior to the pancreas was obliquely anastomosed to the graft PV. There was no PV related complication during the follow-up period. Using a jump vascular graft in an end-to-side manner to connect the small native SMV and the large graft PV is a feasible treatment option in pediatric recipients with inadequate portal flow due to thrombosis or hypoplasia of the PV.