• Bulletin of the Korean Chemical Society
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• v.28 no.2
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• pp.225-228
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• 2007

Lipoic acid (LA) is a multifunctional antioxidant against a variety of ROS. Nitrone acts as free radical spin trap and exhibits neuroprotective activity. Thus, LA-nitrone derivatives (6, 7, 8, and 9) were synthesized and screened as an antioxidant and inhibitors for cholinesterases. Even though the antioxidant effect of LA-nitrone derivatives was not improved, they turned out to be effective inhibitors of acetylcholinesterase (AChE) and butyrylcholinesterase (BuChE) in μM range.

• Journal of the Korean Solar Energy Society
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• v.25 no.4
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• pp.61-67
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• 2005

The purpose of this study is to evaluate the air tightness of Zero Energy Solar House(ZeSH) and to propose the construction improvement of junctions and penetrations where air infiltration was identified. Air leakage rate were measured by means of blower door test in accordance with ASTM E779-87. The results showed that ZeSH has an excellent airtightness with ACH50/20 (air change per hour at a pressure difference of 50 Pa between inside outside) of 0.34hr-1 and leakage class E by normalized leakage area of ASHRAE.

• Bulletin of the Korean Chemical Society
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• v.27 no.11
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• pp.1741-1746
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• 2006

3D-QSARs on the neuroblocking activities by 1-(6-chloro-3-pyridylmethyl)-2-nitroiminoimidazolidine analogues as agonist at the nicotinic acetylcholine receptor (nAChR) were studied quantitatively using CoMFA and CoMSIA methodologies. The statistical results of CoMFA (A5: $r^2\;_{cv.}\;=\;0.707\;&\;r^2\;_{ncv.}$= 0.986) and CoMSIA model (A3: $r^2\;_{cv.}$ = 0.715 & $r^2\;_{ncv.}$ = 0.961) showed the best predictability and fitness for neuroblocking activity based on the cross-validated value and non-cross validated value. The steric and H-bond acceptor nature of a compound were essential for high activity. The study on 3D-QSARs between substrate molecules and their neuroblocking activities appears to be an useful approach for designing better neuroblocking drug development.

• Mycobiology
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• v.37 no.2
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• pp.152-154
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• 2009

Lichen genus Sarcographa Fee, a stromatoid Graphidacean taxa, was newly found in Geomun Island, Jeonnam province. The lichen grew on the bark of Camellia japonica and Eurya emarginata along the coastal line of the island. It was identified as Sarcographa tricosa (Ach.) Mull. Arg. for the first time in Korea.

• Proceedings of the Korean Society of Life Science Conference
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• 2007.10a
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• pp.76.2-76.2
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• 2007

See Full Text

• Proceedings of the Korean Society of Life Science Conference
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• 2007.10a
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• pp.77.1-77.1
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• 2007

See Full Text

• Annals of Clinical Neurophysiology
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• v.9 no.2
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• pp.51-58
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• 2007

Autoimmune myasthenia gravis (MG) is the neuromuscular junction disorder mostly caused by antibody against the acetylcholine receptor (AChR antibody) at the muscle endplate. The goal of treatment is to induce and maintain remission, i.e., absence of symptoms, with the least cost-to-benefit ratio. Although corticosteroids are effective in inducing remission in most patients, they have numerous potentially serious adverse effects with their long-term use. In addition, some patients do not respond or are intolerant to the conventional treatment. In this article, we discuss the difficulties encountered in long-term immunosuppressive treatment of MG, and review useful tips for the use of corticosteroids. Long-term immunosuppressive agents that can be used in steroid-refractory or -dependent patients will be reviewed with their safety profiles and efficacy in MG.

• Toxicological Research
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• v.30 no.3
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• pp.141-148
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• 2014

Endothelium-derived relaxing factors (EDRFs), including nitric oxide (NO), prostacyclin ($PGI_2$), and endothelium-derived hyperpolarizing factor (EDHF), play pivotal roles in regulating vascular tone. Reduced EDRFs cause impaired endothelium-dependent vasorelaxation, or endothelial dysfunction. Impaired endothelium-dependent vasorelaxation in response to acetylcholine (ACh) is consistently observed in conduit vessels in human patients and experimental animal models of hypertension. Because small resistance arteries are known to produce more than one type of EDRF, the mechanism(s) mediating endothelium-dependent vasorelaxation in small resistance arteries may be different from that observed in conduit vessels under hypertensive conditions, where vasorelaxation is mainly dependent on NO. EDHF has been described as one of the principal mediators of endothelium-dependent vasorelaxation in small resistance arteries in normotensive animals. Furthermore, EDHF appears to become the predominant endothelium-dependent vasorelaxation pathway when the endothelial NO synthase (NOS3)/NO pathway is absent, as in NOS3-knockout mice, whereas some studies have shown that the EDHF pathway is dysfunctional in experimental models of hypertension. This article reviews our current knowledge regarding EDRFs in small arteries under normotensive and hypertensive conditions.

• Journal of Life Science
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• v.12 no.1
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• pp.26-31
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• 2002

Choline esters that are used with substrate of BChE-catalyzed hydrolyses were synthesized by two methods. First, 2-chloroethyl thiohexanoate, 2-chloroethyl thioheptanoate, and 2-chloroethyl thiooctanoate were synthesized by the treatment of hexanoyl chloride with ethylene sulfide. Hexanoyl thiocholine and octanoyl thiocholine were synthesized by using 2-chloroethyl thiohexanoate and 2-chloroethyl thiooctanoate with trimethyl amine. Second, after reaction of ethylene sulfide and dimethyl amine, followed by acylation with acid anhydride and then heptanonyl thiocholine, decanoyl thiocholine were synthesized by treatment of methyl iodide.

• Journal of mucopolysaccharidosis and rare diseases
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• v.2 no.2
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• pp.46-49
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• 2016

Achondroplasia is autosomal dominant genetic disease and fibroblast growth factor receptor 3 (FGFR3) is currently known to be the only gene that causes achondroplasia. Gain-of function mutation in fibroblast-growth-factor-receptor 3 (FGFR3) causes the disease and C-type natriuretic peptide (CNP) antagonizes FGFR3 downstream signaling by inhibiting the pathway of mitogen-activated protein kinase (MAPK). As FGFR3-related skeletal dysplasias are caused by growth attenuation of the cartilage, chondrocytes appear to be unique in their response to FGFR3 activation. However, the full spectrum of molecular events by which FGFR3 mediates its signaling is just beginning to emerge. This article summaries the mechanisms of FGFR3 function in skeletal dysplasias, the extraordinary cellular manifestations of FGFR3 signaling in chondrocytes, and finally, the progress toward therapy for ACH.