1.Primary Immunode Ficiency Disorders in Infancy and Childhood.
Hoan Jong LEE ; Jung Shan CHOI ; Jeong Kee SEO ; Kee SEO ; Hyo Sup AHN ; Kwang Wook KO
Journal of the Korean Pediatric Society 1985;28(3):263-282
No abstract available.
2.Lipoprotein Profiles in Minimal Change Nephrotic Syndrome.
Yong CHOI ; Heui Jeen KIM ; Hae Il CHEONG ; Jeong Kee SEO ; Kwang Wook KO
Journal of the Korean Pediatric Society 1983;26(3):237-246
No abstract available.
Lipoproteins*
;
Nephrosis, Lipoid*
3.A Clinical Study of Reye`s Syndrome.
Young Seo PARK ; Hwan Jong LEE ; Sang Pok SUK ; Jeong Kee SEO ; Kwang Wook KO
Journal of the Korean Pediatric Society 1984;27(11):1088-1096
No abstract available.
4.A Case Report of Caroli's Disease.
Hun Jong CHUNG ; Jeong Kee SEO ; Kwang Wook KO ; Kwi Won PARK ; Woo Ki KIM
Journal of the Korean Pediatric Society 1985;28(7):731-736
No abstract available.
Caroli Disease*
5.Primary Peritonitis in Children with Nephrotic Syndrome.
Hae Il CHEONG ; Whan Jong LEE ; Jeong Kee SEO ; Yong CHOI ; Kwang Wook KO
Journal of the Korean Pediatric Society 1985;28(7):695-704
No abstract available.
Child*
;
Humans
;
Nephrotic Syndrome*
;
Peritonitis*
6.Self-administered Enema Related Rectal Perforation.
The Korean Journal of Gastroenterology 2016;67(3):158-160
No abstract available.
Aged
;
Colonoscopy
;
Enema/*adverse effects
;
Humans
;
Intestinal Perforation/*diagnosis/etiology
;
Male
;
Rectal Diseases/*diagnosis/diagnostic imaging/etiology
;
Tomography, X-Ray Computed
7.The Incidence of HBs Antigenemia in Glomerular Desease and Control Group in Children.
Yong CHOI ; Whan Jong LEE ; Jeong Kee SEO ; Kwang Wook KO
Journal of the Korean Pediatric Society 1981;24(2):122-127
HBsAg, HBcAb and HBsAb were examined with radio-immunoassay in 265 patients with glomerular disease, who were admitted to wards or visited to outpatient clinics of department of pediatrics, Seoul National University Hospital, from Jan., 78 to Oct. 80, and in 576 control group, with other than liver disease and without history of transfusion. The incidence in glomerular disease was 10.2%(27 of 265 patients)-nephrotic syndrome 9.2%(12 of 130); acute glomerulonephritis 7.3%(5 of 68), recurrent hematuria 7.7%(2 of 26), H-S nephritis 25%(3 of 12), chronic renal failure 21%(3 of 14), and the others 13.3%(2 of 15), while the incidence of HBs antigenemia in control group was 5.03%(29 of 576 patients)-male 5.5%(21 of 362), female 4.2%(8 of 214). The overall incidence of HBs antigenemia in renal disease was statistically higher than that of control group(p<0.05), though the respective incidences of the above each renal disease group were somewhat higher than that of control group, however they were not statistically significant, The incidence of positive rate of HBsAb and/or HBcAb in control group was 26.7%(56 of 209), and that in renal disease was 23%(18 of 578).
Ambulatory Care Facilities
;
Child*
;
Female
;
Glomerulonephritis
;
Hematuria
;
Hepatitis B Surface Antigens
;
Humans
;
Incidence*
;
Kidney Failure, Chronic
;
Liver Diseases
;
Nephritis
;
Pediatrics
;
Seoul
8.Study on the 3HAcetylcholine Release Induced by Oxygen-Glucose Deprivation in Rat Cerebral Cortical Slices.
Jeong Ju LEE ; Kee Won KIM ; Man Wook SEO ; Young Hyun KIM
Journal of the Korean Neurological Association 1998;16(4):530-535
BACKGROUND: It has been shown that cerebral ischemia alters brain acetylcholine (Ach) metabolism. In an attempt to elucidate the mechanisms for ischemia-induced release of Ach in vitro, the effects of drugs which can influence the cholinergic neurotransmission on the ischemia-induced release of [3H]Ach from cerebral cortical slices of the rat were examined. METHODS: The cortices of decapitated rats were chopped and dispersed in artificial CSF. Then, the tissue suspensions were incubated with [3H]choline. The tissues were transferred and incubated in washing, hypoglycemic (deprivation of glucose), ischemic (deprivation of oxygen and glucose) and extracting plates sequently. Ischemia-induced release of [3H]Ach was expressed as percentage of the total [3H]Ach present in the slices. RESULTS: Ischemia induced significant release (about 9.3% of total tissue content) of [3H]Ach from cerebral cortical slices in vitro. This [3H]Ach release was significantly attenuated by tetrodotoxin, a voltage-sensitive Na+-channel blocker, and Mg2+, a physiological N-methyl-D-aspartate (NMDA) receptor blocker. Vesamicol (1 M), a blocker of vesicular transport of Ach, MK-801 and ketamine, NMDA receptor antagonists, 6,7-nitroquinoxaline-2,3-dione (DNQX) and 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), kainate/AMPA receptor antagonists, and 6-nitro-7-sulphamoylbenzo[f]quinoxaline-2,3-dione (NBQX), a AMPA receptor blocker attenuated the [3H]Ach. Nitrendipine, nimodipine, inhibitor of L-type Ca2+ channels, and -conotoxin GVIA, an inhibitor of N-type Ca2+ channels, significantly attenuated the ischemia-induced release of [3H]Ach. Omission of Ca2+ from incubation media attenuated the ischemia-induced [3H]Ach release. Inhibitors of intracellular Ca2+ release, dantrolene and TMB-8, and a cell-permeable calcium chelator, 1,2-bis (2-aminophenoxy)-ethane-N, N, N+, N+-tetraacetic acid tetrakis (acetoxymethyl) ester (BAPTA-AM), inhibited the ischemia-evoked [3H]Ach release. CONCLUSION: These results suggest that the ischemia can induce Ach rele.
6-Cyano-7-nitroquinoxaline-2,3-dione
;
Acetylcholine
;
Animals
;
Brain
;
Brain Ischemia
;
Calcium
;
Dantrolene
;
Dizocilpine Maleate
;
Ischemia
;
Ketamine
;
Metabolism
;
N-Methylaspartate
;
Nimodipine
;
Nitrendipine
;
Oxygen
;
Rats*
;
Receptors, AMPA
;
Suspensions
;
Synaptic Transmission
;
Tetrodotoxin