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On the 10th of January 2010 Helmut Sick, the German-Brazilian explorer of neotropical birds would have had his 100th anniversary. He made his PhD under supervision of Erwin Stresemann in 1937 about the structure of bird feathers. 1939 he joined a three months expedition to Brazil but was so fascinated about the bird life that he stayed much longer and in 1952 he became citizen of Brazil. Helmut Sick was director at the National Museum Boa Vista and was professor for zoology an the State University in Rio. He became member of the Academia Brasileira de Ciências und honorary citizen of Rio de Janeiro. His probably most important book were the two volumes of „Ornitologia brasiliera, uma introduÇão“, which has been revised in 1993 in an English version “Birds in Brazil. A natural history“. Over 68 years Helmut Sick conducted an ornithological diary with very detailed, sometimes even artistic descriptions of his observations. His notes between 1923 and 1938 comprise 12 diary books with 80 pages each. The authors secured the material and looked through it. Here a short description of the contents is given. A publication list and more material are available online (see bottom of the text). Helmut Sick died in a traffic accident on 5th March 1991 in Rio de Janeiro.
Survivin functions as an apoptosis inhibitor and a regulator of cell division during development and tumorigenesis. Since survivin is a highly relevant target for tumor therapy, we investigated whether interference with it’s dynamic cellular localization represents a novel strategy to inhibit survivin’s cancer promoting functions. We confirmed survivin overexpression in head and neck as well as in colorectal cancers and identified an evolutionary conserved Crm1-dependent nuclear export signal (NES) in survivin. Importantly, nuclear export was required for survivin mediated protection against chemo- and radiotherapy-induced apoptosis by securing efficient interference with cytoplasmic caspases. In dividing cells, the NES was required for tethering of survivin and of the survivin/Aurora-B kinase complex to the mitotic machinery, which was inevitable for proper cell division. The clinical relevance of our findings was supported by showing that preferential nuclear localization of survivin correlated with enhanced survival in a cohort of colorectal cancer patients. Targeting survivin’s nuclear export by the application of NES-specific antibodies promoted its nuclear accumulation and inhibited its cytoprotective function. We here show that nuclear export is essential for the tumor promoting activities of survivin and encourage the identification of chemical inhibitors to specifically interfere with survivin’s nuclear export as a novel class of anticancer therapeutics.