30 research outputs found

    Soleus and EDL muscle weights and function.

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    <p>* indicates significantly different from C57; # indicates significantly different from mdx. C57 (n = 6–7) mdx (n = 6) mdxQ (n = 5–6).</p

    Transcript expression in the soleus.

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    <p>Data are shown as fold change relative to C57. * indicates significantly different from C57; # indicates significantly different from mdx. C57 (n = 7) mdx (n = 6) mdxQ (n = 6).</p

    Dystrophin deficiency increased fibronectin in soleus muscles compared to healthy muscles.

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    <p>A-C) Representative 10x immunohistochemical images for fibronectin (red) and DAPI (blue). All images have been uniformly brightened to make the fibronectin signal easier to see. D) The percent positive pixels were quantified. * indicates significantly different from C57. Width of white bar represents 100 microns. C57 (n = 7) mdx (n = 6) mdxQ (n = 6).</p

    Dystrophin deficiency increased muscle fibrosis.

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    <p>A-C) Representative images from trichrome-stained, reconstructed soleus cross sections. D) Total fibrotic area was calculated by quantifying the blue staining material in the entire muscle cross section. * indicates significantly different from C57. Width of black bar represents 250 microns. C57 (n = 7) mdx (n = 6) mdxQ (n = 6).</p

    Dystrophin deficiency causes histological injury that is not corrected by quercetin.

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    <p>A-C) Representative images from H&E-stained, reconstructed soleus muscle cross sections. E) Extra cellular nuclei, F) centralized nuclei, and G) total contractile area were calculated. * indicates significantly different from C57. Width of black bar represents 250 microns. C57 (n = 7) mdx (n = 6) mdxQ (n = 6).</p

    Animal activity was increased by dietary quercetin enrichment.

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    <p>At the conclusion of the investigation animal behavior was quantified using an ethological approach where a 10 minute observation period was divided into 15 second blocks. A) The number of time blocks spent sitting or exhibiting sedentary behavior was quantified. B) We also quantified the number of active behaviors. * indicates significantly different from C57; # indicates significantly different from mdx. C57 (n = 7) mdx (n = 7) mdxQ (n = 6).</p

    Soleus and EDL muscle function at 14 months of age.

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    <p>A) Specific tension measured in the soleus and B) in the EDL. C) The soleus was then subjected to a fatigue test where it was stimulated once per second for 10 minutes. Force was normalized to force produced in the first contraction. D) The relative force produced in the final contraction is shown. Relative force produced in the final contraction was significantly less in mdx than C57. E) The EDL was subjected to a series of five eccentric contractions and peak force normalized to peak force generated in the first contraction. * indicates significantly different from C57; # indicates significantly different from mdx. C57 (n = 7) mdx (n = 6) mdxQ (n = 6).</p

    Relative protein abundance was altered by dystrophin deficiency.

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    <p>A) Protein abundance of PGC-1α pathway components was largely depressed by dystrophin deficiency independent of intervention compared to muscle from C57 mice. B) Representative blots are included and Ponceau S stain is included to demonstrate equal loading. * indicates significantly different from C57. C57 (n = 5) mdx (n = 6) mdxQ (n = 5).</p

    Relative force reduction in 6 wk old EDL's following lengthening contractions.

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    <p>PGC-1α over-expressing limbs were better able to maintain force during lengthening contractions when compared to control limbs (n = 13/group). Data from age matched C57 animals is included for reference purposes. * indicates p<0.05. Con – contraction.</p

    PGC-1α induced changes in muscle mass.

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    <p>Following four (n = 7) or six (n = 13) weeks of PGC-1α over-expression in mdx mice muscle mass was generally reduced.</p><p>*indicates significantly different from corresponding control. EDL – extensor digitorum longus, Gastroc – gastrocnemius, TA – tibialis anterior.</p
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