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This paper investigates the ethical implications of applying open science (OS) practices on disruptive technologies, such as generative AIs. Disruptive technologies, characterized by their scalability and paradigm-shifting nature, have the potential to generate significant global impact, and carry a risk of dual use. The tension arises between the moral duty of OS to promote societal benefit by democratizing knowledge and the risks associated with open dissemination of disruptive technologies. Van Rennselaer Potter's ‘third bioethics’ serves as the founding horizon for an ethical framework to govern these tensions. Through theoretical analysis and concrete examples, this paper explores how OS can contribute to a better future or pose threats. Finally, we provide an ethical framework for the intersection between OS and disruptive technologies that tries to go beyond the simple ‘as open as possible’ tenet, considering openness as an instrumental value for the pursuit of other ethical values rather than as a principle with prima facie moral significance. [ABSTRACT FROM AUTHOR]

Natural polyamines (PA) are cationic molecules affecting cell growth and proliferation. An association between increased polyamine biosynthesis and inflammation-induced carcinogenesis has been recognised. On the other hand, there are indications that inflammatory stimuli can up-regulate polyamine catabolism and that altered polyamine metabolism could affect pro- and anti-inflammatory cytokines. Since the polyamine content is strictly related to cell growth, a consistent number of evidences relate polyamine metabolism dysfunction with cancer. The increase of polyamine levels in malignant and proliferating cells attracted the interest of scientists during last decades, addressing polyamine depletion as a new strategy to inhibit carcinogenesis. Several studies suggest that PA also play an important role in neurodegeneration, but the mechanisms by which they participate in neuronal death are still unclear. Furthermore, the role of endogenous PA in normal brain functioning is yet to be elucidated. The consequences of an alteration of polyamine metabolism have also been approached in vivo with the use of transgenic animals overexpressing or devoid of some enzymes involved in polyamine metabolism. In the present work we review the experimental investigation carried out on inflammation, cancerogenesis and neurodegeneration using transgenic animals engineered as models for polyamine research. [ABSTRACT FROM AUTHOR]

The elimination of unfit cells from a tissue is a process known in Drosophila and mammals as cell competition. In a well-studied paradigm "loser" cells that are heterozygous mutant for a haploinsufficient ribosomal protein gene are eliminated from developing tissues via apoptosis when surrounded by fitter wild-type cells, referred to as "winner" cells. However, the mechanisms underlying the induction of this phenomenon are not fully understood. Here we report that a CCAAT-Enhancer-Binding Protein (C/EBP), Xrp1, which is known to help maintaining genomic stability after genotoxic stress, is necessary for the elimination of loser clones in cell competition. In loser cells, Xrp1 is transcriptionally upregulated by an autoregulatory loop and is able to trigger apoptosis - driving cell elimination. We further show that Xrp1 acts in the nucleus to regulate the transcription of several genes that have been previously involved in cell competition. We therefore speculate that Xrp1 might play a fundamental role as a molecular caretaker of the genomic integrity of tissues. [ABSTRACT FROM AUTHOR]