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Human Immunology|November 4, 2008
Genetic variants in the HLA-G region are associated with Kawasaki diseaseJae-Jung Kim, Soo-Jong Hong, Young Mi Hong, et al.
Journal of Clinical Immunology|July 17, 2008
The CCR5 (-2135C/T) polymorphism may be associated with the development of Kawasaki disease in Korean childrenWon Kyoung Jhang, Mi-Jin Kang, Hyun-Seung Jin, et al.
Toxicology|July 24, 2002
Aroclor 1254-induced cytotoxicity in catecholaminergic CATH.a cells related to the inhibition of NO productionJu Hee Kang, Wonhyung Jeong, Younjoo Park, et al.
The Pediatric Infectious Disease Journal|August 28, 2007
Kawasaki disease in Korea, 2003-2005Yong-Won Park, Ji-Whan Han, In-Sook Park, et al.
International Journal of Cardiology|September 28, 2011
Low pulmonary vascular compliance predisposes post-Fontan patients to protein-losing enteropathyJeong Jin Yu, Tae-Jin Yun, Sung-Cheol Yun, et al.
Toxicology in Vitro : an International Journal Published in Association with BIBRA|October 25, 2011
Anti-cancer properties of glucosamine-hydrochloride in YD-8 human oral cancer cells: Induction of the caspase-dependent apoptosis and down-regulation of HIF-1αChang-Wook Jung, Jeong-Rang Jo, Sang-Han Lee, et al.
Pediatric Cardiology|March 28, 2012
Variations in the number of CCL3L1 gene copies and Kawasaki disease in Korean childrenHye-Eun Kim, Jae-Jung Kim, Myung Ki Han, et al.
Biochemical and Biophysical Research Communications|March 23, 2004
DNA microarray analysis of the correlation between gene expression patterns and acquired resistance to 5-FU/cisplatin in gastric cancerHark Kyun Kim, Il Ju Choi, Hee Sung Kim, et al.
Journal of Human Genetics|May 17, 2013
Identification of KCNN2 as a susceptibility locus for coronary artery aneurysms in Kawasaki disease using genome-wide association analysisJae-Jung Kim, Young-Mi Park, Dankyu Yoon, et al.
Toxicology in Vitro : an International Journal Published in Association with BIBRA|February 2, 2010
Aspirin induces apoptosis in YD-8 human oral squamous carcinoma cells through activation of caspases, down-regulation of Mcl-1, and inactivation of ERK-1/2 and AKTIn-Sook Park, Jeong-Rang Jo, Hua Hong, et al.
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