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Kwon, So-Youn,Bae, Ok-Nam,Noh, Ji-Yoon,Kim, Keunyoung,Kang, Seojin,Shin, Young-Jun,Lim, Kyung-Min,Chung, Jin-Ho U.S. Dept. of Health, Education, and Welfare, Publ 2015 Environmental health perspectives Vol.123 No.2
<P>Background: Nephrotoxicity associated with lead poisoning has been frequently reported in epidemiological studies, but the underlying mechanisms have not been fully described.</P><P>Objectives: We examined the role of erythrocytes, one of the major lead reservoirs, in lead-associated nephrotoxicity.</P><P>Methods and results: Co-incubation of lead-exposed human erythrocytes with HK-2 human renal proximal tubular cells resulted in renal tubular cytotoxicity, suggesting a role of erythrocytes in lead-induced nephrotoxicity. Morphological and flow cytometric analyses revealed that HK-2 cells actively phagocytized lead-exposed erythrocytes, which was associated with phosphatidylserine (PS) externalization on the erythrocyte membrane and generation of PS-bearing microvesicles. Increased oxidative stress and up-regulation of nephrotoxic biomarkers, such as NGAL, were observed in HK-2 cells undergoing erythrophagocytosis. Moreover, TGF-β, a marker of fibrosis, was also significantly up-regulated. We examined the significance of erythrophagocytosis in lead-induced nephrotoxicity in rats exposed to lead via drinking water for 12 weeks. We observed iron deposition and generation of oxidative stress in renal tissues of lead-exposed rats, as well as the histopathological alterations such as tubulointerstitial lesions, fibrosis, and up-regulation of KIM-1, NGAL, and TGF-β.</P><P>Conclusions: Our data strongly suggest that erythrophagocytosis and subsequent iron deposition in renal tubular cells could significantly enhance nephrotoxicity following lead exposure, providing insight on lead-associated kidney damages.</P><P>Citation: Kwon SY, Bae ON, Noh JY, Kim K, Kang S, Shin YJ, Lim KM, Chung JH. 2015. Erythrophagocytosis of lead-exposed erythrocytes by renal tubular cells: possible role in lead-induced nephrotoxicity. Environ Health Perspect 123:120–127; http://dx.doi.org/10.1289/ehp.1408094</P>
EFL Middle School Learners’ Lexical Profile and Academic Motivation During a Reading Course
Seojin Kim,Yuah V. 언어과학회 2018 언어과학연구 Vol.0 No.85
The purpose of the study is to examine 84 middle school learners’ lexical profiles, academic motivation, and post-instructional reflections of a reading course. After the learners were involved in reading themebased books based on Lexile levels and writing for post-reading controlled writing tasks, the learners were asked to respond to questionnaires on academic motivation and a reflection of the course. The results were triangulated by semi-structured interviews with 14 learners. An analysis of learner writing products with RANGE GSL/AWL indicated that their percentage of words at the 2nd 1,000 and ‘Not in the list’ level had increased at a statistically significant level. Academic motivation analyzed with paired t-tests indicated a significant difference only for ‘amotivation’ by the end of the semester. Learners’ reflection of the course provided further understanding of the reading course for improved reading ability and motivation.
Kim, Se-Hwan,Lim, Kyung-Min,Noh, Ji-Yoon,Kim, Keunyoung,Kang, Seojin,Chang, Youn Kyeong,Shin, Sue,Chung, Jin-Ho Academic Press 2011 TOXICOLOGICAL SCIENCES Vol.124 No.1
<P>Thrombotic risk associated with chemotherapy including doxorubicin (DOX) has been frequently reported; yet, the exact mechanism is not fully understood. Here, we report that DOX can induce procoagulant activity in platelets, an important contributor to thrombus formation. In human platelets, DOX increased phosphatidylserine (PS) exposure and PS-bearing microparticle (MP) generation. Consistently, DOX-treated platelets and generated MPs induced thrombin generation, a representative marker for procoagulant activity. DOX-induced PS exposure appeared to be from intracellular Ca2? increase and ATP depletion, which resulted in the activation of scramblase and inhibition of flippase. Along with this, apoptosis was induced by DOX as determined by the dissipation of mitochondrial membrane potential (δψ), cytochrome c release, Bax translocation, and caspase-3 activation. A Ca2? chelator ethylene glycol tetraacetic acid, caspase inhibitor Q-VD-OPh, and antioxidants (vitamin C and trolox) can attenuate DOX-induced PS exposure and procoagulant activity significantly, suggesting that Ca2?, apoptosis, and reactive oxygen species (ROS) were involved in DOX-enhanced procoagulant activity. Importantly, rat in vivo thrombosis model demonstrated that DOX could manifest prothrombotic effects through the mediation of platelet procoagulant activity, which was accompanied by increased PS exposure and δψ dissipation in platelets.</P>
Seojin Stacey Lee,Joonkyung Kim,Yaeri Kim,Kiwan Park 글로벌지식마케팅경영학회 2023 Global Marketing Conference Vol.2023 No.07
The spread of COVID-19 changes consumer preferences and behaviors greatly across the world. Extant literature has demonstrated that when there is a threat to disease, people stay away from those who do not seem healthy as they can be potentially infectious. Based on the previous literature, this research shows that individuals exposed to disease threat avoid products of which designs are high in visual complexity. When disease threat was present, individuals had lower purchase intention for products with complex designs. The perceived uncleanliness mediated the effect of visual complexity and disease threat on purchase intention. The findings provide a novel insight into the effect of disease salience on consumer perception of product design.
Kim, Keunyoung,Bae, Ok-Nam,Koh, Sung-Hee,Kang, Seojin,Lim, Kyung-Min,Noh, Ji-Yoon,Shin, Sue,Kim, Inho,Chung, Jin-Ho ACADEMIC PRESS 2015 TOXICOLOGICAL SCIENCES Vol.147 No.2
<P>Potential risk of high-dose vitamin C consumption is often ignored. Recently, gram-dose vitamin C is being intravenously injected for the treatment of cancer, which can expose circulating blood cells to extremely high concentrations of vitamin C. As well as platelets, red blood cells (RBCs) can actively participate in thrombosis through procoagulant activation. Here, we examined the procoagulant and prothrombotic risks associated with the intravenous injection of gram-dose vitamin C. Vitamin C (0.5–5 mM) increased procoagulant activity of freshly isolated human RBCs via the externalization of phosphatidylserine (PS) to outer cellular membrane and the formation of PS-bearing microvesicles. PS exposure was induced by the dysregulation of key enzymes for the maintenance of membrane phospholipid asymmetry, which was from vitamin C-induced oxidative stress, and resultant disruption of calcium and thiol homeostasis. Indeed, the intravenous injection of vitamin C (0.5–1.0 g/kg) in rats <I>in vivo</I> significantly increased thrombosis. Notably, the prothrombotic effects of vitamin C were more prominent in RBCs isolated from cancer patients, who are at increased risks of thrombotic events. Vitamin C-induced procoagulant and prothrombotic activation of RBCs, and increased thrombosis <I>in vivo</I>. RBCs from cancer patients exhibited increased sensitivity to the prothrombotic effects of vitamin C, reflecting that intravenous gram-dose vitamin C therapy needs to be carefully revisited.</P>