Is ecology different when studied with citizen scientists? A bibliometric analysis.

Ecology is broad and relies on several complementary approaches to study the mechanisms driving the distribution and abundance of organisms and their interactions. One of them is citizen science (CitSci), the co-production of scientific data and knowledge by nonprofessional scientists, in collaboration with, or under the direction of, professional scientists. CitSci has bloomed in the scientific literature over the last decade and its popularity continues to increase, but its qualitative contribution to the development of academic knowledge remains understudied. We used a bibliometric analysis to study whether the epistemic content of CitSci-based articles is different from traditional, non-CitSci ones within the field of ecology. We analyzed keywords and abstracts of articles published in ecology over the last decade, disentangling CitSci articles (those explicitly referring to citizen science) and non-CitSci articles. Keyword co-occurrence and thematic map analyses first revealed that CitSci and non-CitSci articles broadly focused on biodiversity, conservation, and climate change. However, CitSci articles did so in a more descriptive way than non-CitSci articles, which were more likely to address mechanisms. Conservation biology and its links with socio-ecosystems and ecosystem services was a central theme in the CitSci corpus, much less in the non-CitSci corpus. The situation was opposite for climate change and its consequences on species distribution and adaptation, which was a central theme in the non-CitSci corpus only. We only revealed subtle differences in the relative importance of particular themes and in the way these themes are tackled in CitSci and non-CitSci articles, thus indicating that citizen science is well integrated in the main, classical research themes of ecology.

Measuring epistemic success of a biodiversity citizen science program: A citation study.

This paper offers a comparative evaluation of the scientific impact of a citizen science program in ecology, ''Vigie-Nature", managed by the French National Museum of Natural History. Vigie-Nature consists of a national network of amateur observatories dedicated to a participative study of biodiversity in France that has been running for the last twenty years. We collected 123 articles published by Vigie-Nature in international peer-reviewed journals between 2007 and 2019, and computed the yearly amount of citations of these articles between 0-12 years post-publication. We then compared this body of citations with the number of yearly citations relative to the ensemble of the articles published in ecology and indexed in the ''Web of Science" data-base. Using a longitudinal data analysis, we could observe that the yearly number of citations of the Vigie-Nature articles is significantly higher than that of the other publications in the same domain. Furthermore, this excess of citations tends to steadily grow over time: Vigie-Nature publications are about 1.5 times more cited 3 years after publication, and 3 times more cited 11 years post-publication. These results suggest that large-scale biodiversity citizen science projects are susceptible to reach a high epistemic impact, when managed in specific ways which need to be clarified through further investigations.

SMT and TOFT Integrable After All: A Reply to Bizzarri and Cucina.

In a previous paper recently published in this journal, we argue that the two main theories of carcinogenesis (SMT and TOFT) should be considered as compatible, at the metaphysical, epistemological and biological levels. In a reply to our contribution, Bizzarri and Cucina claim we are wrong since SMT and TOFT are opposite and incompatible paradigms. Here, we show that their arguments are not satisfactory. Indeed, the authors go through the same mistakes that we already addressed. In particular, they confuse reductionism, as an ontological frame, and genetic determinism, as a causal pathway. Beside, they make an inadequate use of the Kuhnian notion of paradigm shift. Finally, we confirm our previous conclusion: there is no strong argument to totally abandon the somatic mutation theory. It describes a partial causal pathway, compatible with the one proposed by TOFT.

SMT or TOFT? How the two main theories of carcinogenesis are made (artificially) incompatible.

The building of a global model of carcinogenesis is one of modern biology's greatest challenges. The traditional somatic mutation theory (SMT) is now supplemented by a new approach, called the Tissue Organization Field Theory (TOFT). According to TOFT, the original source of cancer is loss of tissue organization rather than genetic mutations. In this paper, we study the argumentative strategy used by the advocates of TOFT to impose their view. In particular, we criticize their claim of incompatibility used to justify the necessity to definitively reject SMT. First, we note that since it is difficult to build a non-ambiguous experimental demonstration of the superiority of TOFT, its partisans add epistemological and metaphysical arguments to the debate. This argumentative strategy allows them to defend the necessity of a paradigm shift, with TOFT superseding SMT. To do so, they introduce a notion of incompatibility, which they actually use as the Kuhnian notion of incommensurability. To justify this so-called incompatibility between the two theories of cancer, they move the debate to a metaphysical ground by assimilating the controversy to a fundamental opposition between reductionism and organicism. We show here that this argumentative strategy is specious, because it does not demonstrate clearly that TOFT is an organicist theory. Since it shares with SMT its vocabulary, its ontology and its methodology, it appears that a claim of incompatibility based on this metaphysical plan is not fully justified in the present state of the debate. We conclude that it is more cogent to argue that the two theories are compatible, both biologically and metaphysically. We propose to consider that TOFT and SMT describe two distinct and compatible causal pathways to carcinogenesis. This view is coherent with the existence of integrative approaches, and suggests that they have a higher epistemic value than the two theories taken separately.

Role of compartmentalization on HiF-1α degradation dynamics during changing oxygen conditions: a computational approach.

HiF-1α is the central protein driving the cellular response to hypoxia. Its accumulation in cancer cells is linked to the appearance of chemoresistant and aggressive tumor phenotypes. As a consequence, understanding the regulation of HiF-1α dynamics is a major issue to design new anti-cancer therapies. In this paper, we propose a model of the hypoxia pathway, involving HiF-1α and its inhibitor pVHL. Based on data from the literature, we made the hypothesis that the regulation of HiF-1α involves two compartments (nucleus and cytoplasm) and a constitutive shuttle of the pVHL protein between them. We first show that this model captures correctly the main features of HiF-1α dynamics, including the bi-exponential degradation profile in normoxia, the kinetics of induction in hypoxia, and the switch-like accumulation. Second, we simulated the effects of a hypoxia/reoxygenation event, and show that it generates a strong instability of HiF-1α. The protein concentration rapidly increases 3 hours after the reoxygenation, and exhibits an oscillating pattern. This effect vanishes if we do not consider compartmentalization of HiF-1α. This result can explain various counter-intuitive observations about the specific molecular and cellular response to the reoxygenation process. Third, we simulated the HiF-1α dynamics in the tumor case. We considered different types of mutations associated with tumorigenesis, and we compared their consequences on HiF-1α dynamics. Then, we tested different therapeutics strategies. We show that a therapeutic decrease of HiF-1α nuclear level is not always correlated with an attenuation of reoxygenation-induced instabilities. Thus, it appears that the design of anti-HiF-1α therapies have to take into account these two aspects to maximize their efficiency.