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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, Sung Rae,Yoo, Ji Han,Song, Ho Cheol,Lee, Seong Su,Yoo, Soon Jib,Kim, Young-Du,Lim, Yeon Soo,Kim, Hyung Wook,Yang, Chul Woo,Kim, Yong-Soo,Choi, Euy Jin,Kim, Yong Kyun Springer International ; Oxford University Press 2011 Nephrology, dialysis, transplantation Vol.26 No.11
<P>Obesity and diabetes mellitus (DM) are established risk factors for the development of chronic kidney disease. Visceral adiposity (VAT) and subcutaneous adiposity (SAT) may be associated with the differential metabolic risk. Our study was performed to determine whether VAT or SAT was associated with the decrease of renal function in people with type 2 DM.</P>
Kim, Jin Wook,Kim, Ji Young,Kim, Ja Eun,Kim, Seung-Ki,Chung, Hyun-Tai,Park, Chul-Kee Impact Journals LLC 2014 Genes & cancer Vol.5 No.5
<P>Temozolomide resistance is associated with multiple DNA repair pathways. We investigated homeobox (HOX) genes for their role in temozolomide resistance, focusing on the homologous recombination (HR) pathway, and we tested their therapeutic implications in conjunction with O<SUP>6</SUP>-methylguanine DNA methyltransferase (MGMT) status. Two glioblastoma cell lines with different MGMT statuses were used to test the augmented anticancer effect of temozolomide with HOXA10 inhibition. In vitro experiments, including gene expression studies with RNA interference, were performed to verify the related pathway dynamics. HOXA10 inhibition reinforced temozolomide sensitivity independent of MGMT status and was related to the impaired double-strand DNA breakage repair process resulting from the downregulation of Rad51 paralogs. Early growth response 1 (EGR1) and phosphatase and tensin homolog (PTEN) were the regulatory mediators between HOXA10 and the HR pathway. Moreover, HOXA10 inhibition selectively affected the nuclear function of PTEN without interfering with its cytoplasmic function of suppressing the phosphoinositide 3-kinase/Akt pathway. The mechanism of HR pathway regulation by HOXA10 harbors another target mechanism for overcoming temozolomide resistance in glioblastoma patients.</P>
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.
Kim, Sung-Geun,Park, Cho-Hyun,Kim, Kyung-Mi,Kim, Jae-Gue,Kim, Hyung-Ho,Park, Wong-Sang,Park, Jong-Jae,Lee, Mun-Su,Jung, Hyun-Chul,Jung, Hun-Yong,Han, Sang-Wook,Hyung, Woo-Jin,The Academic Committee of 대한위암학회 2010 Journal of gastric cancer Vol.10 No.3
We have always attempted to create a standard treatment protocol for patients with gastric cancer. However, many debates still exist regarding gastric cancer treatment. For the past 2 years, at the Annual Congress of the Korean Gastric Cancer Association, we have presented a grand symposium on the "Debates on the strategy for treating gastric cancer". In 2008, four major topics were discussed and voted on after discussion. The four major topics were proximal location treatment for early gastric cancer, management choices for pyloric obstruction with advanced gastric cancer, management of liver metastasis, and reconstruction methods after a distal gastrectomy. The opinions of the audience for six minor topics were expressed by an electronic voting system. In 2009, the four main topics were treatment for submucosal tumor sized around 2 cm, laparoscopic gastrectomy in T2N1 gastric cancer, choices for managing gastric lymphoma, and application of a pylorus preserving procedure for early gastric cancer at the antrum. The opinions of the audience for these six minor topics were expressed by an electronic voting system, as was conducted in 2008. It was good opportunity to identify a point of contact about the debates on managing gastric cancer. The results of these debates and studies will identify the best methods to treat patients with gastric cancer.