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Cho, Young-Wuk,Han, Seung-Ho,Min, Byung-Il,Rhee, Jeong-Seop,Norio Akaike 경희대학교 동서의학연구소 2001 東西醫學硏究所 論文集 Vol.2001 No.-
Opioids have been thought to induce analgesia by activating the descending pain control system, especially at the level of periaquenductal gray, and regulate the neurotransmitter release through the inhibition of calcium channel. In the present study, the modulatory effects of protein kinase C and protein kinase A on the μ-opioid agonist-induced inhibition of the high-voltage activated calcium current were examined in the acutely dissociated rat periaqueductal gray neurons with the nystatin-perforated patch-clamp technique. Among 505 neurons tested, the barium current passing through the high-voltage activated calcium channels of 172 neurons (34%) were inhibited by 32±3% with the application of an μ-opioid agonist, [D-_Ala^2, N-MePhe^4, Gly^5 -ol]-enkephalin (DAMGO, 1 μM). The barium currents itself and the DAMGO-induced inhibitory effects were not affected by the application of either an adenylate cyclase activator (forskolin, 1μM) or a protein kinase inhibitor (staurosporin, 10nM) for 2 min. The DAMGO inhibition was completely and irreversibly antagonized by the application of a protein kinase C activator, phorbol-12-myristate-13-acetate (PMA, 1μM) for 2 min without any alteration of the barium current itself. However, the antagonizing effect of PMA was completely abolished by the application of 10 nM staurosporin for 2 min. After then, PMA did not show the antagonizing effect any more. Inversely, when staurosporin was applied before PMA, the antagonizing effect of PMA was also not shown. These results demonstrate that the μ-opiod agonist-induced inhibition of the periaqueductal gray neuronal high-voltage activated calcium current can be antagonized by protein kinase C activation. This finding may provide us a significant clue to understand the action mechanism of opioid-induced analgesia in the periaqueductal gray. ⓒ 2001 Elsevier Science B.V.All rights reserved.
Lithium-induced Increase of Synaptosomal Uptake of Norepinephrine in Rat Brain
Cho, Young-Wuk,Han, Seung-Ho,Kim, Chang-Ju,Min, Byung-Il The Korean Society of Pharmacology 1997 The Korean Journal of Physiology & Pharmacology Vol.1 No.2
Lithium remains the most widely used therapeutic agent for bipolar affective disorder, particularly mania. Although many investigators have studied the effects of lithium on abnormalities in monoamine neuro-transmitter as a pathophysiological basis of affective disorder, the action mechanism of lithium ion remains still unknown. To explore the action mechanism of lithium in the brain, we examined the effects of lithium on the extrasynaptosomal concentrations of catecholamines and their metabolites. Synaptosomes were prepared from the rat forebrains and assays of catecholamines and metabolites were made using HPLC with an electrochemical detector. Lithium of 1mM decreased the extrasynaptosomal concentrations of NE from the control group of $3.07{\pm}1.19$ to the treated group of $0.00{\pm}0.00$ (ng/ml of synaptosomal suspension) but not that of DHPG. It can be suggested that lithium increases synaptosomal uptake of NE. Increased intraneuronal uptake of NE would decrease neurotransmission and extraneuronal metabolism of NE. Because increased brain NE metabolism and neurotransmission have been suggested as important components in the pathophysiology of bipolar affective disorder, especially mania, lithium-induced increase of intraneuronal NE uptake can be suspected as an action mechanism of therapeutic effect of lithium in manic patient, possibly in bipolar affective disorder.
Significance of Biomarkers as a Predictive Factor for Post-Traumatic Sepsis
( Kyung-wuk Lee ),( Sung-hyuk Choi ),( Young-hoon Yoon ),( Jung-youn Kim ),( Young-duck Cho ),( Han-jin Cho ),( Sung-jun Park ) 대한외상학회 2018 大韓外傷學會誌 Vol.31 No.3
Purpose: Many traumatic patients die from sepsis and multiple organ failure. Early recognition of post-traumatic sepsis in traumatic patients will help improve the prognosis. Recently, procalcitonin (PCT), macrophage migration inhibitory factor (MIF), and lactic acid have emerged as predictive factors. Our study aims to explore the significance of PCT, MIF and lactic acid as a predictor of posttraumatic-sepsis in trauma patients. Methods: This study was conducted on prospective observational study patients who visited an emergency medical center in a university hospital from March 2014 to February 2016. We measured the white blood cells, c-reactive protein (CRP), lactic acid, PCT, and MIF with serum taken from the patient’s blood within 1 hour of the occurrence of the trauma. The definition of post-traumatic sepsis was defined as being part of systemic inflammation response syndrome criteria with infections within a week. Results: A total of 132 patients were analyzed, wherein 74 patients were included in the low injury severity score (ISS) group (ISS <15) and 58 patients were included in the high ISS group (ISS ≥15). The mean PCT, MIF, and lactic acid levels were higher in the high ISS group (p<0.05). Meanwhile, 38 patients were included in the early sepsis group and 94 patients were included in the non-sepsis group. The mean MIF levels were higher in the sepsis group than the non-sepsis group (p<0.05) and there were no significant differences in the initial CRP, lactic acid, and PCT levels in these two groups. Conclusions: MIF may be considered as a predictive factor for sepsis in trauma patients.
Developmental change of GABAergic postsynaptic current in rat periaqueductal gray
Hahm, Eu-Teum,Lee, Jong-Ju,Min, Byung-Il,Cho, Young-Wuk EAST-WEST MEDICAL RESEARCH INSTITUTE KYUNG HEE UNI 2005 東西醫學硏究所 論文集 Vol.2005 No.-
The present study was designed to examine developmental changes of GABAergic spontaneous miniature inhibitory postsynaptic currents (mIPSCs) in periaqueductal gray (PAG) neurons mechanically isolated from young (12-to 18-day) and adult (8-to 12-week) rats. While the frequency of mIPSCs was similar, the current amplitude in adult rats was significantly smaller than in young rats. In the study of mIPSC kinetics, all kinetic parameters except for the fast decay time in adult rats were smaller or shorter than in the case of young rats. The present study demonstrates that a decrease in the amplitude of GABAergic mIPSC during development may result from a decrease in the GABA contents of synaptic vesicles and from changes in the kinetics of postsynaptic GABA-activated Cl? channels.
Cho, Kyung Jin,Ryu, Dae Won,Kwak, Hyun Young,Lee, Jin Wuk,Lee, Woo Ram,Lim, Kwang Soo,Koh, Eui Kwan,Kwon, Young Wan,Hong, Chang Seop The Royal Society of Chemistry 2012 Chemical communications Vol.48 No.59
<P>A tetranuclear Fe<SUP>III</SUP><SUB>2</SUB>Mn<SUP>III</SUP><SUB>2</SUB> compound was prepared using highly blocked precursors. The well-isolated molecular entity associated with appropriate magnetic anisotropy allows for single-molecule magnet behavior.</P> <P>Graphic Abstract</P><P>A tetranuclear Fe<SUP>III</SUP><SUB>2</SUB>Mn<SUP>III</SUP><SUB>2</SUB> compound was prepared using highly blocked precursors. The well-isolated molecular entity coupled with appropriate magnetic anisotropy allows for single-molecule magnet behavior. <IMG SRC='http://pubs.rsc.org/services/images/RSCpubs.ePlatform.Service.FreeContent.ImageService.svc/ImageService/image/GA?id=c2cc32503a'> </P>
Cho, Eu‐,Jin,An, Hyo‐,Jin,Shin, Ji‐,Sun,Choi, Hye‐,Eun,Ko, Jane,Cho, Young‐,Wuk,Kim, Hyung‐,Min,Choi, Jung‐,Hye,Lee, Kyung‐,Tae Wiley Subscription Services, Inc., A Wiley Company 2011 Journal of cellular biochemistry Vol.112 No.12
<P><B>Abstract</B></P><P>Roxatidine is a novel, specific, competitive H<SUB>2</SUB>‐receptor antagonist that is used to treat gastric and duodenal ulcers, and which is known to suppress the growth of several tumors by reducing vascular endothelial growth factor (VEGF) expression. Nevertheless, it remains unclear whether roxatidine has anti‐inflammatory effects. In this study, we the authors investigated the anti‐inflammatory effect of roxatidine in lipopolysaccharide (LPS)‐stimulated RAW 264.7 macrophage cells. It was found that roxatidine dose‐dependently inhibited the productions of prostaglandin E<SUB>2</SUB> (PGE<SUB>2</SUB>), nitric oxide (NO), and histamine, and the protein and mRNA expressions of cyclooxygenase‐2 (COX‐2), inducible nitric oxide synthase (iNOS), and histidine decarboxylase (HDC). In addition, roxatidine reduced the productions and expressions of VEGF‐1 and pro‐inflammatory cytokines, including those of tumor necrosis factor‐α (TNF‐α), interleukin‐1β (IL‐1β), and interleukin‐6 (IL‐6). Electrophoretic mobility shift assays (EMSA) and reporter gene assays revealed that treatment with roxatidine attenuated the LPS‐induced DNA‐binding and transcriptional activity of nuclear factor kappa B (NF‐κB). In addition, it was found that pretreatment with roxatidine significantly inhibited the nuclear translocations of the p65 and p50 subunits of NF‐κB, and these inhibitions were not found to be associated with decreases in the phosphorylation or degradation of inhibitory kappa B‐α (IκBα). Furthermore, roxatidine suppressed the phosphorylation of p38 MAP kinase, but not of IκB kinase‐α/β (IKKα/β), c‐Jun NH<SUB>2</SUB>‐terminal kinase (JNK), or extracellular signal‐regulated kinase (ERK). Taken together, these results indicate that the anti‐inflammatory properties of roxatidine in LPS‐treated RAW 264.7 macrophages are mediated by the inhibition of NF‐κB transcriptional activity and the p38 MAP kinase pathway. J. Cell. Biochem. 112: 3648–3659, 2011. © 2011 Wiley Periodicals, Inc.</P>