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- 저자 : Sang-Beom Kim (검색결과 5,001 건)
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( Hyejung Kim ),( Sun-hee Kim ),( Mi Seon Kang ),( Park Seok Ju ),( Min Sung An ),( Ki Beom Bae ) 대한내과학회 2016 대한내과학회 추계학술대회 Vol.2016 No.1
Background: Ischemia-reperfusion injury (IRI) is a leading cause of acute kidney injury with high morbidity and mortality due to limited therapy. AKI emerges in various clinical settings and is complex with outcome linking oxidative stress, inflammation, and cell death. Therefore protection of AKI is still an unsolved problem. Indomethacin is generally known that it inhibits the production of prostaglandins through the inhibition both cyclooxygenase (COX) 1 and 2. Prostaglandins have a wide variety of effect such as regulation of vasodilation, inflammation, regeneration, pain, fever. Therefore effect of indomethacin in AKI is different according to injury model. We investigated whether indomethacin which inhibits the production of prostaglandins aggravate the renal injury in AKI mouse model. Methods: Male C57/BL6 mice (8-10 weeks old, weight 20~25 g) were used. Acute kidney injury is induced by bilateral kidneys pedicle clamping which were subjected to 20 min or 30 min at both kidneys. Mice were treated with indomethacin at before and after injury. Blood and kidney samples were collected at 24 hr after IRI. The expression level of creatinine, N-gal & Kim-1 were detected in serum. And the expression level of PGE2, cAMP and adenosine were detected in kidney. Kidney Injury score were measured by HE staining and TUNEL. Results: In bilateral AKI model, Serum NGAL level and creatinine level were significantly highest in indomethacin treated group compared to non-treated group (NGAL, p<0.05; creatinine, p<0.01). Indomethacin treated group showed significantly more necrosis and apoptosis compared to non-treated group. Furthermore, Indomethacine inhibited the production of prostaglandins, cAMP and adenosine. Conclusions: Indomethacin inhibits adenosine-mediated renal protection by inhibition of prostaglandin production in AKI. Therefore Indomethacin worsened renal injury by inhibition of prostaglandin production in AKI. * This research was supported by a grant of the Korea Health Technology R&D Project through the KHIDI, funded by the Ministry of Health & Welfare, Republic of Korea (grant number :H15C2212)
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Effects of Exercise Types on BNDF and Cognitive Functions in Middle Aged Women
김유범(Yu-Beom Kim1),김경래(Kyeong-Lae Kim),박성태(Sung-Tae Park) 한국교원대학교 뇌기반교육연구소 2020 Brain, Digital, & Learning Vol.10 No.2
This study is to analyse the impact of two types of exercise on BDNF and cognitive functions in middle aged women. Thirty nine healthy women, aged 50~64 years followed by randomly assigned to a task learning exercise group(n=13), non-task learning exercise group(n=13) and control group(n=13). The TEG performed a dance sports and cognitive band resistance exercise and the NTEG performed a walking and band resistance exercise. Blood sampling and auditory verbal learning test(AVLT) were performed at before exercise, after one bout exercise, and 4 weeks after. As a result, an one bout exercise of moderate intensity on middle aged women was not affected transient change of BDNF significantly regardless of exercise types, but a task-learning exercise was affected positive effect on AVLT. A chronic exercise of moderate intensity for 4 weeks on healthy middle aged women was not affected increasing of basal BDNF levels and memory performance significantly.
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Kidney Toxicity Induced by 13 Weeks Exposure to the Fruiting Body of Paecilomyces sinclairii in Rats
Mihye Jeong,Young-Won Kim,Jeong-Ran Min,Min Kwon,Beom-Suk Han,Jeong-Gyu Kim,Sang-Hee Jeong 한국독성학회 2012 Toxicological Research Vol.28 No.3
Paecilomyces sinclairiis (PS) is known as a functional food or human health supplement. However concerns have been raised about its kidney toxicity. This study was performed to investigate the kidney toxicity of PS by 13 week-oral administration to rats. Blood urea nitrogen (BUN), serum creatinine, and kidney damage biomarkers including beta-2-microglobulin (β2m), glutathione S-transferase alpha (GST-α), kidney injury molecule 1 (KIM-1), tissue inhibitor of matrix metalloproteinase 1 (TIMP-1), vascular endothelial growth factor (VEGF), calbindin, clusterin, cystatin C, neutrophil gelatinase-associated lipocalin (NGAL) and osteopontin were measured during or after the treatment of PS. BUN, creatinine and kidney damage biomarkers in serum were not changed by PS. However, kidney cell karyomegaly and tubular hypertrophy were observed dose-dependently with higher severity in males. KIM-1, TIMP-1 and osteopontin in kidney and urine were increased dose dependently in male or at the highest dose in female rats. Increased urinary osteopontin by PS was not recovered at 2 weeks of post-exposure in both genders. Cystatin C in kidney was decreased at all treatment groups but inversely increased in urine. The changes in kidney damage biomarkers were more remarkable in male than female rats. These data indicate that the PS may provoke renal cell damage and glomerular filtration dysfunction in rats with histopathological lesions and change of kidney damage biomarkers in kidney or urine. Kidney and urinary KIM-1 and cystatin C were the most marked indicators, while kidney weight, BUN and creatinine and kidney damage biomarkers in serum were not influenced.
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Kidney Toxicity Induced by 13 Weeks Exposure to the Fruiting Body of Paecilomyces sinclairii in Rats
Jeong, Mi-Hye,Kim, Young-Won,Min, Jeong-Ran,Kwon, Min,Han, Beom-Suk,Kim, Jeong-Gyu,Jeong, Sang-Hee Korean Society of ToxicologyKorea Environmental Mu 2012 Toxicological Research Vol.28 No.3
Paecilomyces sinclairiis (PS) is known as a functional food or human health supplement. However concerns have been raised about its kidney toxicity. This study was performed to investigate the kidney toxicity of PS by 13 week-oral administration to rats. Blood urea nitrogen (BUN), serum creatinine, and kidney damage biomarkers including beta-2-microglobulin (${\beta}2m$), glutathione S-transferase alpha (GST-${\alpha}$), kidney injury molecule 1 (KIM-1), tissue inhibitor of matrix metalloproteinase 1 (TIMP-1), vascular endothelial growth factor (VEGF), calbindin, clusterin, cystatin C, neutrophil gelatinase-associated lipocalin (NGAL) and osteopontin were measured during or after the treatment of PS. BUN, creatinine and kidney damage biomarkers in serum were not changed by PS. However, kidney cell karyomegaly and tubular hypertrophy were observed dose-dependently with higher severity in males. KIM-1, TIMP-1 and osteopontin in kidney and urine were increased dose dependently in male or at the highest dose in female rats. Increased urinary osteopontin by PS was not recovered at 2 weeks of post-exposure in both genders. Cystatin C in kidney was decreased at all treatment groups but inversely increased in urine. The changes in kidney damage biomarkers were more remarkable in male than female rats. These data indicate that the PS may provoke renal cell damage and glomerular filtration dysfunction in rats with histopathological lesions and change of kidney damage biomarkers in kidney or urine. Kidney and urinary KIM-1 and cystatin C were the most marked indicators, while kidney weight, BUN and creatinine and kidney damage biomarkers in serum were not influenced.
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Outcome of Multipair Donor Kidney Exchange by a Web-Based Algorithm
Kim, Beom Seok,Kim, Yu Seun,Kim, Soon Il,Kim, Myoung Soo,Lee, Ho Yung,Kim, Yong-Lim,Kim, Chan Duck,Yang, Chul Woo,Choi, Bum Soon,Han, Duck Jong,Kim, Yon Su,Kim, Sung Joo,Oh, Ha-Young,Kim, Dae Joong American Society of Nephrology 2007 Journal of the American Society of Nephrology Vol.18 No.3
<P>Donor kidney exchange is an established method to overcome incompatibility of donor-recipient pairs (DRP). A computerized algorithm was devised to exchange donor kidney and was tested in a multicenter setting. The algorithm was made according to the consensus of participating centers. It makes all possible exchange combinations not only between two incompatible DRP but also circularly among three DRP and selects an optimum set of exchange combinations, considering several factors that can affect the outcome of the exchanged transplant. The algorithm was implemented as a web-based program, and matching was performed five times. Fifty-three DRP were enrolled from five transplant centers. The numbers of DRP that were enrolled in each matching were 38 (25:13), 39 (34:5), 33 (31:2), 32 (28:4), and 34 (30:4) (carryover:newcomer). The numbers of generated exchange combinations were 4:11, 3:17, 2:12, 2:3, and 2:3 (two-pair exchange:three-pair exchange), and the numbers of DRP in selected exchange combinations were six, 12, six, five, and four in each matching. The numbers of DRP with blood type O recipient or AB donor were five and one, respectively, in selected exchange combinations. Six DRP of two-pair exchange combinations and six DRP of three-pair exchange combinations underwent transplantation successfully. Computerized algorithm of donor kidney exchange was tried not only between two incompatible DRP but also circularly among three DRP. It showed that the algorithm has potential to improve the outcome of donor kidney exchange, especially for disadvantaged DRP with blood type O recipients or AB donors.</P>
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Proteomic analysis of apoptosis related proteins regulated by proto-oncogene protein DEK
Kim, Dong-Wook,Chae, Jung-IL,Kim, Ji-Young,Pak, Jhang Ho,Koo, Deog-Bon,Bahk, Young Yil,Seo, Sang-Beom Wiley Subscription Services, Inc., A Wiley Company 2009 Journal of cellular biochemistry Vol.106 No.6
<P>A nuclear phosphoprotein, DEK, is implicated in certain human diseases, such as leukemia and antoimmune disorders, and a major component of metazoan chromatin. Basically as a modulator of chromatin structure, it can involve in various DNA and RNA-dependent processes and function as either an activator or repressor. Despite of numerous efforts to suggest the biological role of DEK, direct target proteins of DEK in different physiological status remains elusive. To investigate if DEK protein triggers the changes in certain protein networks, DEK was knocked down at both types of cell clones using siRNA expression. Here we provide a catalogue of proteome profiles in total cell lysates derived from normal HeLa and DEK knock-down HeLa cells and a good in vitro model system for dissecting the protein networks due to this proto-oncogenic DEK protein. In this biological context, we compared total proteome changes by the combined methods of two-dimensional gel electrophoresis, quantitative image analysis and MALDI-TOF MS analysis. There were a large number of targets for DEK, which were differentially expressed in DEK knock-down cells and consisted of 58 proteins (41 up-regulated and 17 down-regulated) differentially regulated expression was further confirmed for some subsets of candidates by Western blot analysis using specific antibodies. In the identified 58 spots, 16% of proteins are known to be associated with apoptosis. Among others, we identified apoptosis related proteins such as Annexins, Enolase1, Lamin A, and Glutathione-S-transferase omega 1. These results are consistent with recent studies indicating the crucial role of DEK in apoptosis pathway. We further demonstrated by ChIP analysis that knock-down of DEK caused hyperacetylation of histones around Prx VI promoter which is upregulated in our profile. Using immunoblotting analysis, we have demonstrated the modulation of other caspase-dependent apoptosis related proteins by DEK knock-down and further implicate its role in apoptosis pathway. J. Cell. Biochem. 106: 1048–1059, 2009. © 2009 Wiley-Liss, Inc.</P>
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Kim, Hee Seung,Kang, Sok-Bom,Seo, Sang-Soo,Han, Seung-Su,Kim, Jae Weon,Park, Noh-Hyun,Kang, Soon-Beom,Lee, Hyo-Pyo,Song, Yong Sang Wiley (Blackwell Publishing) 2009 Annals of the New York Academy of Sciences Vol.1171 No.1
<P>The aim of this study was to determine the maximum tolerated dose (MTD) and therapeutic efficacy of a newly developed CKD-602 topoisomerase I inhibitor and cisplatin in patients with recurrent epithelial ovarian cancer. CKD-602 (0.30 mg/m(2) daily for 5 days) and cisplatin (60 mg/m(2) on day 5) were administered to patients every 3 weeks with dose adjustment of CKD-602 by 0.05 mg/m(2) daily until the MTD was reached. Dose-limiting toxicity was defined as grade >or= 3 neutropenia or thrombocytopenia for more than 4 days or accompanied by fever >or= 38.5 degrees C, infection, hemorrhage, or transfusion; grade >or= 3 nonhematological toxicity except for alopecia, nausea, and vomiting. We enrolled 26 patients with recurrent epithelial ovarian cancer who had measurable disease (MD) estimated by computed tomography scan (n= 12) and nonmeasurable disease (NMD) evaluated by serum CA-125 levels (n= 14). All patients received 188 cycles of CKD-602 and cisplatin with a median number of six cycles per patient (range, 2 to 12). MTD of CKD-602 was 0.30 mg/m(2) daily. The overall response rate was 69.2% (18/26) with 58.3% (7/12) and 78.6% (11/14) in MD and NMD, respectively. Among the responsive patients, 14 were platinum sensitive (14/18, 77.7%) and four were platinum resistant (4/8, 50.0%). The most common toxicity was grade >or= 3 neutropenia developing in 17 patients (65.4%) and 72 cycles (38.3%). Grade 3 nausea and anorexia were the most common gastrointestinal toxicities, developing in 15 cycles (8.0%) of four patients (15.4%) and 10 cycles (5.3%) of five patients (19.3%), respectively. The median disease-free interval was 6 months (range 0-26 months). CKD-602 at a concentration of 0.3 mg/m(2) daily for 5 days and cisplatin at 60 mg/m(2) on day 5 every 3 weeks showed high efficacy, with acceptable toxicity, against platinum-sensitive/resistant recurrent epithelial ovarian cancer.</P>
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Kim, Tae-Beom,Park, Ho Ki,Chang, Joo Hyun,Choi, In Ho,Kim, Khae Hawn,Yoon, Sang Jin,Lee, Min Sung,Jung, Han,Kim, Choung-Soo The Korean Urological Association 2010 Korean Journal of Urology Vol.51 No.2
<P><B>Purpose</B></P><P>Dendritic cell (DC)-based tumor vaccine is an attractive modality for the treatment of hormone-refractory prostate cancer (HRPC) because it has some efficacy and few side effects in patients with poor general conditions. The aim of this study was to establish which is the most effective DC vaccine for the treatment of HRPC. We compared DC vaccine sensitized with tumor lysate and a fusion vaccine of DCs and tumor cells.</P><P><B>Materials and Methods</B></P><P>The DU145 cancer cell line was purchased from the American Type Culture Collection. DCs were cultured from peripheral blood monocytes. Peripheral blood monocytes were cultured in RPMI 1640 medium supplemented with interleukin-4 (IL-4), granulocyte-macrophage colony-stimulating factor, and 10% fetal calf serum. Tumor necrosis factor-alpha was added on day 7 to support maturation. Functional activity was measured in three groups: the DC single-culture group, the DC culture group with DC vaccine sensitized with tumor lysates, and the DC culture group prepared with tumor fusion vaccine made from irradiated tumor cells and monocyte-derived DCs by the polyethylene glycol method.</P><P><B>Results</B></P><P>By FACS analysis, the rate of DC-tumor fusion vaccine was 20.3±3%. The IL-12 level produced by the DC-tumor fusion vaccine was significantly higher than that of DCs pulsed with tumor lysate (p<0.05). Also, the generation of interferon-γ by tumor-specific T cells in the DC-tumor fusion vaccine group was superior to that of DCs pulsed with tumor lysate (p<0.05). In addition, the T cells of the tumor lysate-pulsed DCs and tumor fusion vaccine had 1.6 and 2.5 times the functional activity, respectively, of the DC single-culture group in killing tumor cells in the cytotoxicity assay.</P><P><B>Conclusions</B></P><P>The DC-tumor fusion vaccine seems to be more effective than DC single-culture or DC-tumor lysate vaccine in the treatment of HRPC.</P>
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