The American journal of pathology
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A method for the in situ fixation of human meninges for electron microscopic examination is described. It was found that the cranial meninges of humans do not include a subdural space. Instead there is a complex, tight layer of cells, the interface layer, composed in the innermost portion of the dura mater (the dural border cells) and the outermost portion of the arachnoid (the arachnoid barrier layer). ⋯ The fine structural characteristics of these layers are defined. The erroneous macroscopic impression of a subdural space results from an extraordinary lack of cohesion within the dura-arachnoid interface layer conditioned by a) a complete absence of a collagenous reinforcement within this zone, b) the presence of large extracellular cisterns between the dural border cells, and c) a paucity of intercellular contacts within that latter layer. An understanding of the fine structural organization of the interface layer is essential to any consideration of the pathogenesis of subdural lesions: these form within a sheet of torn dural border cells and not within a preexistent tissue compartment.
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Male Swiss-Webster mice were fed diets containing four hypolipidemic agents which are known to induce proliferation of hepatic peroxisomes. Treatment with all four drugs (clofibrate; its structural analogue, nafenopin; and two drugs structurally unrelated to clofibrate, tibric acid and Wy-14,643) produced a marked hepatomegaly in the mice. The extent of the increase in liver weight correlated well with the increases in total hepatic DNA and in the collective volume of hepatocyte peroxisomes. ⋯ Activity of the latter enzyme, however, is not known to be associated with peroxisome fractions. Concomitant administration of actinomycin D or cycloheximide with a single oral dose of clofibrate diminished the increases in liver weight and carnitine acyltransferase which occurred with clofibrate treatment alone. The finding that the major increase in activity of peroxisome enzymes occurred in those associated with metabolism of acyl CoA groups supports the hypothesis that the hypolipidemic action of the drugs and the proliferation of hepatic peroxisomes are related functions.