용접판재(Tailored Blank)를 이용한 Door Inner 개발

김관회(Koan-Hoi Kim),조원석(Won-Seok Cho),김헌영(Heon-Young Kim) 한국소성가공학회 1998 박판성형 심포지엄 Vol.1998 No.2

식물자원에서 세포사멸 조절물질의 개발

김관회(Koan Hoi Kim) 강원대학교 농업생명과학연구원(구 농업과학연구소) 2002 심포지움-생물자원의 보고 장백산 Vol.2002 No.-

Effect of Pyridoxine on Rifampicin Toxicity

Yun, Yeo-Pyo,Kim, Koan-Hoi,Kim, Hack-Seang,Chung, Jin-Ho The Pharmaceutical Society of Korea 1991 Archives of Pharmacal Research Vol.14 No.1

The effects of pyridoxine (PN) on rifampicin (RMF) toxicity were investigated by both in vivo and in vitro methods. RMF (30 mg/kg) was injected intraperitoneally and PN(150 mg/kg) was administered orally to rats for 10 consecutive days. After treatment, clinical chemistry and hematologic profiles were measured. RMF and PN plus RMF did not show any adverse effects at this in vivo experimental condition. Thymidine incorporations of mice bone marrow cells were examined in vitro. RMF showed a decrease in thymidine uptake in a dose-dependent manner, but PN showed a reversal of the thymidine uptake suppression caused by RMF (p<0.01). On the other hand, PN showed a decrease in thymidine uptake at a high concentration level.

Characterization of $ET_B$ Receptor-mediated Relaxation in Precontracted Mesenteric Artery from Streptozotocin-induced Diabetic Rats

Eom, Yang-Ki,Kim, Koan-Hoi,Rhim, Byung-Yong The Korean Society of Pharmacology 2005 The Korean Journal of Physiology & Pharmacology Vol.9 No.5

Diabetes mellitus is associated with vascular complications, including an impairment of vascular function and alterations in the reactivity of blood vessels to vasoactive substances in various vasculature. In the present study, the authors have observed endothelin-B ($ET_B$) receptor agonist-induced relaxation in precontracted mesenteric arterial segments from streptozotocin (STZ)-induced diabetic rats, which was not shown from control rats or in other arterial segments from diabetic rats. Accordingly, the goal of this study was to investigate in what way STZ-induced diabetes altered reactivity of the mesenteric arterial bed and to examine the causal relaxation, if any, between this $ET_B$ receptor-mediated relaxation and endothelial paracrine function, especially nitric oxide (NO) production. The relaxation induced by $ET_B$ agonists was not observed in mesenteric arteries without endothelium. The relaxation to $ET_B$ agonists was completely abolished by pretreatment with BQ788, but not by BQ610. $N_{\omega}-nitro-L-arginine$ methyl ester and soluble guanylate cyclase inhibitors, methylene blue or LY83583 significantly attenuated the relaxant responses to $ET_B$ agonists, respectively. When the expression of eNOS and iNOS was evaluated on agarose gel stained with ethidium bromide, the expression of eNOS mRNA in diabetic rats was significantly decreased, but the expression of iNOS was increased compared with control rats. Furthermore, the iNOS-like immunostaining was densely detected in the endothelium and slightly in the arterial smooth muscle of diabetic rats, but not in control rats. These observations suggest that $ET_B$ receptor may not play a role in maintaining mesenteric vascular tone in normal situation. However, the alterations in $ET_B$ receptor sensitivity were found in diabetic rats and lead to the $ET_B$ agonist-induced vasorelaxation, which is closely related to NO production. In the state of increased vascular resistance of diabetic mesenteric vascular bed, enhanced NO production by activation of iNOS could lead to compensatory vasorelaxation to modulate adequate perfusion pressure to splanchnic area.

Characterization of ET<SUB>B</SUB> Receptor-mediated Relaxation in Precontracted Mesenteric Artery from Streptozotocin-induced Diabetic Rats

Yang Ki Eom,Koan Hoi Kim,Byung Yong Rhim 대한생리학회-대한약리학회 2005 The Korean Journal of Physiology & Pharmacology Vol.9 No.5

Diabetes mellitus is associated with vascular complications, including an impairment of vascular function and alterations in the reactivity of blood vessels to vasoactive substances in various vasculature. In the present study, the authors have observed endothelin-B (ET<SUB>B</SUB>) receptor agonist-induced relaxation in precontracted mesenteric arterial segments from streptozotocin (STZ)-induced diabetic rats, which was not shown from control rats or in other arterial segments from diabetic rats. Accordingly, the goal of this study was to investigate in what way STZ-induced diabetes altered reactivity of the mesenteric arterial bed and to examine the causal relaxation, if any, between this ET<SUB>B</SUB> receptor-mediated relaxation and endothelial paracrine function, especially nitric oxide (NO) production. The relaxation induced by ET<SUB>B</SUB> agonists was not observed in mesenteric arteries without endothelium. The relaxation to ET<SUB>B</SUB> agonists was completely abolished by pretreatment with BQ788, but not by BQ610. Nω-nitro-L-arginine methyl ester and soluble guanylate cyclase inhibitors, methylene blue or LY83583 significantly attenuated the relaxant responses to ET<SUB>B</SUB> agonists, respectively. When the expression of eNOS and iNOS was evaluated on agarose gel stained with ethidium bromide, the expression of eNOS mRNA in diabetic rats was significantly decreased, but the expression of iNOS was increased compared with control rats. Furthermore, the iNOS-like immunostaining was densely detected in the endothelium and slightly in the arterial smooth muscle of diabetic rats, but not in control rats. These observations suggest that ET<SUB>B</SUB> receptor may not play a role in maintaining mesenteric vascular tone in normal situation. However, the alterations in ET<SUB>B</SUB> receptor sensitivity were found in diabetic rats and lead to the ET<SUB>B</SUB> agonist-induced vasorelaxation, which is closely related to NO production. In the state of increased vascular resistance of diabetic mesenteric vascular bed, enhanced NO production by activation of iNOS could lead to compensatory vasorelaxation to modulate adequate perfusion pressure to splanchnic area.

Conditioned Medium from Dying Smooth Muscle Cell Induced Apoptotic Death

Bu, Moon-Hyun,Lee, Kyeong-Ah,Kim, Koan-Hoi,Rhim, Byung-Yong The Korean Society of Pharmacology 2005 The Korean Journal of Physiology & Pharmacology Vol.9 No.6

In this study, the authors investigated whether death of vascular smooth muscle cell (VSMC) had a pathological pertinence. Conditioned media obtained from rat aorta smooth muscle cell (SMC) that were induced death by expressing FADD in the absence of tetracycline (FADD-SMC) triggered death of normal SMC. DNA fragmentation and caspase-3 activation were observed in dying SMC by conditioned media. FADD-SMC showed transcriptional activation of tumor necrosis factor $(TNF)-{\alpha}$. Conditioned medium contained $TNF-{\alpha}$, indicating secretion of the cytokine from dying FADD-SMC. It was investigated if secreted $TNF-{\alpha}$ was functional. Conditioned medium activated ERK and p38 MAPK pathways and induced MMP-9 expression, whereas depletion of the cytokine with its soluble receptor (sTNFR) remarkably inhibited induction of MMP-9 by conditioned medium. These findings suggest that $TNF-{\alpha}$ in conditioned medium seems to be active. Then, contribution of $TNF-{\alpha}$ on death-inducing activity of conditioned medium was examined. Depletion of $TNF-{\alpha}$ with soluble $TNF-{\alpha}$ receptor decreased the death activity of conditioned medium by 35%, suggesting that $TNF-{\alpha}$ play a partial role in the death activity. Boiling of medium almost completely abolished the death-inducing activity, suggesting that other heat labile death inducing proteins existed in conditioned medium. Taken together, these results indicate that SMC undergoing death could contribute to inflammation by expressing inflammatory cytokines and pathological complications by inducing death of neighboring cells.

Identification of mono- or poly-specific monoclonal antibody to Porphyromonas gingivalis heat-shock protein 60

Choi, Jeom-Il,Lee, Sang-Yull,Kim, Koan-Hoi,Choi, Bong-Kyu,Kim, Myung-Jin Korean Academy of Periodontology 2011 Journal of Periodontal & Implant Science Vol.41 No.2

Purpose: The aim of this study was to define the immunoreactive specificity of Porphyromonas gingivalis (P. gingivalis) heat shock protein (HSP) 60 in periodontitis and atherosclerosis. Methods: In an attempt to define the cross-reactive bacterial heat-shock protein with human self-antigen at molecular level, we have introduced a novel strategy for cloning hybridoma producing anti-P. gingivalis HSP 60 which is polyreactive to bacterial HSPs or to the human homolog. Results: Five cross-reactive clones were obtained which recognized the #19 peptide (TLVVNRLRGSLKICAVKAPG) among 37 synthetic peptides (20-mer, 5 amino acids overlapping) spanning the whole molecule of P. gingivalis HSP 60. We have also established three anti-P. gingivalis HSP 60 monoclonal antibodies demonstrating mono-specificity. These clones recognized the #29 peptide (TVPGGGTTYIRAIAALEGLK). Conclusions: Peptide #19 and #29 of P. gingivalis HSP 60 might be important immunoreactive epitopes in the immuno-pathogenic mechanism of bacterial antigen-triggered autoimmune diseases.

Differentially Expressed Genes by Inhibition of C-terminal Src Kinase by siRNA in Human Vascular Smooth Muscle Cells and Their Association with Blood Pressure

Hong, Kyung-Won,Shin, Young-Bin,Kim, Koan-Hoi,Oh, Berm-Seok Korea Genome Organization 2011 Genomics & informatics Vol.9 No.3

C-terminal SRC kinase (CSK) is a ubiquitously expressed, cytosolic enzyme that phosphorylates and inactivates several SRC family protein tyrosine kinases. Recent genomewide association studies have implicated CSK in the regulation of blood pressure. The current study aim is to determine the blood pressure association of the genes regulated by CSK down-regulation. The CSK mRNA expression was downregulated in vascular smooth muscle cells using small interfering RNA (siRNA). CSK mRNA levels fell by 90% in cells that were treated with CSK siRNA; the RNA from these cells was examined by microarray using the Illumina HumanRef-8 v3 platform, which comprises 24,526 reference mRNA probes. On treatment with CSK siRNA, 19 genes were downregulated by more than 2-fold and 13 genes were upregulated by more than 2-fold. Three (CANX, SLC30A7, and HMOX1) of them revealed more than 3 fold differential expression. Interestingly, the HMOX1 SNPs were associated with diastolic blood pressure in the 7551 Koreans using Korea Association REsource data, and the result was supported by the other reports that HMOX1 linked to blood vessel maintenance. Among the remaining 29 differentially expressed genes, seven (SSBP1, CDH2, YWHAE, ME2, PFTK1, G3BP2, and TUFT1) revealed association with both systolic and diastolic blood pressures. The CDH2 gene was linked to blood pressures. Conclusively, we identified 32 differentially expressed genes which were regulated by CSK reduction, and two (HOMX1 and CDH2) of them might influence the blood pressure regulation through CSK pathway.

Stamping Analyses and Die Design of Laser Welded Automotive Body

Kim, Heon Young,Shin, Yong Seung,Kim, Koan Hoi,Cho, Won Seok 대한금속재료학회(대한금속학회) 1998 METALS AND MATERIALS International Vol.4 No.4

Computer simulations and test trials are carried out to get the optimal conditions of the design for the stamping of the laser tailor welded automotive body panels. Through test trials with new manufactured die for Tailor Welded Blanks (TWB), the effects of the initial position of blank, blank holding force, drawbead shape, and corner radius are investigated. The results of computer simulations show good correspondence with those of test trials. The results are directly applied to the modification of the die or changing of the forming conditions, to obtain well controlled sound product free from fracture, wrinkling or excessive weld line movement.

Conditioned Medium from Dying Smooth Muscle Cell Induced Apoptotic Death

Moon Hyun Bu,Kyeong Ah Lee,Koan Hoi Kim,Byung Yong Rhim 대한생리학회-대한약리학회 2005 The Korean Journal of Physiology & Pharmacology Vol.9 No.6

In this study, the authors investigated whether death of vascular smooth muscle cell (VSMC) had a pathological pertinence. Conditioned media obtained from rat aorta smooth muscle cell (SMC) that were induced death by expressing FADD in the absence of tetracycline (FADD-SMC) triggered death of normal SMC. DNA fragmentation and caspase-3 activation were observed in dying SMC by conditioned media. FADD-SMC showed transcriptional activation of tumor necrosis factor (TNF)-α. Conditioned medium contained TNF-α, indicating secretion of the cytokine from dying FADD-SMC. It was investigated if secreted TNF-α was functional. Conditioned medium activated ERK and p38 MAPK pathways and induced MMP-9 expression, whereas depletion of the cytokine with its soluble receptor (sTNFR) remarkably inhibited induction of MMP-9 by conditioned medium. These findings suggest that TNF-α in conditioned medium seems to be active. Then, contribution of TNF-α on death-inducing activity of conditioned medium was examined. Depletion of TNF-α with soluble TNF-α receptor decreased the death activity of conditioned medium by 35%, suggesting that TNF-α play a partial role in the death activity. Boiling of medium almost completely abolished the death-inducing activity, suggesting that other heat labile death inducing proteins existed in conditioned medium. Taken together, these results indicate that SMC undergoing death could contribute to inflammation by expressing inflammatory cytokines and pathological complications by inducing death of neighboring cells.