• The Korean Journal of Pain
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• v.27 no.3
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• pp.210-218
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• 2014

Brachial plexus injury is a potential complication of a brachial plexus block or vessel puncture. It results from direct needle trauma, neurotoxicity of injection agents and hematoma formation. The neurological presentation may range from minor transient pain to severe sensory disturbance or motor loss with poor recovery. The management includes conservative treatment and surgical exploration. Especially if a hematoma forms, it should be removed promptly. Comprehensive knowledge of anatomy and adept skills are crucial to avoid nerve injuries. Whenever possible, the patient should not be heavily sedated and should be encouraged to immediately inform the doctor of any experience of numbness/paresthesia during the nerve block or vessel puncture.

• Proceedings of the PSK Conference
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• 2002.04a
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• pp.148.2-149
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• 2002

• Proceedings of the Korea Environmental Mutagen Society Conference
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• 2002.05a
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• pp.111-111
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• 2002

• Bulletin of the Korean Chemical Society
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• v.30 no.7
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• pp.1445-1451
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• 2009

New benzotriazoles (5-8) or dibenzodiazepine derivatives (11-18) were synthesized starting from 3-[(2-amino- 4,5-disubstitutedphenyl)amino]-5,5-disubstitutedcyclohex-2-enones (1-4) through internal coupling of their diazonium salts or internal Mannich reaction in the presence of aromatic aldehydes. Pharmacological evaluation of benzotriazole and dibenzodiazepine derivatives for their clozapine-like properties revealed that dibenzodiazepine 11 bearing 4-bromophenyl group exhibited the same antipsychotic activity as the reference drug clozapine while the activity of benzotriazole 7 was 25% lesser than that of clozapine. Moreover, compounds 7 and 11 did not show significant CNS depressant activity as well as no or slight neurotoxicity on contrast to clozapine when tested in mice using forced swim, rotarod and horizontal screen tests.

• Journal of The Korean Society of Clinical Toxicology
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• v.3 no.2
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• pp.119-121
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• 2005

Sodium bromate or potassium bromate has been used as hair cold neutralizer. Sodium bromate intoxications occurred in children incidentally early days of marketing, but recently in adult suicidally. This chemical intoxication result in renal failure, ototoxicity, neurotoxicity, hemolytic anemia and so on. We experienced a 39-year-old woman of hairdresser with non-oliguric acute renal failure after ingestion hair neutralizer 500 ml. She received hemodialysis 3 times and discharged without complication on 8th admission days.

• Annals of Clinical Neurophysiology
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• v.16 no.1
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• pp.1-7
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• 2014

Iron is an important element for brain oxygen transport, myelination, DNA synthesis and neurotransmission. However, excessive iron can generate reactive oxygen species and contribute neurotoxicity. Although brain iron deposition is the natural process with normal aging, excessive iron accumulation is also observed in various neurological disorders such as neurodegeneration with brain iron accumulation, Parkinson's disease, Alzheimer's disease, multiple sclerosis, Friedreich ataxia, and others. Magnetic resonance image (MRI) is a useful method for detecting iron deposits in the brain. It can be a powerful tool for diagnosis and monitoring, while furthering our understanding of the role of iron in the pathophysiology of a disease. In this review, we will introduce the mechanism of iron toxicity and the basics of several iron-related MRI techniques. Also, we will summarize the previous results concerning the clinical application of such MR imagings in various neurological disorders.

• Proceedings of the Korean Society of Toxicology Conference
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• 2003.10b
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• pp.64-67
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• 2003

Halogenated aromatic hydrocarbons (HAHs) including TCDD and PCBs are known to cause neurotoxic effects in both man and animals such as cognitive impairment and motor dysfunctions. While theses chemicals may lead to neurodevelopmental and neurobehavioral deficit, structural activity relationship and molecular targets for these chemicals are not elucidated.(omitted)

• Childhood Kidney Diseases
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• v.9 no.1
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• pp.91-96
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• 2005

Cyclosporin A-induced central neurotoxicity has been rarely reported in patients with nephrotic syndrome. We report a pediatric patient who developed acute leukoencephalopathy diagnosed by MRI during CsA therapy for nephrotic syndrome.

• Journal of Yeungnam Medical Science
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• v.35 no.1
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• pp.1-6
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• 2018

Alzheimer's disease (AD) is a neurodegenerative disorder associated with extracellular plaques, composed of amyloid-beta ($A{\beta}$), in the brain. Although the precise mechanism underlying the neurotoxicity of $A{\beta}$ has not been established, $A{\beta}$ accumulation is the primary event in a cascade of events that lead to neurofibrillary degeneration and dementia. In particular, the $A{\beta}$ burden, as assessed by neuroimaging, has proved to be an excellent predictive biomarker. Positron emission tomography, using ligands such as $^{11}C$-labeled Pittsburgh Compound B or $^{18}F$-labeled tracers, such as $^{18}F$-florbetaben, $^{18}F$-florbetapir, and $^{18}F$-flutemetamol, which bind to $A{\beta}$ deposits in the brain, has been a valuable technique for visualizing and quantifying the deposition of $A{\beta}$ throughout the brain in living subjects. $A{\beta}$ imaging has very high sensitivity for detecting AD pathology. In addition, it can predict the progression from mild cognitive impairment to AD, and contribute to the development of disease-specific therapies.

• Biomolecules & Therapeutics
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• v.27 no.2
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• pp.145-151
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• 2019

Methamphetamine (METH) acts strongly on the nervous system and damages neurons and is known to cause neurodegenerative diseases such as Alzheimer's and Parkinson's. Flavonoids, polyphenolic compounds present in green tea, red wine and several fruits exhibit antioxidant properties that protect neurons from oxidative damage and promote neuronal survival. Especially, epicatechin (EC) is a powerful flavonoid with antibacterial, antiviral, antitumor and antimutagenic effects as well as antioxidant effects. We therefore investigated whether EC could prevent METH-induced neurotoxicity using HT22 hippocampal neuronal cells. EC reduced METH-induced cell death of HT22 cells. In addition, we observed that EC abrogated the activation of ERK, p38 and inhibited the expression of CHOP and DR4. EC also reduced METH-induced ROS accumulation and MMP. These results suggest that EC may protect HT22 hippocampal neurons against METH-induced cell death by reducing ER stress and mitochondrial damage.