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Figure 1 | Acta Neuropathologica Communications

Figure 1

From: Lipid accumulation, lipid oxidation, and low plasma levels of acquired antibodies against oxidized lipids associate with degeneration and rupture of the intracranial aneurysm wall

Figure 1

Atherosclerotic changes, lipid accumulation, and degeneration of the aneurysm wall. Intraoperative view of an MCA aneurysm with atherosclerotic changes (A). Lipids accumulate to the aneurysm wall, despite plasma cholesterol levels that did not significantly differ from “normal” (B, bar graphs display mean and error bars SEM). In non-aneurysmal cerebral artery wall, lipid accumulation is mostly observed subendothelially on the luminal side of the internal elastic lamina (C, sample from a middle cerebral artery, polarized light). In most unruptured sIA walls that show features of mild intimal hyperplasia, lipid accumulation in Oil-Red-O stainings is limited to a matrix layer usually between the outer 1/3 and luminal 2/3 of the wall (D). In aneurysms with more myointimal hyperplasia-like wall, intracellular lipid droplets and foam cells are seen (E). In degenerated and decellularized aneurysm walls, Oil-Red-O staining is mostly extracellular and spread around the degenerated matrix (F). Overall, in the Oil-Red-O stainings the accumulation of lipids was associated with loss of mural cells of the sIA wall (G). The bar graph G displays mean values for density of nuclei (number of nuclei per a standardized surface area) and error bars present SEM.

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