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Impact of Dialysate Calcium Concentration on Clinical Outcomes in Incident Hemodialysis Patients
Kim, Hyung Wook,Kim, Su-Hyun,Kim, Young Ok,Jin, Dong Chan,Song, Ho Chul,Choi, Euy Jin,Kim, Yong-Lim,Kim, Yon-Su,Kang, Shin-Wook,Kim, Nam-Ho,Yang, Chul Woo,Kim, Yong Kyun,Malindretos., Pavlos Williams & Wilkins Co 2015 Medicine Vol.94 No.40
<P><B>Abstract</B></P><P>The association between dialysate calcium (DCa) concentration and mortality in hemodialysis (HD) patients is controversial. In this study, we evaluated the impact of DCa concentration on mortality in incident HD patient.</P><P>Incident HD patients were selected from the Clinical Research Center registry—a prospective cohort study on dialysis patients in Korea. Patients were categorized into 3 groups according to the prescribed DCa concentration at the time of enrollment. High DCa was defined as a concentration of 3.5 mEq/L, mid-DCa as 3.0 mEq/L, and low DCa as 2.5 to 2.6 mEq/L. The primary outcome was all-cause mortality and secondary outcomes were cardiovascular or infection-related hospitalization.</P><P>A total of 1182 patients with incident HD were included. The number of patients in each group was 182 (15.4%) in high DCa group, 701 (59.3%) in the mid-DCa group, and 299 (25.3%) in the low DCa group. The median follow-up period was 16 months. The high DCa group had a significantly higher risk of all-cause mortality compared with the mid-DCa group (hazard ratio [HR] 2.23, 95% confidence interval [CI] 1.28–3.90, <I>P</I> = 0.005) and the low DCa group (HR 3.67, 95% CI 1.78–7.55, <I>P</I> < 0.001) after adjustment for clinical variables. The high DCa group was associated with higher risk of cardiovascular and infection-related hospitalization compared with the low DCa group (HR 3.25, 95% CI 1.53–6.89, <I>P</I> = 0.002; and HR 2.77, 95% CI 1.29–5.94, <I>P</I> = 0.009, respectively). Of these 1182 patients, 163 patients from each group were matched by propensity scores. In the propensity score matched analysis, the high DCa group had a significantly higher risk of all-cause mortality compared with the mid-DCa group (HR 2.52, 95% CI 1.04–6.07, <I>P</I> = 0.04) and the low DCa group (HR 4.25, 95% CI 1.64–11.03, <I>P</I> = 0.003) after adjustment for clinical variables.</P><P>Our data showed that HD using a high DCa was a significant risk factor for all-cause mortality and cardiovascular or infection-related hospitalization in incident HD patients.</P>
Kim, Yong Kyun,Kim, Su-Hyun,Kim, Hyung Wook,Kim, Young Ok,Jin, Dong Chan,Song, Ho Chul,Choi, Euy Jin,Kim, Yong-Lim,Kim, Yon-Su,Kang, Shin-Wook,Kim, Nam-Ho,Yang, Chul Woo SAGE Publications 2014 Peritoneal dialysis international Vol.34 No.4
<B>Background</B><P> Previous studies have demonstrated that increased body mass index (BMI) is associated with decreased mortality in hemodialysis (HD) patients. However, the association between BMI and survival has not been well established in patients undergoing peritoneal dialysis (PD). The aim of the study was to determine the association between BMI and mortality in the PD population using the Clinical Research Center (CRC) registry for end-stage renal disease (ESRD) cohort in Korea. </P><B>Methods</B><P> Prevalent patients with PD were selected from the CRC registry for ESRD, a prospective cohort study on dialysis patients in Korea. Patients were categorized into four groups by quartiles of BMI. Cox regression analysis was used to calculate the adjusted hazard ratio (HR) of mortality with a BMI of quartile 2 (21.4 - 23.5 kg/m<SUP>2</SUP>) as the reference. </P><B>Results</B><P> A total of 900 prevalent patients undergoing PD were included. The median follow-up period was 24 months. The multivariate Cox proportional hazard model showed that the lowest quartile of BMI was associated with higher mortality (HR 3.00,95% confidence interval (CI), 1.26 - 7.15). However, the higher quartiles of BMI were not associated with mortality compared with the reference category of BMI quartile 2 (Quartile 3: HR 1.11, 95% CI, 0.43 - 2.85, Quartile 4: H R 1.64,95% CI, 0.66 - 4.06) after adjustment for clinical variables. </P><B>Conclusions</B><P> Lower BMI was a significant risk factor for death, but increased BMI was not associated with mortality in Korean PD patients. </P>
Kim, Hyun-Yi,Yang, Dong-Hwa,Shin, Song-Weon,Kim, Mi-Yeon,Yoon, Jae-Hyun,Kim, Suhyun,Park, Hae-Chul,Kang, Dong Woo,Min, DoSik,Hur, Man-Wook,Choi, Kang-Yell The Federation of American Societies for Experimen 2014 The FASEB Journal Vol.28 No.2
<P>CXXC5 is a member of a small subset of proteins containing CXXC-type zinc-finger domain. Here, we show that CXXC5 is a transcription factor activating <I>Flk-1</I>, a receptor for vascular endothelial growth factor. CXXC5 and Flk-1 were accmulated in nucli and membrane of mouse embryonic stem cells (mESCs), respectively, during their endothelial differentiation. CXXC5 overexpression induced <I>Flk-1</I> transcription in both endothelium-differentiated mESCs and human umbilical vein endothelial cells (HUVECs). <I>In vitro</I> DNA binding assay showed direct interaction of CXXC5 on the <I>Flk-1</I> promoter region, and mutation on its DNA-binding motif abolished transcriptional activity. We showed that bone morphorgeneic protein 4 (BMP4) induced <I>CXXC5</I> transcription in the cells, and inhibitors of BMP signaling suppressed the <I>CXXC5</I> induction and the consequent <I>Flk-1</I> induction by BMP4 treatment. <I>CXXC5</I> knockdown resulted in suppression of BMP4-induced stress fiber formation (56.8±1.3% decrease, <I>P</I><0.05) and migration (54.6±1.9% decrease, <I>P</I><0.05) in HUVECs. The <I>in vivo</I> roles of CXXC5 in BMP-signaling-specific vascular development and angiogenesis were shown by specific defect of caudal vein plex vessel formation (57.9±11.8% decrease, <I>P</I><0.05) in <I>cxxc5</I> morpholino-injected zebrafish embryos and by supression of BMP4-induced angigogensis in subcutaneously injected Matrigel plugs in <I>CXXC5</I><SUP>−/−</SUP> mice. Overall, CXXC5 is a transcriptional activator for <I>Flk-1</I>, mediating BMP signaling for differentiation and migration of endothelial cell and vessel formation.—Kim, H.-Y., Yang, D.-H., Shin, S.-W., Kim, M.-Y., Yoon, J.-H., Kim, S., Park, H.-C., Kang, D. W., Min, D., Hur, M.-W., Choi, K.-Y. CXXC5 is a transcriptional activator of <I>Flk-1</I> and mediates bone morphogenic protein-induced endothelial cell differentiation and vessel formation.</P>
Kim, Taek‐,Keun,Park, Chang Sik,Jang, Jihye,Kim, Mi Ra,Na, Hee‐,Jun,Lee, Kangseung,Kim, Hyun Jung,Heo, Kyun,Yoo, Byong Chul,Kim, Young‐,Myeong,Lee, Je‐,Wook,Kim, Su Jin,Kim, Eu John Wiley and Sons Inc. 2018 MOLECULAR ONCOLOGY Vol.12 No.3
<P>The C‐type lectin‐like domain of CLEC14a (CLEC14a‐C‐type lectin‐like domain [CTLD]) is a key domain that mediates endothelial cell–cell contacts in angiogenesis. However, the role of CLEC14a‐CTLD in pathological angiogenesis has not yet been clearly elucidated. In this study, through complementarity‐determining region grafting, consecutive deglycosylation, and functional isolation, we generated a novel anti‐angiogenic human monoclonal antibody that specifically targets CLEC14a‐CTLD and that shows improved stability and homogeneity relative to the parental antibody. We found that this antibody directly inhibits CLEC14a‐CTLD‐mediated endothelial cell–cell contact and simultaneously downregulates expression of CLEC14a on the surface of endothelial cells. Using various <I>in vitro</I> and <I>in vivo</I> functional assays, we demonstrated that this antibody effectively suppresses vascular endothelial growth factor (VEGF)‐dependent angiogenesis and tumor angiogenesis of SNU182 human hepatocellular carcinoma, CFPAC‐1 human pancreatic cancer, and U87 human glioma cells. Furthermore, we also found that this antibody significantly inhibits tumor angiogenesis of HCT116 and bevacizumab‐adapted HCT116 human colorectal cancer cells. These findings suggest that antibody targeting of CLEC14a‐CTLD has the potential to suppress VEGF‐dependent angiogenesis and tumor angiogenesis and that CLEC14a‐CTLD may be a novel anti‐angiogenic target for VEGF‐dependent angiogenesis and tumor angiogenesis.</P>
Kim, Yudeuk,Kim, Dong Wook,Lee, Moon-Hyeok,Lee, Min Hee,Yoo, Dong Eun,Kim, Ki Nam,Jeon, Sang Chul,Kim, Kyong Hon IOP 2016 Journal of optics Vol.18 No.9
<P>An integrated polarization rotator is demonstrated experimentally by forming a strip waveguide with an asymmetric trench on a silicon-on-insulator wafer. The trench is located asymmetrically in the strip waveguide. It induces the evolution of an orthogonal polarization mode upon a linearly polarized beam input, and thus causes polarization rotation. The device is fabricated using a conventional complementary metal oxide semiconductor process with a single dry etching step. The fabricated device shows a maximum transverse electric (TE)-to-transverse magnetic (TM) polarization conversion efficiency of 21.3 dB and an insertion loss of −0.95 dB at a 1550 nm wavelength with a device length of 67 <I>μ</I>m. The device exhibits a polarization conversion efficiency and insertion loss of 21.1 dB and −2.12 dB, respectively, for the TM-to-TE polarization conversion. The optimum parameters for the waveguide size and trench size are investigated by performing numerical simulations, and by demonstrating experimental fabrication and measurement.</P>
Identification of DNA Aptamers toward Epithelial Cell Adhesion Molecule via Cell-SELEX
Kim, Ji Won,Kim, Eun Young,Kim, Sun Young,Byun, Sang Kyung,Lee, Dasom,Oh, Kyoung-Jin,Kim, Won Kon,Han, Baek Soo,Chi, Seung-Wook,Lee, Sang Chul,Bae, Kwang-Hee Korean Society for Molecular and Cellular Biology 2014 Molecules and cells Vol.37 No.10
The epithelial cell adhesion molecule (EpCAM, also known as CD326) is a transmembrane glycoprotein that is specifically detected in most adenocarcinomas and cancer stem cells. In this study, we performed a Cell systematic evolution of ligands by exponential enrichment (SELEX) experiment to isolate the aptamers against EpCAM. After seven round of Cell SELEX, we identified several aptamer candidates. Among the selected aptamers, EP166 specifically binds to cells expressing EpCAM with an equilibrium dissociation constant (Kd) in a micromolar range. On the other hand, it did not bind to negative control cells. Moreover, EP166 binds to J1ES cells, a mouse embryonic stem cell line. Therefore, the isolated aptamers against EpCAM could be used as a stem cell marker or in other applications in both stem cell and cancer studies.
Kim Ye Seul,Yoon Jung Won,Kim Dasol,Choi Seunghak,Kim Hyoung Kyu,Youm Jae Boum,Han Jin,Heo Soon Chul,Hyun Sung-Ae,Seo Jung-Wook,Kim Deok-Ho,Kim Jae Ho 생화학분자생물학회 2022 Experimental and molecular medicine Vol.54 No.-
Human embryonic stem cell-derived cardiomyocytes (hESC-CMs) have been reported to exhibit immature embryonic or fetal cardiomyocyte-like phenotypes. To enhance the maturation of hESC-CMs, we identified a natural steroidal alkaloid, tomatidine, as a new substance that stimulates the maturation of hESC-CMs. Treatment of human embryonic stem cells with tomatidine during cardiomyocyte differentiation stimulated the expression of several cardiomyocyte-specific markers and increased the density of T-tubules. Furthermore, tomatidine treatment augmented the number and size of mitochondria and enhanced the formation of mitochondrial lamellar cristae. Tomatidine treatment stimulated mitochondrial functions, including mitochondrial membrane potential, oxidative phosphorylation, and ATP production, in hESC-CMs. Tomatidine-treated hESC-CMs were more sensitive to doxorubicin-induced cardiotoxicity than the control cells. In conclusion, the present study suggests that tomatidine promotes the differentiation of stem cells to adult cardiomyocytes by accelerating mitochondrial biogenesis and maturation and that tomatidine-treated mature hESC-CMs can be used for cardiotoxicity screening and cardiac disease modeling.
Human immunodeficiency virus-negative plasmablastic lymphoma in Korea
Kim, Ji Eun,Kim, Young A.,Kim, Wook Youn,Kim, Chul Woo,Ko, Young Hye,Lee, Geon Kook,Choi, Suk-Jin,Jeon, Yoon Kyung Informa UK (TaylorFrancis) 2009 Leukemia & lymphoma Vol.50 No.4
<P>Plasmablastic lymphoma (PBL) is very rare, and predominantly occurs in Human immunodeficiency virus (HIV)-positive individuals. It shows a strong affinity for the oral cavity and for the Epstein-Barr virus (EBV) positive. We investigated the clinicopathologic characteristics of six cases of PBL in Koreans. All patients were HIV-negative and without underlying immunodeficiency. The age distribution was bimodal, and four patients were older than 60 years. Male predominance was observed with male to female ratio of 5:1. The organs primarily involved were the terminal ileum, stomach, oral cavity, tonsil, nasal cavity and meninges. The tumors were histologically typical of PBL. Three of them were composed of monomorphic large immunoblastic or plasmablastic cells, and classified as PBL of the oral mucosa type. Another three cases were classified as PBL with plasmacytic differentiation. Five cases revealed loss of B-cell antigens with CD138 or MUM1 substitution. CD10 was positive in two cases (PBLs of the oral mucosa type), and one of them unexpectedly expressed cytokeratin. EBV was detected in one case (PBL with plasmacytic differentiation). Four patients succumbed to PBL in a relatively short period of time. We suggest that PBL is not strongly associated HIV or EBV in Koreans, and that it shows a variable organ distribution without an oro-nasal predilection.</P>