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. Author manuscript; available in PMC: 2016 May 2.
Published in final edited form as: J Neurotrauma. 2011 Dec 20;29(3):539–550. doi: 10.1089/neu.2011.1976

FIG. 7.

FIG. 7

CD11d monoclonal antibody (mAb) treatment increases myelin sparing at 42 days after spinal cord injury (SCI). (A) Photomicrographs of solochrome-stained spinal cord sections from 1B7 and CD11d mAb-treated mice rostral (− 640 μm), caudal (+ 640 μm), and at the lesion site (0 μm). Very little myelin (indicated by blue staining) was present at the lesion epicenters. However, myelin increased rostral and caudal to the lesion in CD11d mAb-treated mice. (B) Solochrome staining of consecutive transverse sections from anti-CD11d and 1B7 mAb-treated mice was used to plot the amount of myelin from 1400 μm rostral to 1400 μm caudal to the lesion epicenters. The area of myelin in each section was normalized to the area of myelin in a section with normal morphology from the same cord far from the injury site. CD11d mAb treatment (solid line) increased the amount of myelin beginning at 360 μm rostral and caudal to the lesion compared to control treatment (1B7, dashed line; scale bar in A = 100 μm). Values are means ± standard error (*significantly different from controls, p= 0.008 by two-way analysis of variance, and p<0.05 by Fisher’s protected t-test; 5 mice/1B7 group and 6 mice/anti-CD11d group).