Kengo Sato; Hayami Yoshizawa; Tomomi Seki; Remina Shirai; Tomoyuki Yamashita; Taisuke Okano; Koichiro Shibata; Miyu J. Wakamatsu; Yusaku Mori; Toshisuke Morita; Taka-aki Matsuyama; Hatsue Ishibashi-Ueda; Tsutomu Hirano; Takuya Watanabe
Clin Sci (Lond) (2019) 133 (16): 1779–1796.
Pre-clinical effects of highly potent MEK1/2 inhibitors on rat cerebral vasculature after organ culture and subarachnoid haemorrhage
Simon T. Christensen; Kristian A. Haanes; Stine Spray; Anne-Sofie Grell; Karin Warfvinge; Lars Edvinsson; Sara E. Johansson
Clin Sci (Lond) (2019) 133 (16): 1797–1811.
In vitro and in vivo investigation of cardiotoxicity associated with anticancer proteasome inhibitors and their combination with anthracycline
Zuzana Pokorna; Eduard Jirkovsky; Marketa Hlavackova; Hana Jansova; Anna Jirkovska; Olga Lencova-Popelova; Petra Brazdova; Jan Kubes; Dita Sotakova-Kasparova; Yvona Mazurova; Michaela Adamcova; Lucie Vostatkova; Kristyna Holzerova; Frantisek Kolar; Tomas Simunek; Martin Sterba
Clin Sci (Lond) (2019) 133 (16): 1827–1844.
Cover ImageIn the latest issue of Clinical Science (volume 133, issue 16), Pokorna et al. investigate the cardiotoxicity associated with anthracycline anticancer drugs in a rabbit model. Their observations using this well-established model corresponds with the cardiomyopathy in patients treated with high cumulative doses of anthracycline anticancer drugs such as daunorubicin, doxorubicin, idarubicin or epirubicin. The cover image depicts degenerating cardiomyocytes. The profound loss of myofibrils is accompanied by vacuolization of the cytoplasm as necrotic cells are gradually replaced by fibrotic scar tissue (blue-stained collagen fibers).