• Investigative Magnetic Resonance Imaging
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• v.4 no.1
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• pp.27-33
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• 2000

Purpose: To determine the electronic spin relaxation times, $T_{le}$, of three commercially available Gd-chelated MR contrast agents, Gd-DTPA, Gd-DTPA-BMA and Gd-DOTA, using Electron Paramagnetic Resonance(EPR) technique. Material and Methods: The paramagnetic MR contrast agents, Gd-DTFA(Magnevist) , Gd-DTFA-BMA(OMNISCAN) and Gd-DOTA(Dotarem), were used for this study, The EPR spectra of these contrast agents, which were prepared 2:1 methanol/water solution, were obtained at low temperatures, from $-160^{\circ}C~20^{\circ}C$. The glassy-state EPR spectra for these contrast agents were then fitted by the simulation spectra generated with different zero-field splitting (ZFS) parameters by a computer simulation program 'GEN', which generates the EPR powder spectrum using a given ZFS in $3{\times}3$ tensor. Finally, the spin relaxation times of the contrast agents were then determined from the $T_{2e}$, D, and E values of the best simulation spectra using the McLachlan's theory of average relaxation rate. Results: The electronic transverse spin relaxation times, $T_{2e}'s$, of Gd-DTPA, Gd-DTPA-BMA and Gd-DOTA were 0.113ns, 0.147ns and 1.81ns respectively. The g-values were 1.9737, 1.9735 and 1.9830 and the electronic spin relaxation times, $T_{1e}'s$, were 18.70ns, 33.40ns and $1.66{\mu}s$, respectively. Conclusion: The results of these studies reconfirm that the paramagnetic MR contrast agents with larger ZFS parameters should have shorter $T_{1e}'s$. Among three contrast agents used for this study, Gd-DOTA chelated with cyclic ligand structure shows better electronic property then the others with linear structure. Thus, it is concluded that the exact determination of ZFS parameters is the important factor in evaluating relaxation enhancement effect of the agents and in developing new contrast agents.

• Development and Reproduction
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• v.10 no.2
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• pp.105-113
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• 2006

Reactive oxygen species(ROS) generated in cellular metabolism have an effect on cell maturation and development. In human reproductive tract, oxidative injury by ROS may induce female infertility. Also, oxidative injury may be responsible for developmental retardation and arrest of mammalian preimplantation embryos. Activating transcription factor 4(ATF4) is a member of the cyclic-AMP response element-binding(CREB) familiy of basic region- leucine zipper(bZip). ATF4 is known to regulate stress response to protect cell from various stress factors and inducer of apoptisis. The purpose of this study was to investigate whether ATF4 is involved in the defensive mechanism in oxidative stress condition during the development of mouse preimplantation embryos. To verify the expression of ATF4 in oxidative stress condition, 2-cell stage embryos were cultured in HTF media containing 0.1mM, 0.5mM or 1mM hydrogen peroxide($H_2O_2$) for 1hr(2-cell), 8hr(4-cell), 17hr(8-cell), 24hr(morula), 48hr(early blastocyst) or 64hr(late blastocyst). The developmental rate decreased in the 0.1mM $H_2O_2$ treated group compared with control group. In embryos treated with 0.5mM and 1mM $H_2O_2$ showed 2-cell block. As a results of the semi-quantitative RT-PCR analysis of SOD1, ATF4 and Bax gene expression, SOD1, ATF4 and Bax genes were increased in 0.1mM, 0.5mM, 1mM $H_2O_2$ treated groups compared with control group. In 2-cell embryos, expression of SOD1, ATF4 and Bax genes were notably increased in 0.1mM, 0.5mM, 1mM $H_2O_2$ treated groups compared with control group. Immunofluorescence analysis showed that ATF4 protein was localized at the cytoplasm of preimplantation embryos. The increase in ATF4 immunoreactivety was observed in the 0.1mM, 0.5mM, 1mM $H_2O_2$ treated groups compared with control group. It suggests that oxidative stress by $H_2O_2$ induces expression of ATF4 and may be involved in protection mechanism in preimplantation embryos from oxidative injury.

• Journal of Chest Surgery
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• v.42 no.5
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• pp.576-587
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• 2009

Background: The up-regulation of the nitric oxide (NO)-cGMP pathway might be involved in the change of vascular reactivity in rats 3 days after they suffer acute myocardial infarction. However, the underlying mechanism for this has not been clarified. Material and Method: Acute myocardial infarction (AMI) was induced by occluding the left anterior descending coronary artery (LAD) for 30 min (Group AMI), whereas the sham-operated control rats were treated similarly without LAD occlusion (Group SHAM), The concentration-response relationships for phenylephrine (PE), KCl, acetylcholine (Ach) and sodium nitroprusside (SNP) were determined in the endothelium intact E(+) and endothelium denuded E(-) thoracic aortic rings from the rats 3 days after AMI or a SHAM operation. The concentration-response relationships of PE in the E(+) rings from the AMI rats were compared with those relationships in the rings pretreated with nitric oxide synthase (NOS) inhibitor $N{\omega}$-nitro-L-arginine methyl ester (L-NAME) or the cyclooxygenase inhibitor indomethacin. The plasma nitrite/nitrate concentrations were checked via a Griess reaction. The cyclic GMP content in the thoracic aortic rings was measured by radioimmunoassay and the endothelial nitric oxide synthase (eNOS) mRNA expression was assessed by real time PCR. Result: The mean infarct size (%) in the rats with AMI was $21.3{\pm}0.62%$. The heart rate and the systolic and diastolic blood pressure were not significantly changed in the AMI rats. The sensitivity of the contractile response to PE and KCl was significantly decreased in both the E(+) and E(-) aortic rings of the AMI group (p<0.05). L-NAME completely reversed these contractile responses whereas indomethacin did not (p<0.05). Moreover, the sensitivity of the relaxation response to Ach was also significantly decreased in the AMI group (p<0.05). The plasma nitrite and nitrate content (p<0.05), the basal cGMP content (p<0.05) and the eNOS mRNA expression (p=0.056) in the AMI rats were increased as compared with the SHAM group. Conclusion: Our findings indicate that the increased eNOS activity and the up-regulation of the NO-cGMP pathway can be attributed to the decreased contractile or relaxation response in the rat thoracic aorta 3 days after AMI.

• Journal of Korean Society of Environmental Engineers
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• v.27 no.8
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• pp.844-851
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• 2005

The purpose of this study was to determine feasibility of application of regenerated or recycled $TiO_2$ on the successive treatment of Cu(II)-EDTA. The recovery of copper, the reuse of $TiO_2$ and the assessment of acute toxicity was studied in the total eight successive photocatalytic reactions. Aqueous solution of $10^{-4}\;M$ Cu(II)-EDTA was treated using an illuminated $TiO_2$ at pH 6 in a circulating reactor. Two different procedures were applied in the reuse of $TiO_2$: i) recycle of $TiO_2$ without acid wash ii) regeneration of $TiO_2$ with acid wash to remove adsorbed copper in a previous experiment. The averaged decomplexation rate constant($k'_{obs}$) of Cu(II)-EDTA in recycle of $TiO_2$ without acid wash was approximately 45% less than that in regeneration of $TiO_2$ with acid wash. Removal of Cu(II) was near complete after 180 minutes in the total eight successive photocatalytic reactions using the regenerated $TiO_2$ after acid wash. In contrast, removal of Cu(II) was minimum at total fifth successive photocatalytic oxidation using the recycled $TiO_2$ without arid wash. The recovered $TiO_2$ was approximately 86% in average in each procedure. The recovered Cu(II) was 67.9% in average. The acute relative toxicity of the treated water rapidly declined at an initial reaction time up to 60 minutes but little declination was observed after 60 minutes due to little degradation of DOC. Relative toxicity of treated water using the recycled $TiO_2$ without acid wash we some what well correlated with the concentration of dissolved Cu(II). From this work, it is suggested that Cu(II)-EDTA can be effectively treated using an integrated cyclic photocatalytic oxidation with recovery of $TiO_2$ and Cu(II).

• The Korean Journal of Pharmacology
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• v.32 no.1
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• pp.1-11
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• 1996

Since it has been reported that the depolarization-induced norepinephrine (NE) release is inhibited by activation of presynaptic $A_1-adenosine$ heteroreceptor in hippocampus, a large body of experimental data on the post-receptor mechanism of this process has been accumulated. But, the post-receptor mechanism of presynaptic $A_1-adenosine$ receptor on the NE release has not been clearly elucidated yet. Therefore, it was attempted to clarify the post-receptor mechanisms of the $A_1-adenosine$ receptor-mediated control of NE release in this study. Slices from rat hippocampus were equilibrated with $^3H-norepinephrine$ and the release of the labelled products was evoked by electrical stimulation (3 Hz, 5 $Vcm^{-1}$, 2 ms, rectangular pulses), and the influence of various agents on the evoked tritium-outflow was investigated. Adenosine, in concentrations ranging from $1{\sim}30{\mu}M$, decreased the NE release in a dose-dependent manner, without affecting the basal rate of release. The adenosine effects were significantly inhibited by 8-cyclopentyl-1,3-dipropylxanthine (DPCPX, $2{\mu}M$), a selective $A_1-receptor$ antagonist. The responses to N-ethylmaleimide (NEM, 10 & $30{\mu}M$), a SH-alkylating agent of G-protein, were characterized by increments of the evoked NE-release and the basal release, and the adenosine effects were completely abolished by NEM pretreatment. $4{\beta}-Phorbol$ 12,13-dibutyrate (PDB, $1{\mu}M$), a specific protein kinase C (PKC) activator, increased the evoked NE release, whereas polymyxin B sulfate (PMB,0.1 mg), a PKC inhibitor, decreased the release, and the adenosine effects were inhibited by these agents. Nifedipine $(1{\mu}M)$, a $Ca^{2+}-channel$ blocker of dihydropyridine analogue, did not affect the adenosine effect. Tetraethylammonium (TEA, 3 mM) increased the evoked NE release, and inhibited the adenosine effects, but glibenclamide, a ATP dependent $K^+-channel$ blocker, did not. Finally, 8-bromo cyclic AMP (100 & $300{\mu}M$), a membrane-permeable analogue of cAMP, did not alter the NE release, but adenosine effects were inhibited by pretreatment with 8br-cAMP. These results suggest that the decrement of the evoked NE-release by $A_1-adenosine$ receptor is mediated by the C-protein, which is coupled to protein kinase C, adenylate cyclase system and TEA sensitive $K^+-channel$, and that nifedipine-sensitive $Ca^{2+}-channel$ and glibenclamide-sensitive $K^+-channel$ are not involved in this process.

• Pediatric Gastroenterology, Hepatology & Nutrition
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• v.5 no.2
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• pp.174-180
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• 2002

Purpose: Ursodeoxycholic acid (UDCA) is known to decrease hepatic injury by promoting the biliary secretion of retained toxic endogenous bile acids in hepatobiliary diseases complicated by total parenteral nutrition (TPN). However, most studies have focused on treatment for complications after TPN. We investigated the preventive role of early administration of UDCA in TPN-induced hepatobiliary complications by a randomized, double-blind, placebo-controlled trial. Methods: Between May 2000 and May 2002, thirteen patients, who were given TPN more than 10 days in the hospital, were assigned randomly to two groups. One was the case group (7 patients) who were given UDCA simultaneously with TPN regimen, and the other, the control group (6 patients) who were given placebo. Their age ranged from 1 day to 13 years. They were affected with diseases impossible for enteral nutrition, such as prematurity, cerebral palsy, chronic diarrhea, anorexia nervosa, pancreatitis, and cyclic vomiting. The duration of TPN ranged from 10 to 70 days. Hematologic parameters including liver function test were measured at regular intervals, and the duration, composition, administration rate, total calorie of TPN were recorded. The serum levels of total bilirubin, aspartate aminotransferase (AST), alanine aminotransferase (ALT), and alkaline phosphatase were compared between groups after cessation of the study. Results: The autoregressive coefficient of the control group was 0.4419 (p=0.0651) in bilirubin, -0.0431 (p=0.7923) in AST, 0.2398 (p=0.2416) in ALT, and 0.2459 (p=0.1922) in alkaline phosphatase by mixed procedure model when the parameters were referred to the case group. Conclusion: The serum level of total bilirubin did not increase in comparison with that of the control group, but statistically insignificant, when both TPN and UDCA were administered simultaneously from the beginning.

• Journal of the Korean Chemical Society
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• v.36 no.2
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• pp.261-272
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• 1992

Tetradentate Schiff base Cobalt(II)(3MeOSED)$(H_2O)_2$ complexe was synthesized and allowed to react with dry oxygen to form oxygen adducts of Cobalt(III) complexes such as ${\mu}$-peroxo type [Co(III)(3MeOSED)(DMF)]$_2O_2$ and [Co(III)(3MeOSED)(DMSO)]$_2O_2$in DMF and DMSO or superoxo type [Co(III)(3MeOSED)(Py)]$O_2$ in pyridine. The oxygen adducted complex was investigated by cyclic voltammetry and DPP method with glassy carbon electrode in 0.1M TEAP-DMF (-DMSO,-Py) as supporting electrolyte solution. As a result the reduction reaction process occurred to four steps including prewave Of $O_2^-$in 1 : 1 oxygen adducted superoxo type [Co(III)(3MeOSED)(Py)]$O_2$complex and three steps not including prewave of $O_2^-$ in 1 : 2 oxygen adducted ${\mu}$-peroxo type [Co(III)-(3MeOSED)(DMF)]$_2O_2$ and [Co(III)(3MeOSED)(DMSO)]$_2O_2$. A superoxo type [Co(III)(3MeOSED)(L)]$O_2\;(L: CH_3OH)$ was generated with oxygen in methanol. Selectively oxidized hydrazobenzene $(H_2AB)$ to trans-azobenzene(t-AB) and the rate constant k for oxidation reaction of the following equation is $(2.96 {\pm} 0.2)$${\times}$ $10^{-1}$M/sec. $H_2AB$ + Co (II)(3MeOSED)$(L_2)+O_2\;{\rightleftarrow^K}$ [Co(III)(3MeOSED)(L)]$O_2{\cdot}H_2AB{\longrightarrow^K}$ Co(II(3MeOSED)$(L)_2$+t-AB+$H_2O_2 $.

• Journal of Korean Medical Science
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• v.33 no.52
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• pp.346.1-346.11
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• 2018

Background: To evaluate the therapeutic benefits of the treat-to-target (T2T) strategy for Asian patients with early rheumatoid arthritis (RA) in Korea. Methods: In a 1-year, multicenter, open-label strategy trial, 346 patients with early RA were recruited from 20 institutions across Korea and stratified into 2 groups, depending on whether they were recruited by rheumatologists who have adopted the T2T strategy (T2T group) or by rheumatologists who provided usual care (non-T2T group). Data regarding demographics, rheumatoid factor titer, anti-cyclic citrullinated peptide antibody titer, disease activity score of 28 joints (DAS28), and Korean Health Assessment Questionnaire (KHAQ) score were obtained at baseline and after 1 year of treatment. In the T2T group, the prescription for disease-modifying antirheumatic drugs was tailored to the predefined treatment target in each patient, namely remission (DAS28 < 2.6) or low disease activity (LDA) ($2.6{\leq}DAS28$ < 3.2). Results: Data were available for 163 T2T patients and 162 non-T2T patients. At the end of the study period, clinical outcomes were better in the T2T group than in the non-T2T group (LDA or remission, 59.5% vs. 35.8%; P < 0.001; remission, 43.6% vs. 19.8%; P < 0.001). Compared with non-T2T, T2T was also associated with higher rate of good European League Against Rheumatism response (63.0% vs. 39.8%; P < 0.001), improved KHAQ scores (-0.38 vs. -0.13; P = 0.008), and higher frequency of follow-up visits (5.0 vs. 2.0 visits/year; P < 0.001). Conclusion: In Asian patients with early RA, T2T improves disease activity and physical function. Setting a pre-defined treatment target in terms of DAS28 is recommended.