Abstract-Chronically diabetic rats prepared by a single i.v. Injection of strepto zotocin were used to study whether royal jelly (RJ) possesses a hypoglycemic reaction and whether it can augment wound healing. Oral RJ administration of 10, 100 and 1000 mg/kg/day did not show any insulin-like activity (the hypo glycemic reaction). RJ, however, showed some anti-inflammatory activity by decreasing exudation and collagen formation in granulation tissue formation in the cotton pellet method. RJ also shortened the healing period of desquamated skin lesions. Thus, RJ possesses an anti-inflammatory action and is able to augment wound healing, but does not have an insulin-like action in streptozotocin-diabetic rats.

Intracranial meningeal melanocytoma is an uncommon tumor that is considered benign. We formerly reported an intracranial meningeal melanocytoma. Here we report a extremely rare case of malignant transformation of this tumor. A 49-year-old man complained of a headache. Magnetic resonance scanning revealed a mass in the left frontal region. The patient underwent gross total removal of the tomor in 1994. The histological findings showed a meningeal melanocytoma. In 1998, he underwent gamma-knife surgery for local recurrence. An additional operation was performed in 1999 became tumor growth was not stopped. The tumor was partially excised by left frontal craniotomy. Histopathological examination revealed a malignant melanoma originating from a melanocytoma. The tumor was composed of a proliferation of severely atypical melanocytoid cells with slightly irregular nuclei and prominent nucleoli, associated with necrosis and hemorrhage. Mitotic figures were encountered occasionally. After six months, he died from cerebrospinal fluid dissemination of this tumor. To our knowledge, this is the first report of malignant transformation of an intracranial meningeal melanocytoma.

A 44-year-old man presented with traumatic injuries of the bilateral middle meningeal arteries after a traffic accident. Neurological examination found left visual impairement due to left optic nerve injury. Computed tomography demonstrated a small amount of left epidural hemorrhage and bilateral skull fractures. Left external carotid angiography revealed a pseudoaneurysm of the left middle meningeal artery at the sphenoid ridge. Right external carotid angiography demonstrated a dural arteriovenous fistula fed by the right middle meningeal artery colocated with the right frontal convexity fracture. Transarterial embolization of the left middle meningeal artery pseudoaneurysm with four fibered platinum coils and transarterial embolization of the right dural arteriovenous fistula with poly(2-hydroxyethyl methacrylate-co-methyl methacrylate) were performed, resulting in complete obliteration of both lesions. Angiographic cure was obtained and the postoperative course was uneventful.

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A 48-year-old male without marked blood coagulation disorder developed a pseudoaneurysm of the superficial temporal artery (STA) following craniotomy. Cerebral angiography revealed a pseudoaneurysm on the parietal branch of the STA. Total extirpation was performed, and the postoperative course was uneventful. Most pseudoaneurysms of the STA develop after trauma. Lesions rarely develop after craniotomy. However, pseudoaneurysm of the STA should be considered as a possible surgical complication.

To examine the role of axonal ion deregulation in acute spinal cord injury (SCI), white matter strips from guinea pig spinal cord were incubated in vitro and were subjected to graded focal compression injury. At several postinjury times, spinal segments were removed from incubation and rapidly frozen. X-ray microanalysis was used to measure percent water and dry weight elemental concentrations (mmol/kg) of Na, P, Cl, K, Ca, and Mg in selected morphological compartments of myelinated axons and neuroglia from spinal cord cryosections. As an index of axon function, compound action potentials (CAP) were measured before compression and at several times thereafter. Axons and mitochondria in epicenter of severely compressed spinal segments exhibited early (5 min) increases in mean Na and decreases in K and Mg concentrations. These elemental changes were correlated to a significant reduction in CAP amplitude. At later postcompression times (15 and 60 min), elemental changes progressed and were accompanied by alterations in compartmental water content and increases in mean Ca. Swollen axons were evident at all postinjury times and were characterized by marked element and water deregulation. Neuroglia and myelin in severely injured epicenter also exhibited significant disruptions. In shoulder areas (adjacent to epicenter) of severely injured spinal strips, axons and mitochondria exhibited modest increases in mean Na in conjunction with decreases in K, Mg, and water content. Following moderate compression injury to spinal strips, epicenter axons exhibited early (10 min postinjury) element and water deregulation that eventually recovered to near control values (60 min postinjury). Na(+) channel blockade by tetrodotoxin (TTX, 1 microM) perfusion initiated 5 min after severe crush diminished both K loss and the accumulation of Na, Cl, and Ca in epicenter axons and neuroglia, whereas in shoulder regions TTX perfusion completely prevented subcellular elemental deregulation. TTX perfusion also reduced Na entry in swollen axons but did not affect K loss or Ca gain. Thus graded compression injury of spinal cord produced subcellular elemental deregulation in axons and neuroglia that correlated with the onset of impaired electrophysiological function and neuropathological alterations. This suggests that the mechanism of acute SCI-induced structural and functional deficits are mediated by disruption of subcellular ion distribution. The ability of TTX to reduce elemental deregulation in compression-injured axons and neuroglia implicates a significant pathophysiological role for Na(+) influx in SCI and suggests Na(+) channel blockade as a pharmacotherapeutic strategy.

We present autopsy findings in a patient with a dissecting aneurysm of the vertebral artery causing subarachnoid haemorrhage. We sectioned the artery longitudinally and compared it with the angiogram, which showed the "pearl-and-string". Histological examination showed a pseudoaneurysm covered by adventitia alone, forming the "pearl". Internal elastic lamina and media were destroyed, and haematoma extended in the subadventitial space of the wall of the pseudoaneurysm. Media thickened by haematoma caused the "string", narrowing the parent artery. Alcian blue staining showed that stratified internal elastic lamina in the aneurysm and the parent artery, had undergone marked mucoid degeneration, which may have been responsible for the dissection.

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