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. 2012 Jun 26;5(6):804–811. doi: 10.1242/dmm.009712

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© 2012. Published by The Company of Biologists Ltd

This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial Share Alike License (http://creativecommons.org/licenses/by-nc-sa/3.0), which permits unrestricted non-commercial use, distribution and reproduction in any medium provided that the original work is properly cited and all further distributions of the work or adaptation are subject to the same Creative Commons License terms.

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Fig. 5. — Progressive cytoplasmic glycogen accumulation occurs in skeletal of GSD3 dogs. (A–C) Progressive accumulation of glycogen in skeletal muscle over time. MetaMorph measurements were 6.5±3.1%, 20.3±7.6% and 17.3±4.7% tissue area occupied by glycogen at 4, 12 and 16 months, respectively (HRLM, PAS-Richardson’s stain). (D–F) Ultrastructural changes that occur over time. At 4 months, glycogen accumulates in the cytoplasm and dissects in between myofibrils and just beneath the cytoplasmic membrane, forming small blebs (D). At 12 months, the cytoplasmic glycogen begins to pool and disrupts the contractile apparatus, causing fraying of myofibrils (E). At 16 months, entire regions of cells are filled with glycogen, displacing all contractile elements, leaving only mitochondria to float within the pools of glycogen (F). Arrows indicate glycogen pools. Scale bars: 50 μm (A–C), 2 μm (D), 5 μm (E) and 6 μm (F).