Peritumoral brain edema associated with meningioma--histological study of the tumor margin and surrounding brain.

Thirty-nine cases of intracranial meningiomas were analyzed to identify factors causing brain edema. Edema was significantly correlated with tumor size and the destruction of the leptomeninges and cortex. Meningotheliomatous meningioma tended to have more peritumoral edema. There was no correlation between the presence of edema and location of the tumor or histological features including lymphocytic infiltration and the presence of glial fibrillary acidic protein-positive cells in the tumor tissue. Larger tumors destroy the leptomeninges and cerebral cortex, allowing direct transmission of humoral edema-promoting factor or edema fluid into the white matter, resulting in vasogenic edema.     

Horseshoe anomaly of the pancreas.

A 72-year-old man with recurrent pancreatitis and a horseshoe-shaped anomaly of the pancreas is described. The diagnosis was made by endoscopic retrograde cholangiopancreatography (ERCP) and computed tomography scan; laparotomy was confirmatory. The abnormal duct branched to the lower left from an enlarged Santorini's duct; a thin Wirsung's duct was joined at its distal portion to the junction of the abnormal duct. The anomaly was associated with a cystic dilatation of the common bile duct with stone and cholecystolithiasis. This anomaly is considered to be a variation of the dominant dorsal duct syndrome.     

Enhanced clearance of lactic dehydrogenase-5 in severe combined immunodeficiency (SCID) mice: effect of lactic dehydrogenase virus on enzyme clearance.

The lactic dehydrogenase (LDH) level in plasma and the clearance of LDH in C.B-17 scid (severe combined immunodeficiency; SCID) mice were compared with those in C.B-17 or BALB/cCrSlc mice with or without lactic dehydrogenase virus (LDV) infection. The resting enzyme level in SCID mice showed little difference from that in C.B-17 or BALB/cCrSlc mice. The degree of increased plasma LDH level in SCID mice was lower than that in C.B-17 and BALB/cCrSlc mice after LDV infection. To assess the mechanisms of decrease in LDH elevation in SCID mice infected with LDV, virus replication was compared in SCID and BALB/cCrSlc mice. The infectivity titre of plasma in SCID mice was higher (more than 10 times) than that in BALB/cCrSlc mice. Moreover, the percentage of virus antigen positive Kupffer cells was higher in SCID mice than that in BALB/cCrSlc mice. The level of endogenous LDH release as a result of carbon tetrachloride treatment was similar in the SCID and BALB/cCrSlc mice. The clearance rate of endogenous LDH was greater in SCID mice than in BALB/cCrSlc mice with or without LDV infection. The rate of clearance of intravenously injected porcine LDH-5, but not porcine LDH-1, was enhanced in SCID mice as compared with that in BALB/cCrSlc mice. Furthermore, carbon clearance was higher in SCID mice than that in BALB/cCrSlc mice. These results suggest that the smaller increase of plasma LDH after infection might be due, at least in part, to the enhanced LDH-5 clearance function by macrophages in SCID mice.     

Acute myocardial infarction: comparison of results of Tl-201, Tc-99m pyrophosphate and In-111 antimyosin Fab imagings]

To evaluate the extent and characteristics of infarct areas, we performed indium-111 monoclonal antimyosin Fab (InAM), thallium-201 (TL) and Tc-99m pyrophosphate (PYP) imagings in 17 patients with acute myocardial infarction, and tried to find out the mechanism that causes difference of these imagings. In each study, the extent scores as an index of the infarct area were obtained by single photon emission computed tomography (SPECT), and comparisons were made between the results obtained. The overlap between InAM and TL imagings obtained by SPECT was evaluated. Location, severity, extent and patterns of accumulation were compared between InAM and PYP with both planar image and SPECT. The extent scores of InAM correlated well with those of TL (r = 0.73, p < 0.01). However, the overlap of both methods was recognized in 8 of 17 patients, in whom wall thickness of the infarct area as obtained by echocardiography was well preserved. The left ventricular regional asynergy was mild in 6 of these 8 patients. Coronary angiography showed poor or no collateral circulation in these cases. Although there were generally close correlations of the extent scores between InAM and PYP, discrepancy was noted in 2 cases for location; 2 for severity, 5 for extent, and 3 for patterns of accumulation. These differences may be attributed to the timings of imaging, coronary reperfusion and different mechanisms of accumulation. In conclusion, the extent of acute myocardial infarction obtained by InAM correlates well with those obtained by TL and PYP, with some exceptions.     

Nodular fasciitis of the upper labial fascia: cytometric and ultrastructural studies

The rare case of nodular fasciitis in the upper labial fascia is reported. Light microscopic, electron microscopic and cytometric studies were performed. The histopathology corresponded to intermediate and reactive types in the Price and Bernstein classification. Cytometric study of evaluating DNA of fibroblasts revealed a high distinct peak in myxoid and inflammatory areas. Ultrastructurally, fibroblasts and myofibroblasts were identified in the lesion. Reported Japanese cases of orofacial nodular fasciitis are reviewed and compared with the European-American literature.     

Clinical experience with PTFE graft replacement in the descending thoracic aorta

In 6 cases, we have performed polytetrafluoroethylene (PTFE) graft replacement in the descending thoracic aorta, with all patients alive and showing good results. Fifty months have passed since the first graft replacement, but no complications due to the PTFE graft have occurred.     

Effects of systemic hypoxia on pH outside rod photoreceptors in the cat retina.

We studied the effect of systemic hypoxia on intraretinal pH in the intact cat eye using double-barreled H(+)-sensitive microelectrodes. Hypoxia in the dark further acidified the extracellular space surrounding rods in the distal retina and this effect was maximal in the outer nuclear layer (ONL). An acidification occurred in response to essentially any decrease in PaO2 below the normoxic level. Light-evoked alkalinizations in the ONL were larger in amplitude during hypoxia than in normoxia and this difference increased with the severity of hypoxia. Background illumination suppressed the hypoxic acidification of the ONL, completely inhibiting it at rod saturating intensities, at levels of hypoxia down to PaO2s of 40 mmHg. Systemic hyperoxia produced a small alkalinization in the ONL, and a reduction in the amplitude of the light-evoked alkalinizations. This suggests that systemic hyperoxia can partially suppress the ongoing glycolysis of dark-adapted rods. Changes in blood flow during hypoxia also altered intraretinal pH. Hypoxia led to an alkalinization in the choroid in both dark and light adaptation that spread into the distal retina. This alkalinization is most likely caused by the increase in CO2 removal that occurs as systemic blood pressure, and as a consequence, choriocapillaris blood flow increase during hypoxia. The alkalinization attenuated the acidification that was observed outside rods during hypoxia. There was also an alkalinization of the proximal portion of the retina, which spread into the vitreous. This alkalinization was attributed to the autoregulatory increase in blood flow that occurs in the retinal vessels during hypoxia. These findings provide further evidence for the hypothesis that the energy metabolism of dark-adapted rods is exquisitely sensitive to systemic hypoxia so that any small decrease in PaO2 increases rod glycolysis. Rod-saturating illumination can completely suppress this increase in glycolysis for all but severe hypoxia. An increase in blood flow in the choriocapillaris during hypoxia appears to mitigate the effects of hypoxia on the distal retina.     

Case report: myocardial ischemia: an overlooked substrate in syncope of aortic stenosis.

The cause of the syncope in aortic stenosis has been the subject of controversy partly because only a few patients have been monitored during their syncopal episodes. Among the mechanisms proposed are hypersensitive carotid sinus, complete A-V block, ventricular arrhythmias, and ischemic myocardial depression. It is now accepted that the syncope is caused by a vasodepressor response from stimulation of left ventricular baroceptors, resulting in reflex hypotension and bradycardia. This case report describes a patient who developed a syncopal episode during stress testing. Although the mechanism for the syncope is consistent with the vasodepressor response, ischemic changes were observed in the electrocardiogram before the development of syncope. Review of literature shows that, although different mechanisms for syncope have been described, all reported patients manifested myocardial ischemia before the development of their syncopal episodes even when the syncope was nonexertional and clearly caused by a vasodepressor response. The authors conclude that, independent of the mechanism proposed, myocardial ischemia is overlooked as an important substrate in which the syncopes are precipitated in aortic stenosis.