Recently, nine Caenorhabditis elegans genes, grouped into two pathways/clusters, were found to be implicated in healthspan in C. elegans and their homologues in humans, based on literature curation, WormBase data mining and bioinformatics analyses. Here, we further validated these genes experimentally in C. elegans . We downregulated the nine genes via RNA interference (RNAi), and their effects on physical function (locomotion in a swim assay) and on physiological function (survival after heat stress) were analysed in aged nematodes. Swim performance was negatively affected by the downregulation of acox-1.1 , pept-1 , pak-2 , gsk-3 and C25G6.3 in worms with advanced age (twelfth day of adulthood) and heat stress resistance was decreased by RNAi targeting of acox-1.1 , daf-22 , cat-4 , pig-1 , pak-2 , gsk-3 and C25G6.3 in moderately (seventh day of adulthood) or advanced aged nematodes. Only one gene, sad-1 , could not be linked to a health-related function in C. elegans with the bioassays we selected. Thus, most of the healthspan genes could be re-confirmed by health measurements in old worms.

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achieved in 19 patients (60%), while 5 (16%) had postoperative residual disease (n=8 missing data). Sixteen patients (50%) commenced systemic treatment within 90 days from surgery, as documented. Thirty-and 90-day surgical mortality rates were 1 (3%) and 2 (6%), respectively. Within a postoperative median follow-up time of 43.8 months, 12 (38%) deaths were reported. Median overall survival after surgery (OS) was 54.0 months. One-and 2-year OS rates were 91% and 84%, respectively. Conclusion Cytoreductive surgery for subsequent ovarian cancer relapse appears feasible and with low mortality in selected patients who received non-surgical treatment at 1st relapse despite a positive AGO -score. Surgery could be considered as an option in carefully selected patients also later in their journey within a specialized gynecological cancer setting.

among which activation of DNA replication and changes in cell cycle regulation were notable. Organoids which retained regeneration capacity after carboplatin exposure, showed a sustained shift in expression of stemness associated surface marker CD133+ in the subsequent passages as showed by fluorescence-activated cell sorting and Western blot Conclusion We hereby propose OFE assay as a novel functional readout for carboplatin sensitivity. Furthermore, expression profile changes in organoids during acute response to carboplatin provide insights into specific signaling hallmarks that are associated with resistance to carboplatin. and could help identify the cellular mechanism behind the process.