No abstract available.
Osteoblastoma* ; Spine*

No abstract available.
Eosinophilic Granuloma* ; Eosinophils*

No abstract available.

Pleomorphic xanthoastrocytoma is a recently characterized neoplasm with relatively favorable prognosis despite aggressive histological features. Two cases of pleomorphic xanthoastrocytoma involving the left temporal lobe are reported, both occurring in adolescents. The tumor is considered to arise from the subpial astrocytes of the superficial cortex. Electron microscopic examination and immunoperoxidase stains for glial fibrillary acidic protein(GFAP) are helpful in making a definitive histologic diagnosis. In contrast to malignant gliomas, pleomorphic xanthoastrocytoma does not appear to require aggressive postoperative radiation therapy or chemotherapy. Therefore, It is important to recognize and identify this type of glioma as a distinct entity.
Adolescent ; Astrocytes ; Coloring Agents ; Diagnosis ; Drug Therapy ; Glioma ; Humans ; Prognosis ; Temporal Lobe

BACKGROUND: Use of corticosteroid appears to increase the risk of upper gastrosintestinal side effects associated with NSAIDs. But, there is no study for the effects of these drugs to NSAID induced small intestinal damage. Therefore, we examed the effects of corticosteroid to NSAID induced enteropathy and bacterial translocation. METHODS: Rat received no drug, NSAID alone (diclofenac 80 mg/kg per os), corticosteroid alone (dexamethasone 5 mg/kg intraperitoneal, 2 times) or NSAID with corticosteroid. Amounts of food intakes, body weight, intestinal permeability, enteric aerobic bacterial counts in small and large intestine, serum biochemical profiles, and pathologic findings of ileum were measured. Cultures of the mesenteric lymph nodes, as well as liver, spleen and systemic blood were taken. RESULTS: Diclofenac or dexamethasone alone administration caused gut barrier damage, enteric bacterial overgrowth and increased bacterial translocation. The supplements with dexamethasone increased NSAID induced gut barrier damage, villous atrophy, enteric bacterial overgrowth and bacterial translocation to mesenteric lymph nodes, liver, spleen and systemic blood. Also, these increased diclofenac induced body weight loss, but not hypoproteinemia. CONCLUSION: Corticosteroid increase NSAID induced body weight loss, gut barrier dysfunction, villous atrophy, enteric bacterial overgrowth and bacterial translocation in experimental animals.
Animals ; Anti-Inflammatory Agents, Non-Steroidal ; Atrophy ; Bacterial Load ; Bacterial Translocation* ; Body Weight ; Dexamethasone ; Diclofenac ; Hypoproteinemia ; Ileum ; Intestine, Large ; Intestine, Small ; Liver ; Lymph Nodes ; Permeability ; Rats* ; Spleen

The present study was undertaken to investigate the influence of hypothermia on endothelium-independent vascular smooth muscle contractility and to determine the mechanism underlying the relaxation. Denuded aortic rings from male rats were used and isometric contractions were recorded and combined with molecular experiments. Hypothermia significantly inhibited fluoride-, thromboxane A2-, phenylephrine-, and phorbol ester-induced vascular contractions regardless of endothelial nitric oxide synthesis, suggesting that another pathway had a direct effect on vascular smooth muscle. Hypothermia significantly inhibited the fluoride-induced increase in pMYPT1 level and phorbol ester-induced increase in pERK1/2 level, suggesting inhibition of Rho-kinase and MEK activity and subsequent phosphorylation of MYPT1 and ERK1/2. These results suggest that the relaxing effect of moderate hypothermia on agonist-induced vascular contraction regardless of endothelial function involves inhibition of Rho-kinase and MEK activities.
Animals ; Fluorides ; Humans ; Hypothermia* ; Isometric Contraction ; Male ; Muscle, Smooth, Vascular ; Nitric Oxide ; Phosphorylation ; Rats ; Relaxation ; rho-Associated Kinases*

Soybean polyunsaturated phosphatidylcholine (PC) is thought to exert anti-inflammatory activities and has potent effects in attenuating acute renal failure and liver dysfunction. The aim of this study was to investigate the effects of PC in protecting multiple organ injury (MOI) from lipopolysaccharide (LPS). Six groups of rats (N=8) were used in this study. Three groups acted as controls and received only saline, hydrocortisone (HC, 6 mg/kg, i.v.) or PC (600 mg/kg, i.p.) without LPS (15 mg/kg, i.p.) injections. Other 3 groups, as the test groups, were administered saline, HC or PC in the presence of LPS. Six hours after the LPS injection, blood and organs (lung, liver and kidney) were collected from each group to measure inflammatory cytokines and perform histopathology and myeloperoxidase (MPO) assessment. Serum cytokines (TNF-alpha, IL-6 and IL-10) and MPO activities were significantly increased, and significant histopathological changes in the organs were observed by LPS challenge. These findings were significantly attenuated by PC or HC. The treatment with PC or HC resulted in a significant attenuation on the increase in serum levels of TNF-alpha and IL-6, pro-inflammatory cytokines, while neither PC nor HC significantly attenuated serum levels of IL-10, anti-inflammatory cytokine. In the organs, the enhanced infiltration of neutrophils and expression of ED2 positive macrophage were attenuated by PC or HC. Inductions of MPO activity were also significantly attenuated by PC or HC. From the findings, we suggest that PC may be a functional material for its use as an anti-inflammatory agent.
Acute Kidney Injury ; Animals ; Cytokines ; Hydrocortisone ; Inflammation ; Interleukin-10 ; Interleukin-6 ; Kidney ; Liver ; Liver Diseases ; Lung ; Macrophages ; Neutrophils ; Peroxidase ; Phosphatidylcholines ; Rats ; Soybeans ; Tumor Necrosis Factor-alpha

This study was aimed to observe that extremely low frequency magnetic field (ELF-MF) may be relevant to changes of major neurotransmitters in rat brain. After the exposure to ELF-MF (60 Hz, 2.0 mT) for 2 or 5 days, we measured the levels of biogenic amines and their metabolites, amino acid neurotransmitters and nitric oxide (NO) in the cortex, striatum, thalamus, cerebellum and hippocampus. The exposure of ELF-MF for 2 or 5 days produced significant differences in norepinephrine and vanillyl mandelic acid in the striatum, thalamus, cerebellum and hippocampus. Significant increases in the levels of serotonin and 5-hydroxyindoleacetic acid were also observed in the striatum, thalamus or hippocampus. ELF-MF significantly increased the concentration of dopamine in the thalamus. ELF-MF tended to increase the levels of amino acid neurotransmitters such as glutamine, glycine and gamma -aminobutyric acid in the striatum and thalamus, whereas it decreased the levels in the cortex, cerebellum and hippocampus. ELF-MF significantly increased NO concentration in the striatum, thalamus and hippocampus. The present study has demonstrated that exposure to ELF-MFs may evoke the changes in the levels of biogenic amines, amino acid and NO in the brain although the extent and property vary with the brain areas. However, the mechanisms remain further to be characterized.
Animals ; Biogenic Amines ; Brain ; Cerebellum ; Dopamine ; Glutamine ; Glycine ; Hippocampus ; Magnetic Fields* ; Neurotransmitter Agents* ; Nitric Oxide ; Norepinephrine ; Rats ; Serotonin ; Thalamus

Extremely low frequency magnetic fields (ELF-MF) have the ability to produce a variety of behavioral and physiological changes in animals. The stomach, as the most sensitive part of the neuroendocrine organ of the gastrointestinal tract, is crucial for the initiation of a full stress response against all harmful stress. Thus, the purpose of this study was to examine whether ELF-MF stimuli induce changes in the activity of neuroendocrine cells, considering their involvement in endocrine or paracrine effect on surrounding cells. The exposure to ELF-MF (durations of 24 h and 1 or 2 weeks, 60 Hz frequency, 0.1 mT intensity) altered the distribution and occurrence of gastrin, ghrelin and somatostatin-positive endocrine cells in the stomach of rats. The change, however, in the secretion of those hormones into blood from endocrine cells did not appear significantly with ELF-MF exposure. Comparing with sham control, ELF-MF exposure for 1 and 2 week induced an increase in BaSO4 suspension propelling ratio of gastrointestinal tract, indicating that ELF-MF affects gastrointestinal motility. Our study revealed that ELF-MF exposure might influence the activity of endocrine cells, an important element of the intrinsic regulatory system in the digestive tract. The pathophysiological character of these changes and the mechanism responsible for neuroendocrine cell are still unclear and require further studies.
Animals ; Endocrine Cells ; Gastrins ; Gastrointestinal Motility ; Gastrointestinal Tract ; Ghrelin ; Magnetic Fields ; Magnetics ; Magnets ; Neuroendocrine Cells ; Rats ; Salicylamides ; Somatostatin ; Stomach

We evaluated therapeutic and preventive properties of dehydroepiandrosterone (DHEA), a weak androgenic steroid, against isoproterenol-induced cardiomyopathy. The cardiomyopathy was induced by daily i.p. administration of isoproterenol to rats for five days. One group of rats were given with daily s.c. for 5 days during isoproterenol and the other group with daily s.c. DHEA for total 10 days, including 5 days before and during isoproterenol. The animals were killed after each treatment, and cardiac muscle failure was evaluated using histopathologic examination and biochemical indices. DHEA was found to reduce the damaged area and inhibit the elevation in the serum levels of glutamic oxaloacetic transaminase (SGOT), lactate dehydrogenase (LDH), skeletal muscle creatine kinase (CK) and heart creatine kinase (CK-MB) induced by isoproterenol. We also assayed widely used oxidative stress parameters, including thiobarbituric acid reactive substances (TBARS), superoxide dismutase (SOD), catalase and glutathion peroxidase (GPx). DHEA decreased the escalated level of TBARS and enhanced the anti oxidant defense reaction with an increase in Mn-SOD and Cu/Zn-SOD. On the other hand, the treatment with DHEA did not affect catalase and GPx activity. The present study indicates that DHEA has a therapeutic and preventive effect against isoproterenol-induced cardiomyopathy and its effects may depend largely on the increase in SOD activity.
Animals ; Aspartate Aminotransferases ; Cardiomyopathies* ; Catalase ; Creatine Kinase ; Dehydroepiandrosterone* ; Hand ; Heart ; Isoproterenol ; L-Lactate Dehydrogenase ; Muscle, Skeletal ; Myocardium ; Oxidative Stress ; Peroxidase ; Rats* ; Superoxide Dismutase ; Thiobarbituric Acid Reactive Substances