No abstract available.
Female ; Fetal Heart* ; Heart Rate, Fetal* ; Pregnancy ; Telemetry*

Adult Wilms' tumor, unlike that of childhood, is a rare disease. Microscopically, the tumor is fundamentally characterized by triplastic embryonal renal tumor composed of variable amounts of metanephric blastema and its epithelial and stromal derivatives but rarely a small group of tumors composed virtually entirely of differentiated epithelial derivatives, the abundance of tubular structures. These monomorphous epithelial type of Wilms' tumor tended to have an early onset and benign course. Grossly, classic Wilms' tumor is a solid tumor, but very rarely shows cystic change and may lead to misinterpretation as a polycystic kidney or multicystic nephroma. Here, we reports a case of primary renal tumor, grossly very similar to a multicystic kidney but histologically represent a tubular monomorphous epithelial variant of Wilms' tumor occured in 63 year old male adult.
Child ; Adult ; Male ; Female ; Humans

Two cases of Klippel-Trenaunay-Weber Syndrome were presented and its literatures were reviewed. The patients were 25 year old male farmer and 38 year old housewife. Both had hypertrophy, port-wine nevus, and varicosities in case 1, on left lower extremity since birth. The length and cirumference of the affected leg were longer than the other side, and X-ray showed osteohypertrophy of tibia of the involved leg,
Adult ; Humans ; Hypertrophy ; Klippel-Trenaunay-Weber Syndrome* ; Leg ; Lower Extremity ; Male ; Nevus ; Parturition ; Tibia

Two cases of Klippel-Trenaunay-Weber Syndrome were presented and its literatures were reviewed. The patients were 25 year old male farmer and 38 year old housewife. Both had hypertrophy, port-wine nevus, and varicosities in case 1, on left lower extremity since birth. The length and cirumference of the affected leg were longer than the other side, and X-ray showed osteohypertrophy of tibia of the involved leg,
Adult ; Humans ; Hypertrophy ; Klippel-Trenaunay-Weber Syndrome* ; Leg ; Lower Extremity ; Male ; Nevus ; Parturition ; Tibia

No abstract available.
Biopsy ; Biopsy, Fine-Needle ; Diagnosis

OBJECTIVES: This study is aimed to quantify the complex dynamics of beat-to-beat fetal heart rate(FHR) fluctuations by using approximate entropy(ApEn) which is a recently developed mathematical formula quantifying regularity and also to determine the differences between normal fetuses and growth retarded fetuses. BACKGROUND: Recently, some measures of heart rate variability and nonlinear "complexity" of heart rate dynamics have been used as indicators fetal well-being. Approximate entropy is a new mathematical approach and formula to quantify regularity in data. It has been shown to provide new information in fetal heart rate analysis. Because growth retarded fetus accounts for a significant increase in perinatal morbidity and mortality, than normal fetus, we postulated that there existed important differences between normal fetuses and growth retarded fetuses. METHODS: We analyzed FHR tracings for 40 minutes, and approximately 5,000 points in normal fetuses(n=315) and growth retarded fetuses(n=76). The overall "complexity" of each FHR time series was quantified by its approximate entropy, measure of regularity derived from nonlinear dynamics, "chaos theory". RESULTS: Mean baseline FHR increased in growth retarded fetuses than normal fetuses. And the FHR ApEn significantly decreased in growth retarded fetuses(ApEn=0.623) compared to that of the normal fetuses(ApEn=0.868) throughout all gestational ages(p < 0.001). CONCLUSIONS: The ApEn of FHR decreased in growth retarded fetuses throughout all gestational ages. These findings indicated that decreased ApEn values of FHR are associated with sickness and the greater perinatal morbidity risks. Therefore ApEn quantifies subtle changes in FHR regularity and promises for new information in FHR analysis.
Entropy* ; Female ; Fetal Heart* ; Fetus* ; Gestational Age ; Heart Rate ; Heart Rate, Fetal* ; Mortality ; Nonlinear Dynamics ; Pregnancy

To elucidate the effect of copper on the 3'-methyl-4-dimethylaminoazobenzene(3'-MeDAB) induced hepatic carcinogenesis, Sprague-Dawley rats were divided into 4 groups according to 3'-MeDAB and copper administration: I. noraml control, II. copper only, III. 3'-MeDAB only, IV. 3'-MeDAB plus copper. The animals of groups III and IV were fed experimental diet containing 0.06% 3'-MeDAB. Copper was administrated intraperitoneally in a dose of 0.5 mg, twice a weak. Animals were sacrificed at different intervals. Liver weight, hepatic copper content and gross and microscopical changes of the liver were examined and the cell kinetics of various lesions in the hepatic carcinogenesis was studied by applying the immunohistochemical method for bromodeoxyuridine(BrdU). The hepatic copper content was significantly increased in animals given copper but returned to the normal value after cessation of adminstration. 3'-MeDAB administration caused oval cell proliferation and produced hyperplastic nodules, cholangiofibrosis and carcinoma of the liver. Simultaneous administration of copper did not alter the incidence of 3'-MeDAB induced lesions, except for carcinoma. The liver weight and the size of hepatic nodules and masses were smaller in group IV than in group III. The liver weight as well as the nodularity and the mass formation continued to increase affect cessation of 3'-MeDAB administration. Copper did not affect the BrdU labelling indices of the hepatic lesions induced by 3'-MeDAB. The oval cell proliferation and the BrdU labelling indices of the oval cell and the hyperplastic nodule were decreased, but the incidence of cholangiofibrosis and its BrdU labelling index were still elevated after cessation of 3'MeDAB administration. These findings indicate that copper could delay the developement of 3'-MeDAB induced hepatic lesions, but not suppress, since copper does not stay long enough to accumulate in the rat liver, and that copper could not affect the proliferation of 3'-MeDAB induced hepatic lesions once developed.
Rats ; Animals ; Incidence

No abstract available.
Central Venous Catheters* ; Prospective Studies* ; Thrombophlebitis*

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

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*