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. Author manuscript; available in PMC: 2014 Oct 3.
Published in final edited form as: Int J Cardiol. 2013 Apr 15;168(3):2567–2574. doi: 10.1016/j.ijcard.2013.03.049

Table 2.

Pre-treatment with BZ resulted in G-CSF-dependent preservation of cardiomyocytes in T. cruzi-infected mice.

Morphology Myocyte transversal diameter (μm)
NI NI + GCSF I I + GCSF I + BZ(4 m) I + BZ(4 m) + GCSF I + BZ(6 m) I + BZ(6 m) + GCSF
Unaffected Area 9.99 ± 0.85 10.33 ± 1.56 11.02 ± 0.77 11.37 ± 0.22 11.09 ± 0.58 11.66 ± 0.87 11.37 ± 0.22 10.02 ± 0.58
Inflamed Area 9.07 ± 0.62 9.36 ± 0.27* 9.40 ± 1.32 8.80 ± 0.81* 9.19 ± 0.8*

C3H/He uninfected mice and mice infected with T. cruzi were treated at 4 and 6 months post-infection with BZ for 30 days, and with G-CSF for 20 days at 10 months post-infection. Mice were harvested after completion of treatment, and heart tissue sections were subjected to cardiomyocyte measurement by histo-morphometry. Data are presented as mean ± S.D. from analysis of >10 microscopic fields/slide at 400× magnification (3–4 tissue-sections/mouse, n ≥ 6 per group

*

p < 0.05, vs. normal

p < 0.05 vs. infected/unaffected area). NI: uninfected control, NI + GCSF: uninfected/G-CSF-treated, I: infected, I + GCSF: infected/G-CSF treated. I + BZ(4 m)/I + BZ(6 m): infected/BZ-treated at 4 and 6 mo pi, respectively. I + BZ(4 m) + GCSF/I + BZ(6 m) + GCSF: infected/BZ-treated at 4 and 6 mo pi and then treated with G-CSF at 10 mo pi.