Intracranial lipoma is a rare condition, though lipoma in other sites can be found throughout the body. Many authors have reported intracranial lipoma since Rokitansky and Soman who described first in autopsy and living patient respectively. Intracranial lipoma can be diagnosed simply be simple skull and computed tomography. The authors experienced three cases of intracranial lipoma diagnosed by simple skull, tomography, cerebral angiography and computed tomography, and reported with a brief review of the literature.
Autopsy ; Cerebral Angiography ; Humans ; Lipoma* ; Skull ; Soman

Animals ; Female ; Gonads ; physiopathology ; Hypothermia ; chemically induced ; physiopathology ; Male ; Rats ; Rats, Wistar ; Sex Factors ; Soman ; adverse effects ; pharmacology

AIMTo determine the effect of soman on stress induced hyperthermia and the influence of central and peripheral cholinergic antagonists.

METHODSEffects of subcutaneous injection of soman, scopolamine, methylscopolamine and pyridostigmine on stress-induced hyperthermia were observed in rats by radio telemetry in an open-field environment. Plasma cholinesterase (ChE) activity was measured by a spectrophotometry.

RESULTS(1) Core temperature of the control group increased by 0.96 degrees C when exposed to open-field, whereas core temperature only increased by 0.55 degrees C in soman treated animals. Scopolamine, a central cholinergic antagonist, nearly abolished inhibitory effects of soman on core temperature when exposed to open-field. Methylscopolamine, a peripheral cholinergic antagonist, coadministered with soman reduced significantly the hyperthermic response to open-field exposure compared with rats dosed with soman. (2) Pyridostigmine, a peripheral anti-ChE agent that caused a 52% decrease in plasma ChE activity led to a significant enhancement of the hyperthermic response to open-field exposure. Methyl scopolamine nearly abolished the effects of pyridostigmine on stress-induced hyperthermia response.

CONCLUSIONInhibitory effect of soman on the open field hyperthermia suggested that soman treatment hampered the ability of the rat to develop a normal hyperthermic response when placed in the open-field environment. Its inhibitory effects were mediated primarily through a central muscarinic pathway. In addition, peripheral cholinergic nerve was involved in the control of stress hyperthermic response.

Animals ; Cholinergic Antagonists ; pharmacology ; Cholinesterases ; blood ; Female ; Fever ; drug therapy ; Rats ; Rats, Sprague-Dawley ; Soman ; antagonists & inhibitors ; pharmacology ; Stress, Physiological

BACKGROUND: Soman, a potent irreversible acetylcholinesterase (AChE) inhibitor, induces delayed neuronal injury by reactive oxygen species (ROS). Midazolam is used in patients with pathologic effects of oxidative stresses such as infection, hemodynamic instability and hypoxia. We investigated whether midazolam protects the Central Nervous System (CNS) from soman intoxication. The present study was performed to determine whether midazolam protects B35 cells from ROS stress for the purpose of exploring an application of midazolam to soman intoxication. METHODS: Glucose oxidase (GOX) induced ROS stress was used in a B35 neuroblastoma cell model of ROS induced neuronal injury. To investigate the effect of midazolam on cell viability, LDH assays and fluorescence activated cell sorting (FACS) analysis was performed. Western blotting was used for evaluating whether Akt-phosphorylation is involved in cell-protective effects of midazolam. RESULTS: GOX derived ROS injury decreased cell viability about 1.6-2 times compared to control; midazolam treatment (5 and 10 microg/ml) dose-dependently increased cell viability during ROS injury. On western blots, Akt-phosphorylation was induced during pretreatment with midazolam; it was diminished during co-treatment with LY-294002, an inhibitor of Akt-phosphorylation. FACS analysis confirmed that the cell protective effect of midazolam is mediated by an anti-apoptotic effect. GOX-induced apoptosis was inhibited by midazolam and the finding was diminished by LY-294002. CONCLUSIONS: Midazolam protects neuronal cells from GOX-induced ROS injury; this effect is mediated by an anti-apoptotic effect through Akt-phosphorylation. This shows that midazolam may be useful in soman intoxication.
Acetylcholinesterase ; Anoxia ; Apoptosis ; Blotting, Western ; Cell Survival ; Central Nervous System ; Chromones ; Flow Cytometry ; Glucose Oxidase ; Hemodynamics ; Humans ; Midazolam ; Morpholines ; Neuroblastoma ; Neurons ; Oxidative Stress ; Reactive Oxygen Species ; Soman