Representative pictures of Golgi Cox-impregnated layer V pyramidal neurons of the control, CIMT and G-CSF-treated group in the peri-infarct cortex (A) and the corresponding contralateral cortex (B), respectively.

<p>Note the increase of the basilar dendritic arbor in the peri-infarct cortex of G-CSF treated rats. Scale bar: 50 μm.</p

Topographic localization of the photothrombotic infarct.

<p>Note that infarct was mirrored on the contralateral side to analyze Golgi Cox-impregnated cortical layer V pyramidal neurons in the ipsilateral peri-infarct cortex and in the corresponding contralateral cortex (Insets: representative Golgi Cox-impregnated cells).</p

Quantitative analysis of Golgi Cox-impregnated layer V pyramidal neurons in the peri-infarct cortex and in the corresponding contralateral cortex.

<p>There were no differences in the number of basilar dendrites between the various experimental groups neither in the peri-infarct cortex nor in the corresponding contralateral cortex (Values are expressed as mean number of basilar dendrites ± SEM).</p

Sholl analysis of Golgi Cox-impregnated layer V pyramidal neurons in the peri-infarct cortex and in the corresponding contralateral cortex.

<p>Note that corresponding to the increased length of basilar dendrites (c.f. <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0146679#pone.0146679.g003" target="_blank">Fig 3</a>) a significantly increased number of intersections of higher order in the G-CSF group of the peri-infarct cortex were detectable (B) which paralleled the functional outcome as recently published [<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0146679#pone.0146679.ref006" target="_blank">6</a>] (A, B, D, E significant difference compared with control, CIMT, CIMT+G-CSF, CIMT/G-CSF, respectively. Values are expressed as mean number of intersections / μm ± SEM; p<0.05).</p

Brain sections from terminally sick mice (<i>high dose</i> RML6, lowest row) revealed typical signs of a prion disease such as spongiform change (H&E), astrogliosis (GFAP), microgliosis (IBA1) and PrP^Sc deposition (SAF84).

<p> None of these features were observed in <i>tg</i>a<i>20</i> mice inoculated with scFvPOM1-COCS, (scFvPOM1+recPrP_23-230)-COCS, or in untreated mice. Scale bar = 50 μm.</p

IL-6 in cortex or hippocampus.

<p>IL-6 mRNA in cortex (left) or hippocampus (right). * p < 0.05 vs. Ctr.</p

PK-digestion of brain homogenate from a terminally sick <i>tg</i>a<i>20</i> mouse revealed protease resistance.

<p> The residual PrP^Sc showed a typical diagnostic shift in its molecular weight. Neither untreated, scFvPOM1-COCS inoculated (n = 3 brain homogenates) nor (scFvPOM1+recPrP_23-230)-COCS inoculated (n = 3 brain homogenates) <i>tg</i>a<i>20</i> mice showed detectable PrP^Sc.</p

Physiologic parameters given as mean ± SD.

<p>Physiologic parameters given as mean ± SD.</p

IL-1beta in cortex or hippocampus.

<p>IL-1beta mRNA in cortex (left) or hippocampus (right).</p

Wet-to-dry ratio and lung injury score.

<p>Wet-to-dry ratio (left) and histologic assessed lung damage score (right). * p < 0.05 vs. Ctr.</p