1.HLA-DR genotyping from one drop blood by double PCR.
Hoon HAN ; Jung Bin LEE ; Yeun Jun CHUNG ; Byung Uk LIM
Journal of the Korean Society for Microbiology 1991;26(2):205-214
No abstract available.
HLA-DR Antigens*
;
Polymerase Chain Reaction*
2.HLA-DR genotyping from sperm by double PCR.
Hoon HAN ; Byung Uk LIM ; Yeun Jun CHUNG ; Jung Bin LEE
Korean Journal of Immunology 1991;13(1):89-98
No abstract available.
HLA-DR Antigens*
;
Polymerase Chain Reaction*
;
Spermatozoa*
3.Effect of Allopurinol on Methylmercuric Chloride in Cultured O1igodendrocytes.
Seung Taeck PARK ; Yeun Ja MUN ; Jae Min OH ; Jung Joong KIM ; Min Kyu CHOI ; Jae Han SHIM ; Kye Taek LIM ; Yeun Tai CHUNG
Korean Journal of Physical Anthropology 1996;9(2):189-195
In order to examine the neurotoxic mechanism of oxygen radicals on cultured bovine oligodendrocytes, cytoxic effect of oxygen radicals was examined when cultures were treated with various concentrations of xanthine oxidase (XO) and hypoxanthine (HX) in culture medium. In addition, the neuroprotective effect of iron-chelators against the neurotoxicity induced by oxygen radicals was evaluated by MTT assay. Cell viability was remarkably decreased in a time-dependent manner after exposure of cultured bovine oligodendrocytes to 20mU/ml XO and 0.1mM HX for 4 hours. In the neuroprotective effect of iron-chelators on oxidant-induced neurotoxicity, tetrakis (2-pyridylmethyl)ethylenediamine (TPEN) blocked the neurotoxicity induced by oxygen radicals, while DFX was not effective in blocking oxidant-induced neurotoxicity in these cultures. These results suggest that oxygen radicals are toxic in cultured bovine oligodendrocytes, and also selective iron-chelators such as TPEN are effective in blocking the neurotoxicity induced by oxygen radicals.
Allopurinol*
;
Cell Survival
;
Hypoxanthine
;
Neuroprotective Agents
;
Oligodendroglia
;
Reactive Oxygen Species
;
Xanthine Oxidase
4.A Case of Massive Thymic Hyperplasia.
Hye Kyung BAE ; Jung Kyu SUH ; Jae Seung YANG ; Baek Keun LIM ; Yeun Kee KIM ; Chan Il PARK
Journal of the Korean Pediatric Society 1988;31(11):1516-1521
No abstract available.
Thymus Hyperplasia*
5.The Influence of Gestational Age, Birth Weight and Disease on Thyroid Function in Preterm Infants.
Jung Sub LIM ; Yeun Kyng LEE ; Seong Yong LEE ; Choong Ho SHIN ; Beyong Il KIM ; Sei Won YANG ; Jung Hwan CHOI
Journal of Korean Society of Pediatric Endocrinology 2001;6(2):120-128
PURPOSE: To evaluate the influence of gestational age(GA) and disease on thyroid hormone concentration in preterm neonates(preterm), we measured thyroxine (T4) and thyroid stimulating hormone(TSH) concentrations and analyzed the relation to GA and diseases. Additionally, we calculated the reference ranges of T4 in preterm for future investigation. METHODS: Serum T4 and TSH were measured by radioimmunoassay for 107 preterm who admitted neonatal intensive care unit during 1994. We sampled from preterm on 5th day of life. We analysed the relationship of GA and birth weight with the levels of T4 and TSH, and prospectively compared them with each neonatal disease. RESULTS: Serum T4 concentration correlated positively with GA(r=0.62, P<0.001) and birth weight(r=0.29, P<0.01). After controlling GA, birth weight did not correlate to the levels of T4. But after controlling birth weight, GA had correlation with T4(r=0.58, P<0.001). In preterm less than 32 weeks of GA, there was no difference of T4 level between healthy and the diseased(respiratory distress syndrome, patent ductus arteriosus, sepsis, intraventricular hemorrhage, and cerebral palsy). Group of bronchopulmonary dysplasia had significant lower level of T4 compared control group(P<0.01). The reference range of T4 in GA 32-36 weeks is 5.56-15.58 microgdL (9.82+/-.40 microgdL). CONCLUSION: GA positively correlated with serum T4 in preterm, but not to TSH. The measurement of TSH level, using in most of the neonatal care unit as neonatal thyroid screening test, in Korea, is not an adequate test to diagnosis hypothyroidism early in preterm. We recommend serial follow up of TSH and T4 in preterm.
Birth Weight*
;
Bronchopulmonary Dysplasia
;
Diagnosis
;
Ductus Arteriosus, Patent
;
Gestational Age*
;
Hemorrhage
;
Humans
;
Hypothyroidism
;
Infant, Newborn
;
Infant, Premature*
;
Intensive Care, Neonatal
;
Korea
;
Mass Screening
;
Parturition*
;
Prospective Studies
;
Radioimmunoassay
;
Reference Values
;
Sepsis
;
Thyroid Gland*
;
Thyroxine
6.Clinical Analysis of Patch Repair of Ventricular Septal Defect in Infant.
Tae Eun JUNG ; Jang Hoon LEE ; Dong Hyup LEE ; Jung Cheul LEE ; Sung Sae HAN ; Sae Yeun KIM ; Dae Lim JI
Yeungnam University Journal of Medicine 2002;19(2):99-106
BACKGROUND: Simple ventricular septal defect(VSD) is the most common congenital heart disease. Although closure of VSD is currently associated with a relatively low risk, experience with younger and smaller infants has been variably less satisfactory. We assessed the results of surgical closure of VSD in infant. MATERIALS AND METHODS: Between 1996 and 2000, 45 non-restrictive VSD patients underwent patch repair and retrospective analysis was done. Patients were divided into two groups based on weight: group I infants weighed 5kg or less(n=16), and group II infants weighed more than 5kg(n=29). Both groups had similar variation in sex, VSD location, aortic cross clamp time and total bypass time. But combined diseases (ASD, PDA, MR) were more in group I. We closed VSD with patch and used simple continuous suture method in all patients. RESULTS: There were no operative mortality, no reoperation for hemodynamically significant residual shunt and no surgically induced complete heart block. As a complication, pneumonia(group I: 2 cases, group II: 2 cases), transient seizure(group II: 2), wound infection(group I: 1, group II: 1), urinary tract infection(group I: 1) and chylopericardium(group I: 1) developed, and there was no significant difference between two groups(p>0.05). CONCLUSION: Early primary closure with simple continuous suture method was applicable in all patients with non-restrictive VSD without any serious complications.
Heart Block
;
Heart Defects, Congenital
;
Heart Septal Defects, Ventricular*
;
Humans
;
Infant*
;
Mortality
;
Reoperation
;
Retrospective Studies
;
Sutures
;
Urinary Tract
;
Wounds and Injuries
7.Clinical Characteristics of Infant Kawasaki Disease.
Yeun Keun CHOI ; Jung Min HONG ; Hae Kyeung LIM ; Su Mi IHN ; Hong Ryang KIL
Journal of the Korean Pediatric Society 2002;45(1):109-114
PURPOSE: To assess the incidence of coronary artery lesion(CAL) and the efficacy of intravenously administered immune globulin(IVGG) and aspirin therapy, identify risk factors for CAL, and analyze clinical characteristics in infants less than 12 months of age with Kawasaki disease. METHODS: Retrospective chart review of children less than 12 months of age with Kawasaki disease between 1994 and 1998, diagnosed at Chungnam National University Hospital. RESULTS: Of 202 patients with Kawasaki disease, 32(16 percent) were less than 1 year of age, including 7(3 percent) less than 6 months. Sex ratio of male to female was 2.5:1. Age at onset and Harada score were a predictor of the development of CAL:5(71 percent) of 7 children less than 6 months and 10(40 percent) of 25 children between 6 to 12 months of age acquired CAL (P<0.05), and 1(14 percent) of 7 children less than 6 months of age acquired giant CAL. No specific clinical or laboratory features predicted the development of CAL. Persistent(greater than 1 year) CAL were present in 2(7 percent) of 29 IVGG-treated children. The typical clinical features of Kawasaki disease was noted 24(75 percent) of 32 and the atypical one, 8(25 percent) of 32 children less than 12 months of age. CONCLUSION: Patients with Kawasaki disease of less than 12 months of age are at particularly increased risk of having CAL and difficulty in diagnosis due to atypical clinical features. So, it is suggested to intervene in the diagnostic criteria or risk factors for CAL, especially for patients with infant Kawasaki disease of less than 6 months of age.
Aspirin
;
Child
;
Chungcheongnam-do
;
Coronary Vessels
;
Diagnosis
;
Female
;
Humans
;
Incidence
;
Infant*
;
Male
;
Mucocutaneous Lymph Node Syndrome*
;
Retrospective Studies
;
Risk Factors
;
Sex Ratio
8.The relationship between polymorphism of glucose transporter gene and the metabolic profiles such as glucose utilization and insulin secretory capacity in the offsprings of non-insulin dependent diabetic patients.
Hyun Chul LEE ; Young Sik LEE ; Seog Won PARK ; Yoon Sok CHUNG ; Sung Kil LIM ; Kyung Rae KIM ; Kap Bum HUH ; Tae Yeun KIM ; Jung Soo RHIM
Korean Journal of Medicine 1993;45(1):12-24
No abstract available.
Glucose Transport Proteins, Facilitative*
;
Glucose*
;
Humans
;
Insulin*
;
Metabolome*
9.Therapeutic Approaches for Preserving or Restoring Pancreatic beta-Cell Function and Mass.
Kyong Yeun JUNG ; Kyoung Min KIM ; Soo LIM
Diabetes & Metabolism Journal 2014;38(6):426-436
The goal for the treatment of patients with diabetes has today shifted from merely reducing glucose concentrations to preventing the natural decline in beta-cell function and delay the progression of disease. Pancreatic beta-cell dysfunction and decreased beta-cell mass are crucial in the development of diabetes. The beta-cell defects are the main pathogenesis in patients with type 1 diabetes and are associated with type 2 diabetes as the disease progresses. Recent studies suggest that human pancreatic beta-cells have a capacity for increased proliferation according to increased demands for insulin. In humans, beta-cell mass has been shown to increase in patients showing insulin-resistance states such as obesity or in pregnancy. This capacity might be useful for identifying new therapeutic strategies to reestablish a functional beta-cell mass. In this context, therapeutic approaches designed to increase beta-cell mass might prove a significant way to manage diabetes and prevent its progression. This review describes the various beta-cell defects that appear in patients with diabetes and outline the mechanisms of beta-cell failure. We also review common methods for assessing beta-cell function and mass and methodological limitations in vivo. Finally, we discuss the current therapeutic approaches to improve beta-cell function and increase beta-cell mass.
Glucose
;
Humans
;
Insulin
;
Obesity
;
Pregnancy