• YAKHAK HOEJI
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• v.47 no.4
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• pp.195-199
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• 2003

An analysis method for the determination of methylendedioxymethamphetamine (MDMA) and its metabolite methylendedioxymethamphetamine (MDA) in hair by gas chromatography/mass spectrometry was proposed. For MDMA and MDA analysis, hair samples were incubated in MeOH (1％ HCl), derivatized with trifluoroacetic anhydride and assayed by GC/MS. Hair of 18 subjects for drug abuse was analyzed for MDMA and MDA. Calibration curves for the determination of MDMA and MDA in hair showed a good linearity at a concentration range from 0.5 ng to 250 ng ($r^2$=0.999) The extraction recovery was determined from hair blanks at 50, 100 ng. The percentage of recovery were found to be 96.08∼103.48 with CV value of 1.62∼3.89. The concentrations of MDMA and MDA ranged 1.14∼38.06 ng/mg and 0.07∼3.91 ng/mg, respectively in 18 hair samples from MDMA abusers. The ratio of MDMA to MDA ranged from 9.65∼28.46 in all specimen. Hair analysis for MDMA is a useful method for identification of long-term drug abuser.

• Development and Reproduction
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• v.15 no.2
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• pp.173-178
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• 2011

The amphetamine derivative 3,4-methylenedioxymethamphetamine (MDMA) is a potent monoaminergic neurotoxin with the potential to cause serotonergic neurotoxicity, but has become a popular recreational drug. Little has been known about the cellular effects induced by MDMA. This report shows that MDMA inhibits neuronal cell growth and differentiation. MDMA suppressed neuronal cell growth. The results of quantitative real-time PCR analysis showed that Egr-1 expression is elevated in mouse embryo and neuroblastoma cells after MDMA treatment. Transiently transfected Egr-1 interfered with the neuronal differentiation of neuroblastoma cells such as SH-SY5Y and PC12 cells. These findings provide evidence that the abuse of MDMA during pregnancy may impair neuronal development via an induction of Egr-1 over-expression.

• Biomolecules & Therapeutics
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• v.11 no.4
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• pp.214-223
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• 2003

Methamphetamine (METH) and 3,4-methylenedioxymethamphetamine (MDMA) have become popular recreational drugs of abuse in many countries. Although the neurotoxic damage caused by METH and MDMA is characterized by degeneration of the dopaminergic and serotonergic systems in brain, the molecular and cellular mechanisms remain to be clarified. Therefore, the purposes of this study were to confirm the capability of METH and MDMA to induce apoptosis and to clarify the action of its molecular mechanism by using serotonergic JAR cells and dopaminergic SK-N-SH cells. METH and MDMA were dose-dependently cytotoxic to human serotonergic JAR cells and dopaminergic SK-N-SH cells. The morphological change of apoptosis was found in Giemsa staining and TUNEL and further verified in DNA fragmentation analysis. Immunoblotting analysis revealed proteolytic cleavage of caspase-3 and -9 and change of bcl-2 and bax proteins. These results suggest that METH and MDMA may induce caspase-dependent apoptosis via the mitochondrial cell death pathway and METH and MDMA-induced neurotoxicity may happen to broadly and independently of both dopaminergic and serotonergic systems.

• Molecules and Cells
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• v.27 no.5
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• pp.571-575
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• 2009

The amphetamine derivative 3, 4-methylenedioxymethamphetamine (MDMA) has become a popular recreational drug, and has also been shown to cause serotonergic neurotoxicity. This report shows that MDMA impairs brain development in a whole mouse embryo culture. The results of quantitative real-time PCR analysis showed that autophagy-related protein 5 (Atg5) expression is elevated in mouse embryo and neuroblastoma cells after MDMA treatment. This elevated Atg5 expression interferes with the neuronal differentiation of neuroblastoma cells such as SH-SY5Y and PC12 cells. Thus, our results suggest that the use of MDMA during pregnancy may impair neuronal development via an induction of Atg5 expression.

• Proceedings of the PSK Conference
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• 2003.10b
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• pp.112.1-112.1
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• 2003

The qualitative and quantitative analysis of MDMA and MDA in hair samples by GC/MS were reported. Hairs were collected from subjects aged 22-37 years, who were suspected of abusing MDMA. After washing with methanol, hair samples were cut into small pieces, extracted with methanol containing 1 percent hydrochloric acid for 20th, and the solution was evaporated. MDMA or MDA in the extract were determined by GC/MS using selected ion monitoring after derivatization with trifluoroacetic anhydride. (omitted)

• Toxicological Research
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• v.6 no.2
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• pp.205-213
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• 1990

The regulation of neurotoxicants has usually been based upon setting reference doses by dividing a no observed adverse effect level (NOAEL) by uncertainty factors that theoretically account for interspecies and intraspecies extraploation of experimental results in animals to humans. Recently, we have proposed a four-step alternative procedure which provides quantitative estimates of risk as a function of dose. The first step is to establish a mathematical relationship between a biological effect or biomarker and the dose of chemical administered. The second step is to determine the distribution (variability) of individual measurements of biological effects or their biomarkers about the dose response curve. The third step is to define an adverse or abnormal level of a biological effect or biomarker in an untreated population. The fourth and final step is to combine the information from the first three steps to estimate the risk (proportion of individuals exceeding on adverse or abnormal level of a biological effect or biomarker) as a function of dose. The primary purpose of this report is to enhance the certainty of the first step of this procedure by improving our understanding of the relationship between a biomarker and dose of administered chemical. Several factors which need to be considered include: 1) the pharmacokinetics of the parent chemical, 2) the target tissue concentrations of the parent chemical or its bioactivated proximate toxicant, 3) the uptake kinetics of the parent chemical or metabolite into the target cell(s) and/or membrane interactions, and 4) the interaction of the chemical or metabolite with presumed receptor site(s). Because these theoretical factors each contain a saturable step due to definitive amounts of required enzyme, reuptake or receptor site(s), a nonlinear, saturable dose-response curve would be predicted. In order to exemplify this process, effects of the neurotoxicant, methlenedioxymethamphetamine (MDMA), were reviewed and analyzed. Our results and those of others indicate that: 1) peak concentrations of MDMA and metabolites are ochieved in rat brain by 30 min and are negligible by 24 hr, 2) a metabolite of MDMA is probably responsible for its neurotoxic effects, and 3) pretreatment with monoamine uptake blockers prevents MDMA neurotoxicity. When data generated from rats administerde MDMA were plotted as bilolgical effect (decreases in hippocampal serotonin concentrations) versus dose, a saturation curve best described the observed relationship. These results support the hypothesis that at least one saturable step is involved in MDMA neurotoxicity. We conclude that the mathematical relationship between biological effect and dose of MDMA, the first step of our quantitative neurotoxicity risk assessment procedure, should reflect this biological model information generated from the whole of the dose-response curve.

• YAKHAK HOEJI
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• v.47 no.3
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• pp.142-147
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• 2003

Gas chromatography-mass spectrometric (GC-MS) procedure is presented for the simultaneous qualification and quantitation of methamphetamine (MA), amphetamine (AMP), 3,4-methylenedioxymethamphetamine (MDMA), 3,4-methylenedioxyamphetamine (MDA), and 3,4-methylenedioxyethylamphetamine (MDEA) in human hair. The method procedure involves decontamination of hair with distilled water and acetone, acidic hydrolysis, extraction in the presence of deuterated internal standards, and GC-MS analysis after derivatization with trifluoroacetic anhydride (TFAA) in ethylacetate. The limit of detection for 5 drugs were about 0.1∼0.15 ng/mg using 30 mg hair sample. Coefficient variations of correlation ranged from 0.9941 to 0.9993. The recoveries of these drugs were found to be 93.4∼104.4％. The concentrations of AMP, MA, MDA, and MDMA in abusers' hair samples were measured 0.17∼2.88, 2.09∼18.34, 0.24∼3.83, and 3.10∼22.81 ng/mg, respectively. The ratios of MA/AMP and MDMA/MDA ranged 5.67∼49.57 and 4.78∼54.31, respectively. This assay has been successfully utilized in the evaluation of the deposition of amphetamine-type stimulants (ATS) in human hair.

• Analytical Science and Technology
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• v.21 no.1
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• pp.41-47
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• 2008

Although liquid-liquid extraction (LLE) method has been used routinely for the analysis of amphetamine-like drugs (amphetamine; AP, methamphetamine; MA, 3,4-methylenedioxyamphetamine; MDA, 3,4-methylenedioxymethamphetamine; MDMA, 3,4-methylenedioxyethylamphetamine; MDEA), a solid-phase extraction (SPE) method, which can be automated, was applied for the simultaneous determination by GC/MS in human urine. Urine samples (3 mL) and 0.1 M phosphate buffer (1 mL, pH 7.0) were extracted by an automated SPE system. The eluent was evaporated, derivatized with trifluoroacetic anhydride (TFAA), and analyzed by GC/MS. The calibration curves was linear with correlation coefficient ($r^2$) above 0.994 in the ranges of 34.0 (AP), 28.0 (MDA)~1000.0 ng/mL for AP, MDA, and 50.0~2000.0 ng/mL for MA, MDMA, and MDEA. The limits of detection ranged from 4.0 to 10.0 ng/mL, and the limits of quantitation ranged from 12.0 to 34.0 ng/mL. The relative recoveries were 93.5~107.7 %. The precisions and accuracies were 1.9~14.8 % and -8.7~14.8 %, respectively. The present method was successfully applied to identify the MA or Ecstasy (MDMA) abusers in exact as well as rapid.

• Proceedings of the Korean Information Science Society Conference
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• 2005.07a
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• pp.295-297
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• 2005

This paper uses our proposed model for connecting ubiquitous physical objects over the web using URI, while utilizing the already developed frameworks, for ubiquitous service discovery like JINI, UPnP, and RDF/OWL for semantic web. By using this proposed scheme, we have presented architecture of a service oriented modular distributed ubiquitous middleware i.e. MDMA

• The Korean Society of Law and Medicine
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• v.14 no.1
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• pp.43-83
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• 2013

Medical treatment has great potential for conflict. Even the best-trained doctors can commit medical malpractice that result in continuing physical or mental disabilities or even death. Medical conflicts have been increasing over years. The medical conflicts between patient and medical professionals that result from medical professionals' mistakes are often fueled by a violation on the pretext of the injuries form medical malpractice and can lead to litigation. The litigation usually cost a lot of money and time. The extension of the litigation period as well as expensive cost and lack of medical knowledge placing a great burden on patients. Alternative Dispute Resolution(ADR) is more efficient than litigation. In 1988, the medical dispute mediation system has been introduces as the Act on Remedy for Damage from Medical Accident and Medical Dispute Mediation by Korean Medical Association came into effect after 23 years of enactment efforts. Medical Dispute Mediation Act(hereinafter referred to as the "MDMA") has finally entered into force from 8 April 2012. The purpose of the MDMA is to promptly and fairly redress injuries caused by medical malpractice and create a stable environment for medical services of public health or medical professionals by providing for matters regarding the mediation and arbitration of medical disputes(MDMA ${\S}1$). In an effort to secure the fair, speedy and inexpensive resolution of every malpractice case, the Korea Medical Dispute Mediation and Arbitration Agency(hereinafter referred to as the "K-MEDI") was established. Following the MDMA, the K-MEDI shall endeavor to ensure the medical dispute mediation or arbitration proceedings are conducted in a prompt, fair, and efficient manner, and patients and medical professionals shall attend proceedings in good faith with mutual trust and understanding when they participate in medical dispute mediation or arbitration proceedings.