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.
Animals ; Calcium ; Cell Count ; Cell Death ; Cell Survival ; Dantrolene ; Injections, Intraperitoneal ; Malformations of Cortical Development ; Mice ; Models, Theoretical ; Neuroglia* ; Neurons*

Serum IgE levels in 48 patients with scabies were measured by enzyme-linked immunosorbent a.ssay(ELISA) to evaluate the relationship between the scabies and serum IgE. A group of 44 healthy persons was taken as a controls. The results were summarized as follows: In children group(p 15 year-old) of the scabies, serum IgE level was 446 3 +267.2 IU/ml and significantly elevated than in controls, 126, 3 175, 4 IU/rnl, In adult group(over 16 year-old), serum IgE levels of the scabies and controls were 506. 4 + 581. 8 IU/ml, 435, 5+ 548, 8 lU/rnl respetively, and there was no significant difference between them. 2) There were no statistical correlations between the serum IgE levels and intensity of pruritus, duration of illness, number of skin lesions or number of circu1ating eosinophils in patients with scabies.
Adult ; Child ; Eosinophils ; Humans ; Immunoglobulin E* ; Pruritus ; Scabies* ; Skin

To investigate long term effects of CAPD on the left ventricular function in end-stage renal disease patients, M-mode echocardiographic studies and measurement o fsystolic time intervals were performed in 20 CAPD cases, 28 hemodialysis cases and 29 uremic controls. Compared to the uremic control grup, the patients on CAPD treatment revealed significant improvement of ventricular contractility and reduction of volume. On the other hand in hemodialysis group, even though there was improvement of ventricular contractility, volume control was not adequate. In the systolic time interval measurement, it is postulated that increase of PEP/LVET ratio in CAPD group probably results from reduction of volume(preload) rather than from deranged ventricular function.
Echocardiography ; Hand ; Humans ; Kidney Failure, Chronic* ; Peritoneal Dialysis, Continuous Ambulatory* ; Renal Dialysis* ; Systole ; Ventricular Function ; Ventricular Function, Left

BACKGROUND: Mutations in the human Cu, Zn-superoxide dismutase (SOD1) gene have been identified in some cases of familial amyotrophic lateral sclerosis (ALS). Neuronal cells with mutant SOD1 gene promoted cell death during differentiation by dibutyryl cAMP and aphidicolin. The aim of this study is to delineate if there is an impairment of the neural differentiation process in mutant SOD1 cells. METHODS: We studied the motoneuron-neuroblastoma hybrid cells (VSC 4.1) expressing wild-type or mutant SOD1 (G93A) during the differentiation by dibutyryl cAMP and aphidicolin. RESULTS: Mutant SOD1 cell (G93A) showed an impairment in the neurite formation. Western blot analysis revealed that the amount of neurofilament decreased before differentiation. A decrease in the amount of MAP-2 is observed during differentiation. CONCLUSIONS: Our results suggest that the impairment in the neurite formation of mutant SOD1 cell (G93A) is a differentiation failure and is associated with neuronal cell death.
Amyotrophic Lateral Sclerosis ; Aphidicolin ; Blotting, Western ; Cell Death ; Humans ; Hybrid Cells ; Neurites* ; Neurons

Authors reviewed and analyzed 108 cases of secundum ASD(1–15 years old), which had been diagnosed bycineangiography in Seoul Natinal University Children's Hospital from 1979 to 1985. 1) The incidence of theasociation of MVP with secundum ASD was 48%(Male 43%, Female 52%). 2) The incidnece of this association incresedwith age(1–5 years old: 39%, 6–10 : 50%, 11–15: 59%). 3) The incidence of concurrent mitral regurgitation in MVPassociated with ASD was 48%. No special correlation was not found between the degree or incidence of MVP and thatof MR. 4) The incedence of the association of MVP with ASD increased with the increaseing amount of leftventricular geomatry attendant on left to right shunt (QS/QS < 2:33%, 2<=QP/QS < 4:52%, QP/QS >= 4: 100%). Thissuggested that abnormal left ventricular geometry attendant on left to ring shunt would contribute much to theassociation of MVP with secundum ASD.
Female ; Heart Septal Defects, Atrial ; Humans ; Incidence ; Mitral Valve Insufficiency ; Mitral Valve Prolapse ; Mitral Valve ; Seoul

No abstract available.
Laser Therapy*

No abstract available.
Extremities* ; Myokymia*

PURPOSE: Cathepsin D, a lysosomal protease has been proposed to play a role in the local invasion and metastatic dissemination in primary breast cancer. Although there are many conflicting results, the overexpression of cathepsin D has been considered to be related with a poorer prognosis of breast cancer. This study was designed to verify whether cathepsin D expression is related to other prognostic factors in breast cancer. METHODS: Cathepsin D was assessed by immunohistochemistry using murine monoclonal anti-cathepsin D antibody (ZyMED) in 79 paraffin-embedded primary breast cancer specimens. Cathepsin D expression was compared to other prognostic parameters such as tumor size, axillary lymph node metastasis, tumor histologic grades, hormone receptors (ER & PR), p53, c-erb B2, Ki-67, MVD (microvessel density), and Pgp (P-glycoprotein). RESULTS: A high-expression of cathepsin D was found in 35 of 79 patients (44.3%) with primary breast cancer. Cathepsin D expression was not related to tumor size, axillary lymph node metastasis, tumor histologic grades, hormone receptors, p53, Ki-67, or CD31. However, a significant relationship was found between cathepsin D expression and c-erb B2 (p=0.007), and between cathepsin D expression and Pgp (p=0.003). CONCLUSION: These results suggest that cathepsin D expression may be an indicator of a poor prognosis in breast cancer. However, further studies are required to verify the xact role of cathepsin D in the prognosis of breast cancer.
Breast Neoplasms* ; Breast* ; Cathepsin D* ; Cathepsins* ; Humans ; Immunohistochemistry ; Lymph Nodes ; Neoplasm Metastasis ; Prognosis

Primary Pigmented Nodular Adrenal Dysplasia (PPNAD) is a rare cause of Cushing's syndrome in infants and young adults. The familial occurrence, it may be variably associated with a complex of other pathologic characteristics that manifests extraadrenal disorders (includes cardiac myxomas, lentigines, mammary myxoid lesions, testicular tumors, pituitary adenomas, and neuroectodermal tumors) was considered indicative of Carneys complex. This was based on the failure of cortisol suppression by high-dose dexamethasone, either normal or suppressed basal adrenocorticotropic hormone (ACTH) levels, and normal radiographic studies of the sellar turcica, and adrenals glands is almost normal or slightlg eulaged.. Bilateral adrenalectomy has thus the only effective means of cure. The disease may be a component of a rare, but potentially dangerous complex of abnormalities that follow an autosomal-dominant mode of inheritance. Recently we experienced a case of Carney's complex composed by Cushings syndrome due to PPNAD with familial purple colored lentigines on their lips and report it with reviews of the literatures.
Adrenalectomy ; Adrenocorticotropic Hormone ; Cushing Syndrome* ; Dexamethasone ; Humans ; Hydrocortisone ; Infant ; Lentigo ; Lip ; Myxoma ; Neural Plate ; Pituitary Neoplasms ; Testicular Neoplasms ; Wills ; Young Adult

BACKGROUND: Recently, the mechanism involved in nitric oxide (NO)-mediated motor neuron death is under extensive investigation. The role of Cu/Zn superoxide dismutase (SOD) mutation, which is found in about 2% of all ALS patients, has been implicated in selective motor neuron death and it is said to play an important role in NO-mediated motor neuron death. Estrogen is reported to have neuroprotective effect in various neurological diseases. However, neuroprotective effect on estradiol on spinal motor neuron exposed to NO has rarely been studied. METHODS: Motor neuron-neuroblastoma hybrid cell expressing wild-type or mutant (G93A or A4V) SOD gene was treated with 200 micro M Snitrosoglutathione. After 24 hours, cell viability was measured by MTT assay. To see the neuroprotective effect of estradiol, pretreatment with 5 nM or 50 nM 17 beta-estradiols was done 24 hours before S-nitrosoglutathione treatment. RESULTS: S-nitrosoglutathione showed significant neurotoxic effect in all three cell lines. Percentage of cell death was significantly different in each cell line. Both 5 nM and 50 nM estradiols showed neuroprotective effect in G93A cell line. In wild-type cell line, 50 nM estradiol showed neuroprotective effect, but 5 nM estradiol did not. In A4V cell line, estradiol did not showed neuroprotective effect. CONCLUSIONS: This study showed that NO-mediated motor neuron death could be influenced by presence or absence of mutation and type of mutation in SOD gene. Neuroprotective effect of estradiol is also influenced by SOD gene mutation. This study implies that estrogen might be beneficial to some ALS patients.
Cell Death ; Cell Line ; Cell Survival ; Estradiol ; Estrogens* ; Humans ; Hybrid Cells ; Motor Neurons* ; Neuroprotective Agents* ; Nitric Oxide ; S-Nitrosoglutathione ; Superoxide Dismutase* ; Superoxides*