Renal Anomalies in Neonates with Isolated Preauricular Tags / 소아과

PURPOSE: The aim of this study was to determine the role of renal ultrasonography in neonates with isolated preauricular tags. METHODS: We performed a retrospective study of 10,997 newborn infants delivered from January 1995 to June 2003 in Wonkwang University Hospital. Nineteen newborns born with isolated preauricular tags were assessed for renal anomalies by performing renal ultrasonography within one week after birth. The study group was compared with a control group of 25 healthy neonates without preauricular tags during the same period, also using renal ultrasonography. RESULTS: Preauricular tags were detected in 19 of 10,997(0.17%) neonates; 57.9% were found on the right side. Renal anomalies in neonates with isolated preauricular tags were detected in four infants (21.1%); this incidence was higher, but was not significant, compared with the control group. Types of anomalies were mild hydronephrosis of grade 1(3 cases) and 2(1 case) which were normalized within one year. CONCLUSION: Routine renal ultrasonography is not recommended for newborn infant with isolated preauricular tags.

A Case of Thyroid Papillary Carcinoma Presenting as a Miliary Pulmonary Infiltration in 8 Year Old Girl / 소아알레르기및호흡기학회지

Papillary carcinoma of the thyroid is the most common thyroid cancer in children. It usually occurs in the teenage female and presents as a mass within the thyroid itself. In the great majority of cases the only presenting sign is a neck mass. In a high percentage (60-80%) there are also palpable lymph nodes. A 8 years old female patient was admitted because of palpable neck mass and miliary shadow in chest X-ray. On examination, a soft nontenter nodular mass 1x1 cm in size was palpated at supraclavicular area of left mid-neck. In chest X-ray and CT, well demarcated nodular milialy infiltration was fully distributed in both lung. After the initial treatment failure for the miliary tuberculosis, the fine needle aspiration biopsy was performed. The Papillary carcinoma of the thyroid was diagnosed. Total thyroidectomy and entire lymph node excision were performed, followed by radioiodine ablation and hormonal therapy. The patient has been improved clinically. We are reporting a case of thyroid papillary carcinoma presenting as a pulmonary miliary infiltration with brief review of the literature.

The Effect of Intrauterine Irradiation on Cortical Neurons and Glial Cells / 대한소아신경학회지

PURPOSE: Our study was an experimental model for the mechanism of cortical dysplasia. We examined the changes of neuronal cells and glial cells by intrauterine irradiation. This paper will elucidate the effect of these changes on the development of cortical dysplasia. METHODS: The cytotoxic effect of irradiation was examined by viability and numbers in cerebral cortical neurons and glial cells, which were derived from a mouse exposed to 225 cGy of gamma-irradiation on embryonic day 17. In addition, the protective effect of an inhibitor of intracellular calcium release, dantrolene sodium(DS), on irradiation-induced neurotoxicity was examined after DS(10 mg/kg) was administrated via intraperitoneal injection after intrauterine irradiation. RESULTS: 1) Irradiation induced the decrement of the cell number and cell viability of cerebral cortical neurons in the developing stages. 2) The number of glial cells in the mouse treated with intrauterine irradiation was increased in E20-P4 stages compared with the control group, but there was no difference in cell viability. 3) The glial fibrillary acidic protein(GFAP)-positive cells were seen in developing stages (E20-P4). 4) In the protective effect from neuronal cell death by intrauterine irradiation, DS attenuated cell death by an increase of neuronal cells. CONCLUSION: From these results, it is suggested that intrauterine irradiation has the neurotoxic effect as neuronal cell death and induced glial cell proliferation. A selective inhibitor of intracellular calcium release such as DS is effective in protecting neuronal cell death induced by irradiation of the intrauterine period. Cortical dysplasia induced by intrauterine irradiation may be involved in neuronal cell death and the hyperproliferation of glial cells. Intracellular calcium influx may contribute to the pathogenesis of irradiation-induced neuronal cell death.

Effect of Vitamin E on Cerebral Hypoxia-Ischemia in Neonatal Rats

PURPOSE: In order to evaluate the hypoxia-ischemia induced neurotoxic effect and the protective effect of vitamin E as an antioxidant, cell number and cell viability were measured in cerebral neurons and astrocytes derived in neonatal rats. METHODS: 7-day old neonatal rats were subjected to unilateral common carotid artery occlusion, and exposed to hypoxic condition for 3 hours. The protective effect of vitamin E, as an antioxidant was examined by XTT [2,3-bis(2-methoxy-4-nitro-5-sulfophenyl)-5-(phenylami-nocarbonyl) 12H-tetrazolium hydroxide] assay and cell number on 14 days after hypoxia-ischemia when the rats received an intraperitoneal injection of vitamin E immediately following hypoxia-ischemia. RESULTS: Hypoxic-ischemic condition positively decreased the cell number and cell viability of rat cerebral neurons in a time-dependent manner when rats were killed 72 hours after hypoxia- ischemia. 72 hours after hypoxia-ischemia, the cell number and viability of astrocytes were slightly decreased, compared with the saline treated group. In rats treated with vitamin E, the cell number and cell viability of neurons were significantly increased compared with those of the saline- or non-treated group. In hypoxic-ischemic treated rats after 14 days from hypoxia- ischemia, astrocytes were significantly proliferated, but vitamin E showed the protective effect on hypoxic-ischemia induced cell proliferation and cell viability. CONCLUSION: It is suggested that hypoxic-ischemic condition is more toxic in neurons than astrocytes, and selective antioxidants such as vitamin E, especially when it was administered within two hours after hypoxia-ischemia, is highly effective in preventing the cell death of neurons and astrocytes from hypoxia-ischemic condition in neonatal rats.

Cytotoxicity of Diamide and the Protective Effect of Thioredoxin on Diamide-Induced Vasculotoxicity in Vascular Endothelial Cells

BACKGROUND AND OBJECTIVES: This study was designed to examine the effects of diamide and thioredoxin (TRX) on vascular endothelial cells in order to clarify the mechanism by which vascular damage is mediated by oxygen free radicals. MATERIALS AND METHODS: The pulmonary artery endothelial cell (PAEC) line derived from bovine serum was cultured for 8 hours in media supplemented with various concentrations of diamide and TRX. The XTT assay, MTS assay, SRB assay, LDH activity and lipid peroxidation tests were perfomed. RESULTS: In XTT and MTS assays, diamide significantly decreased the cell viability of cultured PAEC in a dose- and time-dependent manner. Diamide showed a decrease in the amount of total protein, although it showed an increase of lipid peroxidation and LDH activity in cultured PAEC. In regards to the protective effect of TRX on diamide-induced cytotoxicity, this showed an increase of total protein, however it showed a decrease of lipid peroxidation and LDH activity. CONCLUSION: Our results suggest that diamide has a vasculotoxic effect on cultured bovine PAEC and that TRX is very effective in the protection of diamide-induced cytotoxicity by duye to the increase of total protein and the decrease of lipid peroxidation and LDH activity in these cultures.

The Protective Effect of Vitamin E and Desferrioxamine on Cultured Cerebral Neurons of Neonatal Mouse Damaged by Ischemic Condition

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 from cerebrum of neonatal mouse. Tissues were diced into small pieces and were incubated in phosphate buffered saline at 37degrees C. Isolated cells were resuspended in the medium and plated in poly-L-lysine coated 96 well multichambers at a cell density of 5x104cells/well. Cells were grown in a 5% CO2/95% air atmosphere at 37degrees C. Cytotoxic effects were examined in the cultured cerebral neurons with time interval in the ischemic condition with a 95% nitrogen/5% CO2. And the protective effect of vitamin E and desferrioxamine as an antioxidant was examined by MTT assay and neurofilament enzymeimmunoassay(EIA). Microscopic examinations were also done. RESULTS: Ischemic condition markedly decreased the cell viability in a time-dependent manner in cultured cerebral neurons. MTT50 value was estimated at 10 minutes, when cerebral neurons were incubated for various time intervals in ischemic condition. Under light microscopy, the number of cells and neurites were decreased when cerebral neurons were cultured for 10 minutes in the ischemic condition. Vitamin E was an effective antioxidant in blocking ischemic condition-induced neurotoxicity, while desferrioxamine was not in these cultures. CONCLUSION: It is suggested that ischemic conditions are neurotoxic and selective antioxidant such as vitamin E is effective in protecting against the neurotoxicity induced by ischemic condition in cultured cerebral neurons of neonatal mouse.

The Effects of Glutamate Receptor Antagonists on Cultured Cerebral Cortical Neurons of Neonatal Mouse Damaged by Oxidative Stress

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 37degrees C. Isolated cells were resuspended in Eagle's minimum essential medium and plated poly-L-lysine coated plastic coverslips in 96 well multichambers at a cell density of 3x105 cells/well. Cells were grown in a 5% CO2/95% air atmosphere at 37degrees C. Cytotoxic effects were examined in cerebral cortical neurons cultured for 3 hours in media containing various concentration of XO and HX. The protective effects of glutamate receptor antagonist were also examined by MTT assay and neurofilament enzymeimmunoassay(EIA). Microscopic examinations were also done. RESULTS: Oxygen radicals markedly induced decrement of the cell viability of cultured mouse cerebral cortical neurons in a dose-dependent manner. Midpoint cytotoxicity value was 30mU/ml XO/0.1mM HX, when mouse cerebral cortical neurons were incubated for 3 hours with various concentrations of XO and HX. The number of cells and neurites was decreased when cerebral cortical neurons were cultured for 3 hours in a medium containing 30mU/ml XO/0.1mM HX. MK- 801 was very effective in blocking oxidant-induced neurotoxicity, while CNQX falied to show any protective effect in these cultures. CONCLUSION: It is suggested that oxygen radicals are neurotoxic, and selective N-methyl-D-aspartate antagonists such as MK-801 are very effective in protecting neurotoxicity induced by oxygen radicals in cultured cerebral cortical neurons of neonatal mouse.

Effect of Oxygen Radicals on Cultured Cerebral Neurons of Neonatal Mouse

PURPOSE: In order to elucidate the neurotoxic mechanism of oxygen radicals which are pathological factor of ischemia, we evaluated the oxidant-induced neurotoxicity and the neuroprotective effect of antioxidant on cultured cerebral neurons derived from neonatal mouse. METHODS: Neurotoxic effect was investigated after cultured mouse neuronal cells were exposed to oxygen radicals which were generated enzymatically by reaction of xanthine oxidase (XO) and hypoxanthine (HX). And also the neuroprotective effect of antioxidant was assessed with catalase. Both effects determined by cell viability were assessesd by MTT assay and neurofilament enzymeimmuno assay (EIA). In order to see the histologic change microscopic exam also done on the cerebral neuronal cells. RESULTS: 1) Oxygen radicals were toxic on cultured mouse cerebral neurons in dose- and time-dependent manner. 2) The value of lethal concentration50 (LC50) of oxygen radicals was estimated at a concentration of 25mU/ml xanthine oxidase (XO) and 0.2mM hypoxanthine (HX) in these culture. 3) Catalase was effective in blocking the neurotoxicity induced by oxygen radicals at a concentration of 50ug/ml. 4) Oxygen radicals induced the decrease of cell number and the loss of neurites in cultured mouse cerebral neurons. CONCLUSION: It is suggest that oxygen radicals cause the neurotoxicity and the selective antioxidants such as catalase are very effective in blocking oxidant-mediated neurotoxicity on cultured cerebral neurons of neonatal mouse.