OBJECTIVE: Sarcoma of uterus is originated from uterine muscles and/or connective tissues and rare and most lethal of all primary uterine tumors. The purpose of this study was to evaluate the clinical outcome of 12 patients diagnosed primary uterine sarcoma at the Department of Obstetrics and Gynecology in Kyungpook National University Hospital between 1984 and 1998 for 15 years. METHODS: After review of chart in twelve patients, data including clinical and histologic findings, treatment and outcome were analysed. RESULTS: The most common histologic finding was leiomyosarcoma(6cases, 50%) and the age of patients ranged 24 to 69 years and the average age was 43.25 years and two patients were nulliparous. The most common sign was abnormal uterine or vaginal bleeding(48%), and pelvic cavity or vaginal mass(16%), pelvic pain(16%), no symptom(16%), in order of frequency. The distribution by FIGO clinical stage was four cases(33%) for stage I, one case (8%) for stageII, one case(8%) for stage III, six cases (50%) for stage N. The nine cases received hysterectomy with or without BSO. Two cases received myomectomy to preserve fertility. The mean follow-up duration was 39.6 months. CONCLUSION: Uterine sarcoma is an uncommon and aggressive tumors with a poor prognosis. Leiomyosarcoma is the most frequent histologic type(50%). Stage I uterine sarcoma with or without adjuvant chemotherapy has better prognosis than other stages.
Animals ; Chemotherapy, Adjuvant ; Connective Tissue ; Female ; Fertility ; Follow-Up Studies ; Gyeongsangbuk-do ; Gynecology ; Humans ; Hysterectomy ; Leiomyosarcoma ; Mice ; Myometrium ; Obstetrics ; Prognosis ; Sarcoma* ; Uterus*

A 41 year-old man had dark pigmented papules and plaques, 4 to 15 mm in size, on the proximal portion of the dorsum of the penile shaft and pubic area of 8 months duration. Over next several months, flesh colored, macerated papules, 2 to 4 mm in size, appeared on the left side of the scrotum Light microscopic examination from a pigmented lesion of the penile shaft showed typical findings of Bowen's disease. Ultrastructural findings included: widening of intercellular space, a decrease in the number of desmosomes with microvillous projections, aggregation of tonofilaments, an increase in the mitotic keratinocytes, an increase in the number of melanin granules, and disorganized bundles of tonofilaments surrounding chromosomes. Virus-like particles were not observed. Based on the ultrastructural findings and review of literatures, it seems to be probable that bowenoid papulosis is a clinical variant of Bowens disease.
Adult ; Bowen's Disease ; Desmosomes ; Extracellular Space ; Genitalia* ; Humans ; Intermediate Filaments ; Keratinocytes ; Melanins ; Scrotum

BACKGROUND: To get the information about the clinical characteristics of the paroxysmal junctional tachycardia in children and to get the general principle in managing these children. METHOD: Analysis of the medical records of the 43 patients(male 30, female 13) with paroxysmal junctional tachycardia(JT) who had been followed-up in this hospital for a mean of 4.6 years(range 1 month up to 12 years) was done. RESULT: In 19 patients, JT started before 1 years of age : in 2, during gestational period, in 15, within 4 months of age, in 2, after 4 months of age. The next peak was 7 in the age of 5 years. The associated cardiac abnormalities were complex congenital defects in 2, tumor in 1, dilated and hypertrophic cardiomyopathy in 1 each. The significant hemodynamic disturbances during JT were noticed in 25. Among those whose surface electrocardiogram during JT were available, mean heart rate during JT was 232rpm(range 160-310) ; narrow QRS complex in 33 and wide in 1 ; P` wave in ST segment or T wave in 22. The delta waves were noticed after stopping JT and during followe up in 20. The types of delta waves were A in 7, B in 9, and indeterminate in 4. The different forms of delta waves unrelated to the degree of fusion were noticed in 6 ; disappearance or intermittent form of delta wave in 4. The efficacy of stopping JT was as follows : ATP 84.4%(38/45), diving reflex 50%(7/14), other vagal stimulation 71.4%(5/7), digoxin 72.7%(8/11), verapamil 54.5%(12/22), D/C cardioversion 62.5%(5/8), neosynephrine 100%(2/2). There were 2 deaths due to associated cardiac defects and 2 elective catheter ablations during the followe up period. The preventive medication with digoxin, beta blocker, and/or verapamil was succesful in 14, partially succesful in 11, failed in 14. The 7 persistent JT were treated with amiodarone in 3, with amiodarone and beta blocker in 1, with flecainide and digoxin in 1. In 1, surgical ablation of accessory pathway was done due to persistent JT. At present, JT do not recur or occur transiently without drugs in 29 ; with drugs, JT become controlled without recurrence in 4, with transient episodes in 4 and with intermittent episodes in 1. CONCLUSION: Althouh the JT in children is benign in most cases spite of the severity during the early period, JT is persistent in cases and needs potent drugs to control JT. Ablation of the foci may be necessary in these cases. Even in patients whose long-term results are benign, it is necessary to choose the optimal drugs to terminate and prevent the JT during the intervening period.
Adenosine Triphosphate ; Amiodarone ; Cardiomyopathy, Hypertrophic ; Catheters ; Child* ; Congenital Abnormalities ; Digoxin ; Diving ; Electric Countershock ; Electrocardiography ; Female ; Flecainide ; Heart Rate ; Hemodynamics ; Humans ; Medical Records ; Phenylephrine ; Recurrence ; Reflex ; Tachycardia* ; Verapamil

No abstract available.
Histiocytosis*

No abstract available.
Neurothekeoma* ; Scalp

In the rat brain, partial ischemia causes a delayed neuronal degeneration that occurs hours to days after reoxygenation. It is generally thought that the ischemic damage is initiated by neurotoxicity mediated through glutamate receptors, particulaly NMDA subtypes. Calcium entry through the NMDA receptor is responsible for the synaptic plasiticity and neuronal pathology. Degradation of MAP-2 and NF200, a major components of neuronal cytoskeleton, by Ca2+-dependent protease after NMDA receptor activation has been postulated in delayed neuronal damage. Calcium-activated protease calpain, excessive degradation of MAP-2, together with the calpain-sensitive microtubule and neurofilaments, would be expected to disrupt intracellular transport- and membrane-related functions that is vital to neurons. Changed of NR subunit 2A, 2B, MAP2 and NF200 in rat hippncampal postsynaptic density[PSD] after partial ischemic injury were investigated though immunoblot analyses. To understand the effect of Ca2+, influx through NMDA receptors on neuronal damage which is manifested by cytoskeletal disruption, morphological change was examined through immunohistochemistry and routine staining method. We found that immunoreactivity to NR2B receptor subuit in the hippocampal formation PSD was upregulated while MAP2 and NF200 was down-regulted at 18 hours after initial partial ischemic insult. On the other hand, morphological changes of neuronal cell in partial ischemic conditions were manifested as eosinophilic inclusion bodies in the cytoplasm which is progression of neuronal damage after 6 days. Calcium influx through NR1/NR2B receptor channel may activate intracellular proteases which would degrade cytoskeleton. Proteolysis of cytoskeleton leads to its reorganization and eventually damages normal function of cell membrane which cause neuronal cell death.
Animals ; Brain ; Calcium ; Calpain ; Cell Death ; Cell Membrane ; Cytoplasm ; Cytoskeleton ; Eosinophils ; Hand ; Hippocampus* ; Immunohistochemistry ; Inclusion Bodies ; Ischemia ; Microtubules ; N-Methylaspartate ; Neurons ; Pathology ; Peptide Hydrolases ; Proteolysis* ; Rats* ; Receptors, Glutamate ; Receptors, N-Methyl-D-Aspartate

Transient cerebral ischemia was induced by bilateral common carotid artery ligation with reperfusion to understand its effect on the expression of NMDA receptor subunits 2A (NR2A), 2B (NR2B), and NF200 The changes of the expressions of NR2A, NR2B, and NF200 in cerebral postsynaptic density (PSD) were evaluated through immunoblot analyses. The expressions of NR2A and NF200 were markedly decreased until 18 hours after reperfusion, while that of NR2B was increased. The immunohistochemistry with NFIGO antibody showed that NF200 protein, which is a marker for neuronal damage, was also significantly decreased at this time point indicating neuronal damages, and the morphological damages of neuronal cells were evident by hyperchromatic condensation of nucleus, irregular cell membrane, displacement of nucleus, and chromatolysis of Nissl substances in toluidine blue stain. However, from 18 hours to 3 day after reperfusion, immunoblot analyses showed that NF200 was increased significantly, while the expression of NR2A were recovered to the control level and that of NR2B was returned to somewhat higher level than control. The NR1/NR2B-type receptor is known to have a longer offset decay time than NR1/NR2A-type ones, and to be more potent in Ca2 influxing. Therefore, our results suggest that, until 18 hours, neurons are damaged by overinflux of Ca2 through NR1/NR2B receptors which helps to degrade NF200 by Ca2 sensitive professes resulting in damages to intracellular transport. The fact that the expression of NF200 was increased even though the NR2A and NR2B are control level during 18 hours to 3 days after damage suggests that NMDA receptor subunits expressed at this time may not form functional receptors. The worsening of some neuronal damages after 3 days may indicate that an abnormal reorganization of elevated NF200 between 18 hours to 3 days further disturb intracellular transport and functions of cell membrane which cause cell death.
Animals ; Carotid Artery, Common ; Cell Death ; Cell Membrane ; Cerebral Cortex* ; Immunohistochemistry ; Ischemic Attack, Transient* ; Ligation ; N-Methylaspartate* ; Neurons ; Post-Synaptic Density ; Rats* ; Reperfusion ; Tolonium Chloride

In the rat brain, global hypoxia cause a delayed neuronal degeneration that occurs hours to days after reoxygenation. It is generally thought that the ischemic damage is initiated by neurotoxicity mediated through glutamate receptors, particulary NMDA subtypes. Calcium entry through the NMDA receptor is responsible for the synaptic plasiticity and neuronal pathology. Degradation of MAP-2 and NF200, a major components of neuronal cytoskeleton, by Ca2+-dependent protease after NMDA receptor activation has been postulated in delayed neuronal damage. Changes of NR subunit 2B, MAP2 and NF200 in rat brain postsynaptic density[PSD] after hypoxic injury were investigated through immunoblot analyses. To understand the effect of Ca2+ influx through NMDA receptors on neuronal damage which is manifested by cytoskeletal disruption, morphological change was examined through immunohistochemistry and H & E staining. We found that immunoreactivity to NR2B antibody in the cerebral cortex PSD was up-regulated while MAP2 and NF200 was down-regulated at 30 hours after initial hypoxic insult. At this time, morphological changes of neuronal cells in hypoxic conditions were manifested as down-regulation of MAP2 and NF200 immunoreactivities, hyperchromatic condensation of cytoplasm and nucleus, homogenizing cell change, expansion of perineuronal space and dispersion of chromatin. From 3 days, NR2B, MAP2, NF200 were up-regulated simultaneously. On the other hand, morphological alterations in hypoxic neurons were progress further. Our present results suggests that Calcium influx through NR1/NR2B receptor channel is effective whithin 30 hours but ineffective from 30 hours. Delayed neuronal cell death triggered by Ca2+ influx through NR1/NR2B receptor channel within 30 hours, which may activate intracellular profeases. Proteolysis of cytoskeleton by activated protease leads to its abnormal reorganization and eventually damages normal function of cell membrane which causes neuronal cell death.
Animals ; Anoxia ; Brain ; Calcium ; Cell Death ; Cell Membrane ; Cerebral Cortex* ; Chromatin ; Cytoplasm ; Cytoskeleton* ; Down-Regulation ; Hand ; Immunohistochemistry ; N-Methylaspartate* ; Neurons ; Pathology ; Proteolysis ; Rats* ; Receptors, Glutamate ; Receptors, N-Methyl-D-Aspartate ; Up-Regulation*

The peritoneal equilibration test(PET) has been recommended in adults as a standardized means of estimating solute transport. However, it appears that norrns for pediatric PD patients may be different. We performed a PET on 16 children aged 3 to 18 years using a dwell volume for 30ml/kg of 2.596 dialysate. Our children transported glucose more rapidly than adults, however, creatinine transport was not significantly different. Age did not correlate with D/13% glucose or drainage volume. There was negative correlation between D/D% glucose and D/P Cr. There was no significant difference between initial and maintenance CAPD patients. There was slight difference in patients with previous peritonitis. In conclusion, there was difference in glucose transport between children and adults.
Adult ; Child* ; Creatinine ; Drainage ; Glucose ; Humans ; Peritoneal Dialysis, Continuous Ambulatory* ; Peritonitis

No abstract available.
Amiodarone* ; Arrhythmias, Cardiac* ; Child* ; Humans