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The angiogenesis of the rat cerebrum was studied under pathologic conditions caused by the administration of the neurotoxin methylazoxymethanol acetate (MAMAc) in the time (E14) of neuroblast migration. The sinovenous junction of the main superficial cerebral veins and the morphological changes of the veins were examined by a quantitative analytic method. The hypoplastic areas of the brains showed extremely malformed venous systems with pathologic changes of the sinovenous junctions depending on the degree of disturbance of the neuroblast migration. These findings suggest the primary role of the neuronal maturation in the angioarchitectonic development and the direct dependency of the vascular differentiation on the neuroblast migration of the drained territory.

A necrotizing, nonprogressive myopathy with unusual paracrystalline inclusion bodies is described in a patient who underwent long-term treatment with megadoses of vitamin E. The clinical course and morphological findings suggest a close relationship to the administration of the vitamin. The theoretical pathogenesis of muscle damage and the possible origin of paracrystalline inclusion bodies are discussed.

A 66-year-old man had developed a myopathy while undergoing several periods of etofibrate and clofibrate therapy over the past 5 years. Discontinuation of etofibrate treatment failed to reverse his muscle illness which, however, did not progress. A muscle biopsy revealed a chronic myopathy marked by abundant, abnormally structured muscle mitochondria. His mitochondrial myopathy may represent a forme fruste of the Kearns-Sayre syndrome or other types of mitochondrial myopathy, clinically made evident by the etofibrate/clofibrate therapy, or a permanent, adverse side effect of clofibrate treatment. If the latter assumption proves to be correct, it will indicate that clofibrate therapy may induce an acutely painful but reversible neuromuscular illness, or also, though rarely, a chronic mitochondrial myopathy.

The angioarchitecture of the superficial and basal arterial system of the hypoplastic rat brain caused by the administration of the neurotoxin, methylazoxymethanol acetate (MAMAc), at the time of neuroblast migration was studied. Increased variation of the arterial branching of the basal main stem of arteries and local vessel changes were observed. The findings suggest a close relationship between vascular and neuronal development, showing a generalized disturbance and local adaptation of vasculature to the altered neuronal architecture of the corresponding hypoplastic areas.

Differentiated and anaplastic oligodendrogliomas revealed intracytoplasmic and nuclear presence of endogenous carbohydrate-binding proteins by application of labelled (neo)glycoproteins in histochemical analysis. The histochemical patterns showed differences between the differentiated and anaplastic forms of the same tumor type. Xylose-, lactose- and asialofetuin-specific carbohydrate-binding proteins could be detected in both types of tumors with the same staining intensity. However, maltose-specific carbohydrate-binding proteins were present only in the differentiated form. An inverse intensity of the histochemical reaction was observed with galactose-6-phosphate-, galactose-beta(1.3)-N-acetylglucosamine-N-acetylglucosamine- and mannose-(BSA-biotin) and fucose-(BSA-biotin) respectively, when the differentiated and anaplastic oligodendrogliomas were compared with each other. These differences document changes in the pattern of histochemically detectable carbohydrate-binding proteins, suggesting a role for endogenous carbohydrate-binding proteins in the tumor cell differentiation. These data indicate the potential usefulness of labelled (neo)glycoproteins as a new type of marker for histopathological diagnosis.