@article{RegnLaggerbauerJentzschetal.2016,
  author    = {Regn, Michael and Laggerbauer, Bernhard and Jentzsch, Claudia and Ramanujam, Deepak and Ahles, Andrea and Sichler, Sonja and Calzada-Wack, Julia and Koenen, Rory R. and Braun, Attila and Nieswandt, Bernhard and Engelhardt, Stefan},
  title     = {Peptidase inhibitor 16 is a membrane-tethered regulator of chemerin processing in the myocardium},
  series = {Journal of Molecular and Cellular Cardiology},
  volume    = {99},
  journal   = {Journal of Molecular and Cellular Cardiology},
  doi       = {10.1016/j.yjmcc.2016.08.010},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-187039},
  pages     = {57-64},
  year      = {2016},
  abstract  = {A key response of the myocardium to stress is the secretion of factors with paracrine or endocrine function. Intriguing in this respect is peptidase inhibitor 16 (PI16), a member of the CAP family of proteins which we found to be highly upregulated in cardiac disease. Up to this point, the mechanism of action and physiological function of PI16 remained elusive. Here, we show that PI16 is predominantly expressed by cardiac fibroblasts, which expose PI16 to the interstitium via a glycophosphatidylinositol (-GPI) membrane anchor. Based on a reported genetic association of PI16 and plasma levels of the chemokine chemerin, we investigated whether PI16 regulates post-translational processing of its precursor pro-chemerin. PI16-deficient mice were engineered and found to generate higher levels of processed chemerin than wildtype mice. Purified recombinant PI16 efficiently inhibited cathepsin K, a chemerin-activating protease, in vitro. Moreover, we show that conditioned medium from PI16-overexpressing cells impaired the activation of pro-chemerin. Together, our data indicate that PI16 suppresses chemerin activation in the myocardium and suggest that this circuit may be part of the cardiac stress response.},
  language  = {en}
}
@article{LohrTerekhovWengetal.2019,
  author    = {Lohr, David and Terekhov, Maxim and Weng, Andreas Max and Schroeder, Anja and Walles, Heike and Schreiber, Laura Maria},
  title     = {Spin echo based cardiac diffusion imaging at 7T: An ex vivo study of the porcine heart at 7T and 3T},
  series = {PLoS ONE},
  volume    = {14},
  journal   = {PLoS ONE},
  number    = {3},
  doi       = {10.1371/journal.pone.0213994},
  url       = {http://nbn-resolving.de/urn:nbn:de:bvb:20-opus-201376},
  pages     = {e0213994},
  year      = {2019},
  abstract  = {Purpose of this work was to assess feasibility of cardiac diffusion tensor imaging (cDTI) at 7 T in a set of healthy, unfixed, porcine hearts using various parallel imaging acceleration factors and to compare SNR and derived cDTI metrics to a reference measured at 3 T. Magnetic resonance imaging was performed on 7T and 3T whole body systems using a spin echo diffusion encoding sequence with echo planar imaging readout. Five reference (b = 0 s/mm\(^2\)) images and 30 diffusion directions (b = 700 s/mm\(^2\)) were acquired at both 7 T and 3 T using a GRAPPA acceleration factor R = 1. Scans at 7 T were repeated using R = 2, R = 3, and R = 4. SNR evaluation was based on 30 reference (b = 0 s/mm\(^2\)) images of 30 slices of the left ventricle and cardiac DTI metrics were compared within AHA segmentation. The number of hearts scanned at 7 T and 3 T was n = 11. No statistically significant differences were found for evaluated helix angle, secondary eigenvector angle, fractional anisotropy and apparent diffusion coefficient at the different field strengths, given sufficiently high SNR and geometrically undistorted images. R≥3 was needed to reduce susceptibility induced geometric distortions to an acceptable amount. On average SNR in myocardium of the left ventricle was increased from 29±3 to 44±6 in the reference image (b = 0 s/mm\(^2\)) when switching from 3 T to 7 T. Our study demonstrates that high resolution, ex vivo cDTI is feasible at 7 T using commercial hardware.},
  language  = {en}
}