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Original Article
Hu.4-1BB-Fc fusion protein inhibits allergic inflammation and airway hyperresponsiveness in a murine model of asthma
Byoung-Ju Kim, Ji-Won Kwon, Ju-Hee Seo, Won-Ah Choi, Young-Jun Kim, Mi-Jin Kang, Jinho Yu, Soo-Jong Hong
Clin Exp Pediatr. 2011;54(9):373-379.   Published online September 30, 2011
Purpose

4-1BB (CD 137) is a costimulatory molecule expressed on activated T-cells. Repression by 4-1BB is thought to attenuate Th2-mediated allergic reactions. The aim of this study was to investigate the effect of 4-1BB on allergic airway inflammation in a murine asthma model.

Methods

BALB/c mice were sensitized to and challenged with ovalbumin (OVA). Hu.4-1BB-Fc was administered 1 day before the first OVA...

The effects of early allergen/endotoxin exposure on subsequent allergic airway inflammation to allergen in mouse model of asthma
Yeong-Ho Rha, Sun-Hee Choi
Clin Exp Pediatr. 2010;53(4):481-487.   Published online April 15, 2010
Purpose : Recently many studies show early exposure during childhood growth to endotoxin (lipopolysaccharides, LPS) and/or early exposure to allergens exhibit important role in development of allergy including bronchial asthma. The aim of this study was to evaluate the role of endotoxin and allergen exposure in early life via the airways in the pathogenesis of allergic airways inflammation and airway hyperresposiveness...
The Protective Effect of Vitamin E and Desferrioxamine on Cultured Cerebral Neurons of Neonatal Mouse Damaged by Ischemic Condition
So-ra Lee, Yeon-kyun Oh, Seung-taek Park
Clin Exp Pediatr. 1999;42(10):1426-1433.   Published online October 15, 1999
Purpose : Perinatal asphyxia is an important cause of neurologic morbidity. Experiments in animal models of hypoxic-ischemic brain injury demonstrate that brain damage starts during hypoxia-ischemia. In order to evaluate the ischemic condition-induced neurotoxic effect in view of oxi- dative stress, we examined the cytotoxic effect in cultured cerebral neurons of neonatal mouse. Methods : Dissociated cell cultures were prepared...
The Effects of Glutamate Receptor Antagonists on Cultured Cerebral Cortical Neurons of Neonatal Mouse Damaged by Oxidative Stress
Dae-ho Choi, Yeon-kyun Oh, Seung-taek Park
Clin Exp Pediatr. 1999;42(8):1096-1103.   Published online August 15, 1999
Purpose : To evaluate neurotoxic effects induced by oxygen-radicals, which were generated by adding xanthine oxidase(XO) and hypoxanthine(HX), and protective effects of glutamate receptor antagonist such as MK-801 and 6-cyano-7-nitroquinoxaline(CNQX). Methods : Dissociated cell cultures were prepared from cerebrum of neonatal mouse. Tissues were dissected and diced into small pieces in phosphate buffered saline and were incubated at 37℃. Isolated cells...
Cell Proliferation and Apoptosis in Heart of Trisomy 16 in Mice
Eun Jung Bae, Yong Soo Yun, Jung Sun Kim, Jeong-Wook Seo
Clin Exp Pediatr. 1999;42(5):621-630.   Published online May 15, 1999
Purpose : Although abnormal developments of cushion and atrioventricular septum have been suggested, the exact mechanism for the development of atrioventricular septal defect is not well known. We aimed to identify the role of cell proliferation and apoptosis on cardiac morphogenesis in trisomy 16 mice(an animal model for Down's syndrome in human). Methods : We examined the difference in cardiac...
Etretinate Induced Cardiovascular Malformations in Mouse Embryo
Il Kyung Kim, Chang Sung Son, Young Chang Dockgo, Yong Hyuk Jeon
Clin Exp Pediatr. 1995;38(10):1370-1377.   Published online October 15, 1995
Purpose : Etretinate(Tigason? is an aromatic retinoid currently in therapeutic use for psoriasis but studies have shown that it is a potent teratogen in human and in experimental animal. So we carried this study to observe teratogenic effects of etretinate and to search a possibility of etretinate for using as an experimental model to induce cardiovascular malformation. Methods : In order...
Experimental study on the effect of phenobarbital on Na+, K+-activated adenosine triphosphatase in microsome fractions of mouse brain.
Seo Kyu Kim, Sa Jun Chung, Chang Il Ahn
Clin Exp Pediatr. 1991;34(7):959-970.   Published online July 31, 1991
Na+, K+-activated adenosine triphosphatase (Na+, K+-ATPase) is known to play a role as a trigger in neurotransmitter release and may also affect the transport of calcium ion (Ca++). By doing so, Na+, K+-ATPase, as an anticonvulsant, can modify the excitability level of cells in epilepsy. In order to elucidate the possible mechanisms of neuropharmacological interaction between Na+, K+.ATPase and phenobarbital, serial experimental studies were...
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