63 results on '"Ho Seon Park"'
Search Results
52. The role of plasma in microwave systems for materials processing
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Ho-Seon Park, Monika Willert-Porada, J. Grosse-Berg, and T. Gerdes
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Materials science ,Materials processing ,visual_art ,Microwave heating ,visual_art.visual_art_medium ,Sintering ,Ceramic ,Plasma ,Atmospheric temperature range ,Engineering physics ,Microwave ,Carbide - Abstract
Summary form only given, as follows. Since 1990 processing of materials using microwave heating is under development, with only few industrial applications till today in the high temperature range, e.g., with process temperatures T>1000/spl deg/C. Among the most promising technologies sintering of PM-products (cemented carbides, ceramic, metals) and melting of glass using microwaves of 2.45 GHz frequency should be mentioned. The peculiarities for industrial use of microwave materials processing technology are mainly of economical origin but there are also some basic technological problems, which need to be solved in order to promote microwave heating as a widely used materials processing technology.
- Published
- 2003
53. Ex vivo pre-conditioning of hematopoietic stem/progenitor cells impairs long-term hematopoietic repopulation after transplantation (TRAN3P.881)
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Hakmo Lee, Ho Seon Park, Ju Eun Oh, Jongwoo Park, Sung Soo Chung, Kyong Soo Park, and Hye Seung Jung
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Immunology ,Immunology and Allergy - Abstract
A number of investigators have tried to facilitate engraftment with limited numbers of available HSPCs by enhancing responsiveness of HSPCs to CXCL12. Recently, granulocyte derived cationic peptide, LL-37, has been suggested as a useful pre-conditioning component to overcome the shortage of available HSPCs. In this study, we first evaluated the character of LL-37 pre-conditioned HSPCs and found that LL-37 pre-conditioning effects are specific only to the clonogenic stem cells which are considered relatively dormant. This raised our concern regarding the fate of LL-37 pre-conditioned cells after transplantation and led us to evaluate their repopulation capacity as HSPCs. Not betraying our expectations, hematopoietic recovery of LL-37 pre-conditioned cells gradually decreased from 4 weeks after transplantation in competitive repopulation experiments. Further, in vitro studies revealed that LL-37 lead HSPCs to be more vulnerable to extracellular stimuli such as extracellular glucose followed by increased calcium influx from extracellular sources, which dampen self-renewal capacity by activating mammalian target of rapamycin and its downstream signaling. These results suggest that a future strategy must focus on maintaining HSPCs in dormant and protecting them from various stimuli during their long journey to the bone marrow niches rather than activating them before transplantation for successful transplantation outcome.
- Published
- 2014
54. Granulocyte derived cationic peptide LL-37 prime hematopoietic progenitor cells through up-regulating glucose uptake and AMPK signaling (P2202)
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Hakmo Lee, Ho Seon Park, Ok Kyung Choi, Jongwoo Park, Ju Eun Oh, Won-Woo Lee, Sung Soo Chung, Hye Seung Jung, and Kyong Soo Park
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Immunology ,Immunology and Allergy - Abstract
It has been reported that activated granulocytes derived cationic peptide LL-37 positively prime responsiveness of hematopoietic progenitor cells (HPCs) to CXCL12 gradient through an ambiguous pathway. The goal of this study was to elucidate the mechanism of enhanced migration of LL-37 primed HPCs to CXCL12 gradient. We performed in vitro migration assay and found out that LL-37 pretreatment enhanced migration of HPCs to CXCL12 only in the presence of D-glucose, but not in the absence of glucose or in the presence of glucose uptake inhibitor, 2-deoxy-D-glucose (2-DG). This signifies that LL-37 may affect intracellular energy production machinery. So we tested if the priming effect of LL-37 is related to mTOR signaling since mTOR is a central regulator of nutrient sensing and glycolysis promoting glucose uptake and ATP production to match energy demands for cell migration. As we expected, LL-37 induced glucose uptake in mTOR signaling dependent manner. Also, LL-37 induced the activation of nutrient sensing AMPK and its downstream substrates. In line with this, pretreatment of AMPK activator AICAR promoted migration of HSPCs as well. These findings demonstrate that the priming mechanism of LL-37 is closely associated with increasing ATP production and the optimization of glucose uptake and ATP production for HPCs prior to transplantation would be particularly important in HPCs transplantation where the number of cells available for transplantation is usually limited.
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- 2013
55. Effect of Adipose Differentiation-Related Protein (ADRP) on Glucose Uptake of Skeletal Muscle
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Sang Gyu Park, Kyong Soo Park, Inkyu Lee, Sung Soo Chung, Sena Kim, Hong Kyu Lee, Kim Min, Yun Hyi Ku, Han Jong Kim, Ho Seon Park, Dong Hoon Shin, and Young Min Cho
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chemistry.chemical_classification ,congenital, hereditary, and neonatal diseases and abnormalities ,medicine.medical_specialty ,Insulin ,medicine.medical_treatment ,Glucose uptake ,Peroxisome proliferator-activated receptor ,Adipose tissue ,Skeletal muscle ,Metabolism ,Biology ,medicine.disease ,eye diseases ,Endocrinology ,medicine.anatomical_structure ,Insulin resistance ,chemistry ,Internal medicine ,Lipid droplet ,medicine - Abstract
Background: Skeletal muscle is the most important tissue contributing to insulin resistance. Several studies have shown that accumulation of intramyocellular lipid is associated with the development of insulin resistance. Thus, proteins involved in lipid transport, storage and metabolism might also be involved in insulin action in skeletal muscle. Adipose differentiation-related protein (ADRP), which is localized at the surface of lipid droplets, is known to be regulated by peroxisome proliferator activated receptor γ (PPARγ). However, it is not known whether ADRP plays a role in regulating glucose uptake and insulin action in skeletal muscle. Methods: ADRP expression in skeletal muscle was measured by RT-PCR and western blot in db/db mice with and without PPARγ agonist. The effect of PPARγ agonist or high lipid concent ration (0.4% intralipos) on ADRP expression was also obtained in cultured human skeletal mu scle cells. Glucose uptake was measured when ADRP was down-regulated with siRNA or when ADRP was overexpressed with adenovirus. Results: ADRP expression increased in the skeletal muscle of db/db mice in comparison with normal controls and tended to increase with the treatment of PPARγ agonist. In cultured human skeletal muscle cells, the treatment of PPARγ agonist or high lipid concentration increased ADRP expression. siADRP treatment decreased both basal and insulin-stimulated glucose uptake whereas ADRP overexpression increased glucose uptake in cultured human skeletal muscle cells. Conclusion: ADRP expression in skeletal muscle is increased by PPARγ agonist or exposure to high lipid concentration. In these conditions, increased ADRP contributed to increase glucose uptake. These results suggest that insulin-sensitizing effects of PPARγ are at least partially achieved by the increase of ADRP expression, and ADRP has a protective effect against intramyoce llular lipid-induced insulin resistance. (Korean Diabetes J 33:206-214, 2009)
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- 2009
56. Microwave antenna array for high temperature material processing.
- Author
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Gerdes, T., Ho-Seon Park, Rosin, A., Schmidt, A., and Willert-Porada, M.
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- 2010
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57. Electrophoretic Deposition for the Growth of Carbon nanofibers on Ni-Cu/C-fiber Textiles.
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Ki-Mok Nam, Karina Mees, Ho-Seon Park, Willert-Porada, Monika, and Chang-Seop Lee
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ELECTROPHORETIC deposition ,CARBON nanofibers ,TEXTILES ,TEXTILE fibers ,BIOCHEMICAL substrates - Abstract
In this study, Ni, Ni-Cu and Ni/Cu catalysts were deposited onto C-fiber textiles via the electrophoretic deposition method, and the growth characteristics of carbon nanofibers on the deposited catalyst/C-fiber textiles were investigated. The catalyst deposition onto C-fiber textiles was accomplished by immersing the C-fiber textiles into Ni or Ni-Cu mixed solutions, producing the substrate by post-deposition of Ni onto C-fiber textiles with pre-deposited Cu, and passing it through a gas mixture of N
2 , H2 and C2 H4 at 700 °C to synthesize carbon nanofibers. For analysis of the characteristics of the synthesized carbon nanofibers and the deposition pattern of catalysts, SEM, EDS, BET, XRD, Raman and XPS analysis were conducted. It was found that the amount of catalyst deposited and the ratio of Ni deposition in the Ni-Cu mixed solution increased with an increasing voltage for electrophoretic deposition. In the case of post-deposition of Ni catalyst onto substrates with pre-deposited Cu, both bimetallic catalyst and carbon nanofibers with a high level of crystallizability were produced. Carbon nanofibers yielded with the catalyst prepared in Ni and Ni-Cu mixed solutions showed a Y-shaped morphology. [ABSTRACT FROM AUTHOR]- Published
- 2014
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58. 4-deoxypyridoxine improves the viability of isolated pancreatic islets ex vivo.
- Author
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Hakmo Lee, Ho Seon Park, Shin Hee Hong, Ok Kyung Choi, Sung-Dae Cho, Jongwoo Park, Ju Eun Oh, Sung Soo Chung, Hye Seung Jung, and Kyong Soo Park
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- 2013
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59. Endothelial Progenitor Cell Cotransplantation Enhances Islet Engraftment by Rapid Revascularization.
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Shinae Kang, Ho Seon Park, Jo, Anna, Shin Hee Hong, Han Na Lee, Yeon Yi Lee, Joong Shin Park, Hye Seung Jung, Sung Soo Chung, and Kyong Soo Park
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REVASCULARIZATION (Surgery) , *ENDOTHELIAL cells , *NEOVASCULARIZATION , *HEPATOCYTE growth factor , *BASAL lamina - Abstract
Impaired revascularization of transplanted islets is a critical problem that leads to progressive islet loss. Since endothelial progenitor cells (EPCs) are known to aid neovascularization, we aimed to enhance islet engraftment by cotransplanting EPCs with islets. Porcine islets, with (islet-EPC group) or without (islet-only group) human cord blood-derived EPCs, were transplanted into diabetic nude mice. The islet-EPC group reached euglycemia by ~11 days post-transplantation, whereas the islet-only group did not. Also, the islet-EPC group had a higher serum porcine insulin level than the islet-only group. Islets from the islet-EPC group were more rapidly revascularized at the early period of transplantation without increment of final capillary density at the fully revascularized graft. Enhanced revascularization rate in the islet-EPC group was mainly attributed to stimulating vascular endothelial growth factor-A production from the graft. The rapid revascularization by EPC cotransplantation led to better graft perfusion and recovery from hypoxia. EPC cotransplantation was also associated with greater β-cell proliferation, probably by more basement membrane production and hepatocyte growth factor secretion. In conclusion, cotransplantation of EPCs and islets induces better islet engraftment by enhancing the rate of graft revascularization. These findings might provide a directly applicable tool to enhance the efficacy of islet transplantation in clinical practice. [ABSTRACT FROM AUTHOR]
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- 2012
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60. A Newly Identified CG301269 Improves Lipid and Glucose Metabolism Without Body Weight Gain Through Activation of Peroxisome Proliferator-Activated Receptor α and γ.
- Author
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Hyun Woo Jeong, Joo-Won Lee, Woo Sik Kim, Sung Sik Choe, Kyung-Hee Kim, Ho Seon Park, Hyun Jung Shin, Gha Young Lee, Dongkyu Shin, Hanjae Lee, Jun Hee Lee, Eun Bok Choi, Hyeon Kyu Lee, Heekyoung Chung, Seung Bum Park, Kyong Soo Park, Hyo-Soo Kim, Seonggu Ro, and Jae Bum Kim
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PEROXISOMES ,CELL receptors ,METABOLIC disorders ,BIOLOGICAL assay ,FATTY acids ,OXIDATION ,GENES ,LABORATORY mice - Abstract
OBJECTIVE--Peroxisome proliferator-activated receptor (PPAR)-α/γ dual agonists have been developed to alleviate metabolic disorders. However, several PPARα/γ dual agonists are accompanied with unwanted side effects, including body weight gain, edema, and tissue failure. This study investigated the effects of a novel PPARα/γ dual agonist, CG301269, on metabolic disorders both in vitro and in vivo. RESEARCH DESIGN AND METHODS--Function of CG301269 as a PPARα/γ dual agonist was assessed in vitro by luciferase reporter assay, mammalian one-hybrid assay, and analyses of PPAR target genes. In vitro profiles on fatty acid oxidation and inflammatory responses were acquired by fatty acid oxidation assay and quantitative (q)RT-PCR of proinflammatory genes. In vivo effect of CG301269 was examined in db/db mice. Total body weight and various tissue weights were measured, and hepatic lipid profiles were analyzed. Systemic glucose and insulin tolerance were measured, and the in vivo effect of CG301269 on metabolic genes and proinflammatory genes was examined by qRT-PCR. RESULTS--CG301269 selectively stimulated the transcriptional activities of PPARa and PPAR7. CG301269 enhanced fatty acid oxidation in vitro and ameliorated insulin resistance and hyper-lipidemia in vivo, hi db/db mice, CG301269 reduced inflammatory responses and fatty liver, without body weight gain. CONCLUSIONS--We demonstrate that CG301269 exhibits beneficial effects on glucose and lipid metabolism by simultaneous activation of both PPARα and PPARγ. Our data suggest that CG301269 would be a potential lead compound against obesity and related metabolic disorders. [ABSTRACT FROM AUTHOR]
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- 2011
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61. Lysophosphatidic acid regulates blood glucose by stimulating myotube and adipocyte glucose uptake.
- Author
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Kyungmoo Yea, Jaeyoon Kim, Seyoung Lim, Ho Seon Park, Kyong Soo Park, Pann-Ghill Suh, and Sung Ho Ryu
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LYSOPHOSPHOLIPIDS ,BLOOD sugar ,FAT cells ,GLUCOSE ,PHOSPHORYLATION - Abstract
Lysophosphatidic acid (LPA) is known to have diverse cellular effects, but although LPA is present in many biological fluids, including blood, its effects on glucose metabolism have not been elucidated. In this study, we investigated whether LPA stimulation is related to glucose regulation. LPA was found to enhance glucose uptake in a dose-dependent manner both in L6 GLUT4 myc myotubes and 3T3-L1 adipocytes by triggering GLUT4 translocation to the plasma membrane. Moreover, the effect of LPA on glucose uptake was completely inhibited by pretreating both cells with LPA receptor antagonist Ki16425 and G
i inhibitor pertussis toxin. In addition, LPA increased the phosphorylation of AKT-1 with no effects on IRS-1, and LPA-induced glucose uptake was abrogated by pretreatment with the PI 3-kinase inhibitor LY294002. When low concentration of insulin and LPA were treated simultaneously, an additive effect on glucose uptake was observed in both cell types. In line with its cellular functions, LPA significantly lowered blood glucose levels in normal mice but did not affect insulin secretion. LPA also had a glucose-lowering effect in streptozotocin-treated type 1 diabetic mice. In combination, these results suggest that LPA is involved in the regulation of glucose homeostasis in muscle and adipose tissues. [ABSTRACT FROM AUTHOR]- Published
- 2008
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62. Novel Strategy for Successful Long-Term Hematopoietic Recovery after Transplanting a Limited Number of Hematopoietic Stem/Progenitor Cells
- Author
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Hye Seung Jung, Ju Eun Oh, Kyong Soo Park, Hakmo Lee, Sung Soo Chung, Ho Seon Park, and Ok Kyung Choi
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Male ,AMPK ,Transplantation Conditioning ,mTORC1 ,Biology ,Hematopoietic stem cell ,medicine ,Animals ,Humans ,Progenitor cell ,Transplantation ,Stem Cells ,Hematopoietic Stem Cell Transplantation ,LL-37 ,Hematology ,Hematopoietic Stem Cells ,Cell biology ,Haematopoiesis ,medicine.anatomical_structure ,Immunology ,Bone marrow ,Homing (hematopoietic) - Abstract
Various investigators have attempted to overcome the shortage of available hematopoietic stem/progenitor cells (HSPCs) by facilitating their engraftment after transplantation. Preconditioning of HSPCs with the granulocyte-derived cationic peptide LL-37 has been suggested as a useful strategy to facilitate engraftment of transplanted cells by enhancing their responsiveness to CXCL12. In this study, we evaluated whether LL-37 preconditioning is acceptable for clinical application. We found that the effect of LL-37 preconditioning was specific to clonogenic cells and was mediated specifically by increased calcium influx with the activation of downstream signaling through mammalian target of rapamycin complex 1 (mTORC1). Because hyperactivation of mTORC1 and the disruption of 5′ adenosine monophosphate-activated protein kinase (AMPK) are known to deplete HSPC pools, we compared the repopulation capacity of HSPCs preconditioned with LL-37 and those preconditioned with AMPK activator (AICAR). In vivo competitive repopulation experiments revealed that LL-37 preconditioning impairs long-term repopulation of transplanted HSPCs, suggesting that this strategy might not acceptable for clinical applications in which long-term repopulation capacity is a prerequisite. AICAR preconditioning dramatically enhanced the long-term repopulation of transplanted HSPCs, however. Taken together, these results suggest that future strategies to ensure successful transplantation outcomes should focus on protecting HSPCs from various stimuli during their homing to the bone marrow niches rather than activating them before transplantation.
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63. Lysophosphatidylcholine Activates Adipocyte Glucose Uptake and Lowers Blood Glucose Levels in Murine Models of Diabetes.
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Kyungmoo Yea, Jaeyoon Kim, Jong Hyuk Yoon, Taewan Kwon, Jong Hyun Kim, Byoung Dae Lee, Hae-Jeong Lee, Seung Jae Lees, Jong-In Kim, Lee, Taehoon G., Moon-Chang Baek, Ho Seon Park, Kyong Soo Park, Ohba, Motoi, Pann-GhiII Suh, and Sung Ho Ryu
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DIABETES , *BLOOD sugar , *HOMEOSTASIS , *FAT cells , *PROTEIN kinase C , *CHROMATOGRAPHIC analysis , *ANIMAL models in research - Abstract
Glucose homeostasis is maintained by the orchestration of peripheral glucose utilization and hepatic glucose production, mainly by insulin. In this study, we found by utilizing a combined parallel chromatography mass profiling approach that lysophosphatidylcholine (LPC) regulates glucose levels. LPC was found to stimulate glucose uptake in 3T3-L1 adipocytes dose- and time-dependently, and this activity was found to be sensitive to variations in acyl chain lengths and to polar head group types in LPC. Treatment with LPC resulted in a significant increase in the level of GLUT4 at the plasma membranes of 3T3-L1 adipocytes. Moreover, LPC did not affect IRS-i and AKT2 phosphorylations, and LPC-induced glucose uptake was not influenced by pretreatment with the P1 3-kinase inhibitor LY294002. However, glucose uptake stimulation by LPC was abrogated both by rottlerin (a protein kinase Cδ inhibitor) and by the adenoviral expression of dominant negative protein kinase C. In line with its determined cellular functions, LPC was found to lower blood glucose levels in normal mice. Further- more, LPC improved blood glucose levels in mouse models of type 1 and 2 diabetes. These results suggest that an understand- ing of the mode of action of LPC may provide a new perspective of glucose homeostasis. [ABSTRACT FROM AUTHOR]
- Published
- 2009
- Full Text
- View/download PDF
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