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At the end of the permeability assay midbrain organoids were removed from the bottom of acceptor compartments, homogenized in DW containing Triton X-100 (10 mg/ml)

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Because typical early atherosclerotic lesion formation observed in hyperhomocysteinemic animals can be prevented by an antiplatelet therapy with dipyridamole, the authors concluded that platelet-mediated proliferation of smooth muscle cells is a potential cellular mechanism involved in the atherogenicity of hyperhomocysteinemia