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Lim, Mi-Hee,Jeung, In Cheul,Jeong, Jinyoung,Yoon, Sung-Jin,Lee, Sang-Hyun,Park, Jongjin,Kang, Yu-Seon,Lee, Hansu,Park, Young-Jun,Lee, Hee Gu,Lee, Seon-Jin,Han, Baek Soo,Song, Nam Woong,Lee, Sang Chul Elsevier 2016 Acta Biomaterialia: structure-property-function re Vol.46 No.-
<P><B>Abstract</B></P> <P>Despite the rapid expansion of the biomedical applications of graphene oxide (GO), safety issues related to GO, particularly with regard to its effects on vascular endothelial cells (ECs), have been poorly evaluated. To explore possible GO-mediated vasculature cytotoxicity and determine lateral GO size relevance, we constructed four types of GO: micrometer-sized GO (MGO; 1089.9±135.3nm), submicrometer-sized GO (SGO; 390.2±51.4nm), nanometer-sized GO (NGO; 65.5±16.3nm), and graphene quantum dots (GQDs). All types but GQD showed a significant decrease in cellular viability in a dose-dependent manner. Notably, SGO or NGO, but not MGO, potently induced apoptosis while causing no detectable necrosis. Subsequently, SGO or NGO markedly induced autophagy through a process dependent on the c-Jun N-terminal kinase (JNK)-mediated phosphorylation of B-cell lymphoma 2 (Bcl-2), leading to the dissociation of Beclin-1 from the Beclin-1–Bcl-2 complex. Autophagy suppression attenuated the SGO- or NGO-induced apoptotic cell death of ECs, suggesting that SGO- or NGO-induced cytotoxicity is associated with autophagy. Moreover, SGO or NGO significantly induced increased intracellular calcium ion (Ca<SUP>2+</SUP>) levels. Intracellular Ca<SUP>2+</SUP> chelation with BAPTA-AM significantly attenuated microtubule-associated protein 1A/1B-light chain 3-II accumulation and JNK phosphorylation, resulting in reduced autophagy. Furthermore, we found that SGO or NGO induced Ca<SUP>2+</SUP> release from the endoplasmic reticulum through the PLC β3/IP<SUB>3</SUB>/IP<SUB>3</SUB>R signaling axis. These results elucidate the mechanism underlying the size-dependent cytotoxicity of GOs in the vasculature and may facilitate the development of a safer biomedical application of GOs.</P> <P><B>Statement of Significance</B></P> <P>Graphene oxide (GO) have received considerable attention with respect to their utilization in biomedical applications. However, GO-related safety issues concerning human vasculature are very limited. In this manuscript, we report for the first time the differential size-related biological effects of GOs on endothelial cells (ECs). Notably, Subnanometer- and nanometersized GOs induce apoptotic death in ECs via autophagy activation. We propose a molecular mechanism for the GO-induced autophagic cell death through the PLCβ3/IP3/Ca<SUP>2+</SUP>/JNK signaling axis. Our findings could be provide a better understanding of the GO sizedependent cytotoxicity in vasculature and facilitate the future development of safer biomedical applications of GOs.</P> <P><B>Graphical abstract</B></P> <P>[DISPLAY OMISSION]</P>
He, Yinsheng,Yoo, Keun-Bong,Park, Joong Cheul,Lee, Byung-Ho,Yoon, Jeong-Bong,Kim, Jung-Gu,Shin, Keesam Elsevier 2018 Materials characterization Vol.142 No.-
<P><B>Abstract</B></P> <P>This study investigated the corrosion behavior and underline mechanisms of low alloy steels with a minor addition of 0.4 wt% Cu, 0.2 wt% Ni, 0.1 wt% Sb and 0.05 wt% Co developed for a flue gas desulfurization (FGD) system. Corrosion tests were carried out in an aggressive solution of 16.9 vol% H<SUB>2</SUB>SO<SUB>4</SUB> + 0.35 vol% HCl + Bal. H<SUB>2</SUB>O at 60 °C for up to 48 h. The experimental results revealed enrichment of the additional elements (Cu, Sb and Ni) in the corrosion layer, whose concentration increased with test time. As the concentrations of Cu increased, the crystallization and growth of the Cu particles (from several nm to 320 nm)) within the corrosion layer was accelerated. At the initial stage of the test, a continuous amorphous layer rich with the additional elements formed and covered the surface of the steel, which then gradually developed defects, pores and cracks, as the crystallization and growth of Cu particles with the elapse of time. The results indicated that the corrosion resistance of the low alloy steel depends on the existence form of Cu in the corrosion layer, i.e., as solute atoms or as nanoparticles strengthened the corrosion layer and increased corrosion resistance. As the coarsening of Cu particles weakened the corrosion layer and deteriorated the corrosion resistance.</P> <P><B>Highlights</B></P> <P> <UL> <LI> Corrosion mechanism of low alloy steels for flue gas desulfurization was studied. </LI> <LI> An amorphous corrosion layer enriched with Fe, O, S formed on the blank specimen. </LI> <LI> Added Cu concentrated, crystallized and grown to particles in corrosion layer. </LI> <LI> Corrosion resistance of the steels depended on the form of Cu in corrosion layer. </LI> <LI> Sb addition slows the crystallization and growth of Cu particles in corrosion layer. </LI> </UL> </P>
Mitomycin-C에 의한 용혈성 요독 증후군(Hemolytic Uremic Syndrome) 1예
한상훤,김경욱,김철홍,박재홍,이민재,김구,양윤식,손창학 인제대학교 백병원 2003 仁濟醫學 Vol.24 No.1
Hemolytic Uremic Syndrome(HUS) is a clinical syndrome characterized by the presence of microangiopathic hemolytic anemia, thrombocytopenia and acute renal failure. This syndrome spontaneously arise in a few patients with advanced cancer, but it is more commonly related to the use of certain chemotherapeutic agents. Mitomycin-C is the most common causative agent. Hemolytic uremic syndrome may be induced 4 to 8 weeks after administration of mitomycin-C, and it usually develop in clinical remission state of cancer. We report a patient who developed HUS after adjuvant chemotherapy containing mitomycin-C for gastric cancer.
Kang, Young-Ju,Jeung, In Cheul,Park, Arum,Park, Young-Jun,Jung, Haiyoung,Kim, Tae-Don,Lee, Hee Gu,Choi, Inpyo,Yoon, Suk Ran Oxford University Press 2014 Human reproduction Vol.29 No.10
<P><B>STUDY QUESTION</B></P><P>Is the decreased natural killer (NK) cell cytolytic activity in the peritoneal fluid (PF) of endometriosis patients due to primary cytokine activity?</P><P><B>SUMMARY ANSWER</B></P><P>An increased level of interleukin-6 (IL-6) in the PF of patients with endometriosis suppresses NK cell cytolytic activity by down-regulating cytolytic granule components, such as granzyme B and perforin, through the modulation of Src homology region 2-containing protein tyrosine phosphatase-2 (SHP-2) expression.</P><P><B>WHAT IS ALREADY KNOWN</B></P><P>Endometriosis is known to be related to a defect in NK cell cytolytic activity. Additionally, the levels of inflammatory cytokines are elevated in the PF of women with endometriosis.</P><P><B>STUDY DESIGN, SIZE, DURATION</B></P><P>The effects of PF on the differentiation and functional activity of NK cells were investigated in patients with or without endometriosis, and cytokines that reduce NK cell cytolytic activity in endometriosis patients were examined. The study included women who underwent laparoscopic examination for the diagnosis of endometriosis from August 2012 to July 2013 (33 women with, and 15 women without, endometriosis).</P><P><B>PARTICIPANTS/MATERIALS, SETTING, METHODS</B></P><P>Women of reproductive age (20–40 years old) who underwent laparoscopic examination for endometriosis were included. Cytokines present in the PF were identified by enzyme-linked immunosorbent assay. The cytolytic activity of NK cells in the PF was also analyzed using a calcein-acetoxy methyl ester (AM) release assay.</P><P><B>MAIN RESULTS AND THE ROLE OF CHANCE</B></P><P>PF from patients with endometriosis suppressed the differentiation and cytotoxicity of NK cells compared with PF from controls (<I>P</I> < 0.05). Increased levels of IL-6 were also found in the PF of patients with endometriosis (<I>P</I> < 0.01), and IL-6 levels were negatively correlated with the cytolytic activity of NK cells (<I>r</I><SUB>s</SUB> = −0.558, <I>P</I> = 0.03). Furthermore, IL-6 reduced the cytolytic activity of NK cells, concomitantly with the down-regulation of granzyme B and perforin (<I>P</I> < 0.05), by modulating SHP-2. Importantly, the addition of anti-IL-6 to the PF of endometriosis patients restored the activity of NK cells (<I>P</I> < 0.01), suggesting that IL-6 plays a crucial role in the reduction of NK cell activity in the PF of patients with endometriosis.</P><P><B>LIMITATIONS, REASONS FOR CAUTION</B></P><P>PF contains various inflammatory cytokines in addition to IL-6 and so it is possible that other cytokines may affect the differentiation and activity of NK cells.</P><P><B>WIDER IMPLICATIONS OF THE FINDINGS</B></P><P>Our results imply that the suppression of IL-6 using an anti-IL-6 antibody or soluble IL-6 receptor could rescue the impairment of NK cell activity in patients with endometriosis.</P><P><B>STUDY FUNDING/COMPETING INTEREST(S)</B></P><P>This work was supported by the KRIBB Creative Research Program (KCS3051312); the STP project (DTM0111221) of the Ministry of Knowledge & Economy and the Basic Science Research Program (RBM0271312) of the National Research Foundation of Korea (NRF) from the Ministry of Education, Science & Technology. There are no conflicts of interest.</P>