No abstract available.
Follow-Up Studies* ; Hepatitis*

No abstract available.
Female ; Germ Cells* ; Neoplasms, Germ Cell and Embryonal* ; Ovary*

No abstract available.

It is known that excitotoxicity and oxygen radicals were two major pathogenic events related to mesial temporal sclerosis(MTS), which was the most common histopathologic features in intractable temporal lobe epilepsy. The experiment was designed to investigate the neuroprotective effect of 2-methylaminochroman U-78S17F, a second generation series of nonsteroidal lazaroid compounds, against excitotoxic and oxygen radical injuries on the human fetal hippocampal neurons in vitro. Neuron-enriched cultures were seeded on both 96 well multichamber plates and poly-L-Iysine coated Aclar cover slips to determine cytotoxicity by MTT(3-4, 5-dimethylthiazol-2-yl-2, 5-diphenyl tetrazolium bromide) assay and cytopathologic features respectively. Dose-dependent neuronal injuries were developed by treatment of 100, 200, and 500 microM glutamate (p<0.01), and 100 microM hypoxanthine plus 10 to 20 mU xanthine oxidase (p<0.01). The glutamate-induced cytotoxicity was completely blocked by pretreatment of 20 microM MK-801 (p<0.01), however, U-78S17F did not attenuate the glutamate toxicity. The fetal hippocampal neurons were protected from oxygen radical injuries by pretreatment of 2 to 16 microM U-78517F (p<0.01). The cytopathologic changes observed by phase-contrast inverted microscope, neurofilament protein (NF) immunocytochemistry, and MTT stain correlated well with the degree of neuronal injuries in experimental groups. Considerably swollen neurons with disintegrated neurites were noted by the excitotoxic and oxygen radical injuries, however, there was no characteristic cytologic difference between them. These data indicated that U-78S17F had only a significant protective effect from oxygen radical injury on fetal hippocampal neurons in culture, and it was suggested that the early treatment of both glutamate-antagonists and antioxidants would be beneficial to reduce MTS following epileptic seizures.
Antioxidants ; Dizocilpine Maleate ; Epilepsy ; Epilepsy, Temporal Lobe ; Glutamic Acid ; Humans* ; Hypoxanthine ; Immunohistochemistry ; Neurites ; Neurons* ; Neuroprotective Agents* ; Oxygen ; Reactive Oxygen Species ; Xanthine Oxidase

No abstract available.
alpha-Fetoproteins* ; Infant, Newborn ; Jaundice, Neonatal* ; Plasma*

BACKGROUND: The vascular endothelial growth factor (VEGF) is known as a potent mediator of brain tumor angio-genesis, vascular permeablity, and glioma growth. This study was designed to study the balance between growth and death signals in different grades of astrocytic tumors. METHODS: Using immunohistochemistry, the relationship between the expression of VEGF and microvessel count and density were evaluated in 62 cases of astrocytic tumors including 33 low grade astrocytomas, 6 anaplastic astrocytomas, and 23 glioblastomas. In order to determine the apoptotic index (AI), the in situ end-labeling method was applied. RESULTS: VEGF was expressed on the tumor cell cytoplasm. Of 62 tumors, 44 (77%) were weak to strong postive for VEGF, but 18 cases were not reactive. VEGF positivity was correlat-ed with WHO grades of the astrocytic tumors; low grade astrocytomas (52%), anaplastic astrocytomas (83%), and glioblastomas (96%). Mean microvessel count and density were significantly higher in VEGF-positive tumors (75.7 and 4.1%) than in VEGF-negative tumors (43.9 and 2.5%). Apoptotic cells were readily found in the astrocytic tumors; the highest value of AI was observed in glioblastomas (8.6%) and the lowest in anaplastic astrocytomas (1.9%). It seemed that the grade of malignancy was not related with AI values. CONCLUSIONS: These results suggest that VEGF promotes angiogenesis with tumor cell growth against apoptotic cell death in the human astrocytomas.
Apoptosis* ; Astrocytoma ; Brain Neoplasms ; Cell Death ; Cytoplasm ; Glioblastoma ; Glioma ; Humans ; Immunohistochemistry ; Microvessels ; Vascular Endothelial Growth Factor A*

Five brains from established cases of Senile Dementia of Alzheimer Type (SDAT) and six branis from cases of no clinical or neuropathological evidences of SDAT were studied immunocytochemically using anti-somatostatin (SST) antibody. Fifty micrometer sections of immersion fixed brains (autopsy delay: 10-16 hours) were cut and then stored in 0.1 M tris-HCI buffer (pH7.4) until the immunocytochemical study. Lmmunostatinings were performed according to Sternberger's peroxidase-antiperoxidase (PAP) technique. The primary antiserum was rabbit antiserum to synthetic somatostatin (Cambridge Research Biochemicals). Diluted to 1: 1.000. The secondary antiserum was goat anti-rabbit IgG (Sternbeger-Meyer) in dilutions of 1: 400 to 500. Controls followed complete staining protocol. But without incubation in the specific antibody. SST-immunoreactive (IR) neurons in aged normal brains were distributed in all layers of cortices. These cells were multipolar, bitufted, or wramidal in shape. The changes of SST-IR neurons were profound in frontal, parietal, and temporal cortices of SDAT brains, but were absent in the Cal of hippocampus. Neuritic plaque-like structure formation was the most common changes seen in the cortices, especially in the temporal cortex. The morphology of altered SST-IR neuronal elements were similar to that of the neuritic plaques demonstrated by the Bielshowsky's silver impregnation method. Apparently intact SST-IR neurons were also found in SDAT brains, thus giving rise to the speculation that these neurons may have unusual survival and reorganization potential. Unexpectedly, there were no degenerative changes of SST-IR neurons in CA! region of SDAT hippocampus. These results strongly suggest that among SST-IR neurons only neocortical short association neurons are affected in the neuronal degenerative changes of SDAT.
Alzheimer Disease* ; Brain ; Goats ; Hippocampus ; Immersion ; Immunoglobulin G ; Neurons* ; Plaque, Amyloid ; Rabeprazole ; Silver ; Somatostatin

No abstract available.
Anemia, Aplastic* ; Preleukemia*

BACKGROUND: Steroid myopathy is an unexpected side effect to the prolonged therapeutic use of steroids. To treat steroid myopathy, the followings are recommended; reduction of the steroid dose, usage of a nonfluorinated steroid, and conversion to an alternate day regimen. As muscle loading is encouraged in maintaining normal muscle properties, it is also apparent that physical exercise may be useful in the prevention and treatment of steroid myopathy. METHOD: The experiment was designed to investigate the effects of exercise on steroid myopathy. Rats being treated with triamcinolone acetonide (TA) (5 mg/kg/day) for 7 days exercised on a treadmill (speed 20m/min, 30 min/day, 3 days/week) for 2 weeks. The extensor digitorum longus (EDL) and soleus were then examined histochemically and ultrastructurally. RESULTS: Rats treated with TA showed significant loss of body and muscle weight. In the TA treated group, cross-sectional areas of type II fibers of both EDL and soleus were decreased in comparison with the controls. Necrotic changes were found only in type II fibers of the soleus. Recovery from the weight loss with type II fiber atrophy was more pronounced in the exercise group than that of the sedentary group, but was not significant statistically. Ultrastructural abnormalities, that consisted of subsarcolemmal mitochondrial accumulation, mitochondrial vacuolation, increased number of mitochondria in autophagic vacuoles, and dilatation of sarcoplasmic reticulum, were seen in TA treated muscles. These injuries were significantly reduced by the exercise, however, complete recovery could not be seen. CONCLUSIONS: These results suggest that treadmill exercise for 2 weeks partially ameliorate steroid myopathy in.
Animals ; Atrophy ; Dilatation ; Exercise* ; Mitochondria ; Muscles ; Muscular Diseases* ; Rats ; Sarcoplasmic Reticulum ; Steroids ; Triamcinolone Acetonide ; Vacuoles ; Weight Loss

Cerebral venous thrombosis is come from thromboplebitis of infectious origin and bland occlusion of cerebral vein by various causes. Although the main cause of cerebral venous thrombosis is thrombophlebitis, the bland occlusion causes it infrequently as a form of an infarct state. We report a case of cerebral venous infarction caused by splenectomy induced thrombocytosis.
Cerebral Veins ; Infarction ; Splenectomy ; Thrombocytosis* ; Thrombophlebitis ; Venous Thrombosis