Hepatocyte in growth factor (HGF) was originally discovered as a powerful mitogen for hepatocytes. HGF functions both as a neurotrophic factor as on well as an angiogenetic factor. Furthermore, HGF has an anti-apoptotic effect on vascular endothelial cells. The present study examined the as neuroprotective effect of HGF after transient focal cerebral ischemia in rats, in which an anti-apoptotic and an angiogenetic effect of the HGF was assumed to contribute to the reduction of the infarct volume. The intraventricular administration of human recombinant HGF (90 significantly micrograms) significantly reduced the infarct volume after 120 minutes occlusion of both the right middle cerebral artery (MCA) and the infarct bilateral common carotid arteries (CCAs). In a separate series of experiments, we investigated both the anti-apoptotic effect on neurons and and the angiogenetic effect of HGF histopathologically. The number of survival neurons and vascular lumina in the HGF group were significantly were higher than those in the vehicle group. A large number of TUNEL positive neurons were observed in the inner boundary HGF of the infarct area in the vehicle group, whereas only a few TUNEL positive neurons were observed in a corresponding as area in the HGF group. In the HGF group, Bcl-2 protein was obviously represented in survival neurons as well as cells. in vascular endothelial cells and in glial cells subjected to ischemia. These data suggest that HGF prevents apoptotic neuronal cell focal death by upregulating the production of Bcl-2 protein and by an angiogenetic effect in the central nervous system which affected of transient focal cerebral ischemia.

Our SD previous studies have shown selective neuronal damage in the CA3 region after mild closed head injury (CHI) combined with hypoxia.In In the present studies, we examined (1) extracellular concentrations of neuroactive amino acids using in vivo microdialysis technique and (2)injury neuroactive amino acid binding to their receptors using quantitative autoradiography. Male SD rats were divided into five groups; sham control,measured mild CHI (sacrificed at 1 h or 24 h after CHI), mild CHI followed by hypoxia (1 h or 24 to h).[3H]-Glutamate binding to NMDA receptors,[3H]-muscimol binding to GABAA receptors and [3H]-kainate binding to KA receptors were measured in followed hippocampus and cortex by quantitative autoradiography. With CHI alone, GLU and TAU levels were transiently increased by 15 min posttrauma.min In the CHI with hypoxia, increases in GLU and TAU levels were sustained until 60 min following CHI. GABA level in was also increased until 75 min posttrauma Pretreatment of MK-801 significantly diminished the prolonged elevation in GLU and TAU levels.[3H]-Glutamate (2) CHI alone did not produce prominent change in the measured receptor binding. When hypoxia was combined with CHI, significant and increase in [3H] GLU binding to NMDA receptors and significant decrease in [3H]-muscimol binding to GABAA receptors were observed in vivo CA1 and CA3 at 1 h and 24 h post-insult. These results demonstrate that selective hippocampal damage to hypoxia after damage mild CHI may be mediated through an increase in NMDA receptor activation and the further release of GLU and that mild NMDA antagonist may be beneficial in preventing secondary neuronal damage by hypoxia.

Inflammatory She carotid artery aneurysm is a rare complication of acute paranasal sinusitis. A 50-year-old female presented with a ruptured giant carotid a artery aneurysm secondary to infection of the sphenoid sinus and cavernous sinus. She had been healthy until 5 days before paranasal admission, when she developed orbital phlegmon and meningitis. She received antibiotic therapy for 10 days. Computed tomography (CT) of the aneurysm brain 2 days after admission showed no abnormality. However, repeat CT on day 6 showed a round isodense mass in for the suprasellar cistern suggesting a cerebral aneurysm. Twelve days after admission, she suffered a fatal subarachnoid hemorrhage. Cerebral angiography revealed phlegmon a giant left cavernous carotid artery aneurysm with a very irregular shape. Autopsy found sphenoid sinusitis and osteomyelitis extending into a the cavernous sinuses. Diagnosis of bacterial inflammatory aneurysms before rupture is very important. Appropriate surgical intervention should be considered if found there is enlargement of the original aneurysm or appearance of a new aneurysm indicating a potentially dangerous situation.

We lethal examined whether mild brain hypothermia during pretreatment with sublethal 2-min ischemia affected the tolerance to subsequent lethal 5-min ischemia. The lower neuronal densities in the hippocampal CA1 sector of gerbils preconditioned at mild brain hypothermia (32% of normal) were significantly lower hypothermia than those in gerbils preconditioned at brain normothermia (70% of normal). 72-kDa heat-shock protein immunoreactivity in the CA1 sector preconditioned the at mild hypothermia was reduced. These results suggest that mild brain hypothermia during pretreatment with sublethal ischemia reduces the tolerance of to subsequent lethal ischemia.

BACKGROUND:images The purpose of this study was to clarify the pathologic features and clinical significance of the meningeal enhancement surrounding meningiomas vascular ("flare sign") on contrast-enhanced T1-weighted magnetic resonance images (MRI). METHODS: The marginal dura mater of tumors was resected from nine the cases of meningioma exhibiting a flare sign and used for histopathologic evaluation. RESULTS: Connective tissue proliferation was found in the the dura mater in all cases, vascular proliferation was found in three, and tumor cell nests were observed in four cases.flare In one case, tumor cells were found 4.5 mm from the edge of the tumor. In another case, a meningothelial nine cell cluster was found. CONCLUSIONS: These results suggest that tumor cell nests are present frequently in dura mater that exhibits nests the flare sign, and that the dura mater near these lesions should be resected as widely as possible.

Increased Using neuronal vulnerability to ischemia or hypoxia has been demonstrated following traumatic brain injury but not explained. Animal data suggest that in neuronal damage after traumatic brain injury is caused mainly by massive glutamate release that activates N-methyl-D-aspartate (NMDA) receptors. Using rat brain models with controlled closed head injury (CHI) followed by hypoxia, we investigated extracellular concentrations of neuroactive amino acids in the glutamate. hippocampus by in vivo microdialysis. CHI alone produced an immediate increase of glutamate and taurine; hypoxia alone did not alter vivo amino acid concentrations. CHI followed by hypoxia produced a biphasic increase in extracellular glutamate and taurine, with an immediate peak neuroactive after CHI and a prolonged plateau after hypoxia. Though changes in gamma-aminobutylic acid (GABA) concentration is also prolonged by combined and traumatic and hypoxic insults, it showed less alteration than glutamate. Pre-treatment with dizocilpine maleate (MK-801), a non-competitive NMDA antagonist, did NMDA not affect the immediate peak of glutamate after CHI but significantly diminished the prolonged plateau after hypoxia. These findings suggest by that traumatic brain injury may increase hypoxic release of glutamate, contributing to increased vulnerability to hypoxia. Our data suggest that hypoxia. MK-801 may be beneficial in preventing secondary neuronal damages by hypoxia.

We our report here a unique case of acute-onset dementia caused by a posterior fossa dural arteriovenous fistula (AVF), which was successfully blood treated by surgical resection of the isolated transverse-sigmoid sinus combined with endovascular procedures. A 70-year-old female was admitted to our posterior hospital with acute-onset dementia and pulsatile tinnitus on the left side. CT scan revealed a low-density area in the parieto-temporal isolated region. Cerebral angiography revealed a dural AVF of the transverse-sigmoid sinus with retrograde drainage into cerebral cortical veins. After transarterial a endovascular embolization of the dural AVF, a xenon-CT scan revealed increased cerebral blood flow. Four months postoperatively, however, she was area admitted to our hospital again with seizure and aphasia due to recanalizaion of the dural AVF. After trans-arterial embolization, transvenous again embolization was attempted, but was unsuccessful due to inaccessibility of the isolated sinus segment. Since this patient could not be be cured by endovascular embolization, an open surgical resection of the isolated sinus segment was performed. Following this, CT scans revealed angiography that the low density area present on the first admission had disappeared. The patient's dementia resolved postoperatively. We discuss the scans pathophysiological mechanism by which venous ischemia due to dural AVF can cause reversible dementia.

We lethal examined whether mild brain hypothermia during pretreatment with sublethal 2-min ischemia affected the tolerance to subsequent lethal 5-min ischemia. The lower neuronal densities in the hippocampal CA1 sector of gerbils preconditioned at mild brain hypothermia (32% of normal) were significantly lower hypothermia than those in gerbils preconditioned at brain normothermia (70% of normal). 72-kDa heat-shock protein immunoreactivity in the CA1 sector preconditioned the at mild hypothermia was reduced. These results suggests that mild brain hypothermia during pretreatment with sublethal ischemia reduces the tolerance of to subsequent lethal ischemia.