First we identified one seed region in the left inferior parietal (IPL) cortex (BA7) showing activation differences between grapheme-color synesthetes and controls. Furthermore, we found activation differences in brain areas involved in processing of letters and pseudo-letters,
in particular the right IPL cortex (BA7), but also two more clusters in the right hemispheric BA SU5402 solubility dmso 18 and BA 40. Functional connectivity analysis revealed an increased connectivity between the left IPL seed region and primary/secondary visual areas (BA 18) in synesthetes. Also the right BA 7 showed a stronger connectivity with primary/secondary visual areas (BA 18) in grapheme-color synesthetes. The results of this study support the idea that the parietal lobe plays an important role in synesthetic experience. The data suggest furthermore that the information flow in grapheme-color synesthetes was already modulated at the level of the FRAX597 in vivo primary visual cortex which is different than previously thought. Therefore, the
current models of grapheme-color synesthesia have to be refined as the unusual communication flow in synesthetes is not restricted to V4, fusiform cortex and the parietal lobe but rather involves a more extended network. (C) 2012 Elsevier Ltd. All rights reserved.”
“Objectives: Ventricular remodeling after myocardial infarction begins with massive extracellular matrix deposition and resultant fibrosis. This loss of functional tissue and stiffening
of myocardial elastic and contractile elements starts the vicious cycle Metformin mw of mechanical inefficiency, adverse remodeling, and eventual heart failure. We hypothesized that stromal cell-derived factor 1 alpha (SDF-1 alpha) therapy to microrevascularize ischemic myocardium would rescue salvageable peri-infarct tissue and subsequently improve myocardial elasticity.
Methods: Immediately after left anterior descending coronary artery ligation, mice were randomly assigned to receive peri-infarct injection of either saline solution or SDF-1 alpha. After 6 weeks, animals were killed and samples were taken from the peri-infarct border zone and the infarct scar, as well as from the left ventricle of noninfarcted control mice. Determination of tissues’ elastic moduli was carried out by mechanical testing in an atomic force microscope.
Results: SDF-1 alpha-treated peri-infarct tissue most closely approximated the elasticity of normal ventricle and was significantly more elastic than saline-treated peri-infarct myocardium (109 +/- 22.9 kPa vs 295 +/- 42.3 kPa; P<.0001). Myocardial scar, the strength of which depends on matrix deposition from vasculature at the peri-infarct edge, was stiffer in SDF-1 alpha-treated animals than in controls (804 +/- 102.2 kPa vs 144 +/- 27.5 kPa; P<.0001).