21 research outputs found

    Empowering citizens to inform decision-making as a way forward to support invasive alien species policy

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    Observations reported by citizens are crucial to the ability of scientists to inform policy on biodiversity. This is particularly relevant in the case of preventing and controlling biological invasions; that is, the introduction and spread of species outside their natural ranges as a consequence of human activity. Such invasions of natural ecosystems represent one of the main threats to biodiversity, economy, and human well-being globally, and policies on tackling this issue require a strong evidence base that increasingly is built on citizen science. Many citizens are motivated to collect data for their own interest, while presumably, few expect to make a major impact on policy. The needs of policy-makers are not always aligned with the approaches used by citizens to collect and share data. Therefore, how can we motivate citizen science for the needs of policy without compromising the enjoyment that citizens gain from collecting biodiversity observations? How can policy-makers support citizens to collect the data they need? Solutions require two components, a combination of social and technological innovation. Initiatives aimed at supporting decision-making processes should involve more societal actors and be built in a more collaborative or even co-created manner with citizens, scientists, and policy-makers. Technological solutions can be achieved through regular, rapid, and open publication of biodiversity data products. We envisage frequent publication of maps and indicators from rapidly mobilized data, with clear pointers to gaps in knowledge. Improving the links between data collection and delivery of policy-relevant information demonstrates – to citizens and their organizations – the need for their data, and gives them a clear view on the impact of their data on policy. This visibility also empowers stakeholder organizations in the policy development process

    Understanding hadronic gamma-ray emission from supernova remnants

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    We aim to test the plausibility of a theoretical framework in which the gamma-ray emission detected from supernova remnants may be of hadronic origin, i.e., due to the decay of neutral pions produced in nuclear collisions involving relativistic nuclei. In particular, we investigate the effects induced by magnetic field amplification on the expected particle spectra, outlining a phenomenological scenario consistent with both the underlying Physics and the larger and larger amount of observational data provided by the present generation of gamma experiments, which seem to indicate rather steep spectra for the accelerated particles. In addition, in order to study to study how pre-supernova winds might affect the expected emission in this class of sources, the time-dependent gamma-ray luminosity of a remnant with a massive progenitor is worked out. Solid points and limitations of the proposed scenario are finally discussed in a critical way.Comment: 30 pages, 5 figures; Several comments, references and a figure added. Some typos correcte

    Farnesyl Transferase Inhibitors Enhance Death Receptor Signals and Induce Apoptosis in Multiple Myeloma Cells

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    Multiple myeloma is an incurable plasma cell malignancy in which Ras may be constitutively active either via interleukin-6 (IL-6) receptor signaling or by mutation. Inactivation of Ras may be achieved with farnesyl transferase (FTase) inhibitors a class of drugs which have shown promise in clinical trials particularly in patients with acute leukemia. This report investigates the efficacy of two distinct classes of FTase inhibitors in diverse myeloma cell lines and primary isolates. While Ras signaling has traditionally been linked to myeloma cell growth, we found that these compounds also potently triggered cell death. Death induced by perillic acid (PA) was caspase dependent without evidence of death receptor activation. Apoptosis was associated with mitochondrial membrane depolarization and activation of caspase-9 and 3 but proceeded despite over-expression of Bcl-X L a known correlate of relapsed and chemorefractory myeloma. In addition, Fas ligand and TRAIL mediated apoptosis was potentiated in death receptor resistant (U266) and sensitive (RPMI 8226/S) cell lines. Of clinical relevance, the FTase inhibitor R115777 induced cell death in myeloma lines at doses observed in clinical trials. Furthermore, both R115777 and PA induced cell death in primary isolates with relative specificity. Taken together these preclinical data provide evidence that FTase inhibitors may be an effective therapeutic modality for the treatment of multiple myeloma
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