Social innovation for biodiversity: a literature review and research challenges

There are calls for social innovation to help with the effort to halt biodiversity loss. However, research on social innovation and biodiversity is dispersed and covers a multitude of disciplines. A systematic overview of research on social innovation and biodiversity is missing and this paper contributes by focusing on social innovation to tackle the drivers of biodiversity loss and unsustainability. The paper reviews research on social innovation in changing land use (agriculture, forestry, aquatic ecosystems and cities), in tackling exploitation of organisms (fishing, hunting, harvesting), and in addressing threats of climate change, pollution and invasive species. Across these drivers, we find a) a strong emphasis on social innovation as civic action for changing practices in addressing unsustainability, b) that social innovation research tends to focus on local experimentation although there are bodies of literature on policy-driven innovations and consumer/producer-driven innovations, and c) that there is very little research taking a critical perspective to explore negative or unintended consequences of social innovation. Drawing on the review, we propose three cross cutting issues that can be a focus for future research, practice and supportive policy: social innovation for nature-based solutions, social innovation for participatory governance, and social innovation for technology that tackles biodiversity loss

Calbindin-D32k Is Localized to a Subpopulation of Neurons in the Nervous System of the Sea Cucumber Holothuria glaberrima (Echinodermata)

Members of the calbindin subfamily serve as markers of subpopulations of neurons within the vertebrate nervous system. Although markers of these proteins are widely available and used, their application to invertebrate nervous systems has been very limited. In this study we investigated the presence and distribution of members of the calbindin subfamily in the sea cucumber Holothuria glaberrima (Selenka, 1867). Immunohistological experiments with antibodies made against rat calbindin 1, parvalbumin, and calbindin 2, showed that these antibodies labeled cells and fibers within the nervous system of H. glaberrima. Most of the cells and fibers were co-labeled with the neural-specific marker RN1, showing their neural specificity. These were distributed throughout all of the nervous structures, including the connective tissue plexi of the body wall and podia. Bioinformatics analyses of the possible antigen recognized by these markers showed that a calbindin 2-like protein present in the sea urchin Strongylocentrotus purpuratus, corresponded to the calbindin-D32k previously identified in other invertebrates. Western blots with anti-calbindin 1 and anti-parvalbumin showed that these markers recognized an antigen of approximately 32 kDa in homogenates of radial nerve cords of H. glaberrima and Lytechinus variegatus. Furthermore, immunoreactivity with anti-calbindin 1 and anti-parvalbumin was obtained to a fragment of calbindin-D32k of H. glaberrima. Our findings suggest that calbindin-D32k is present in invertebrates and its sequence is more similar to the vertebrate calbindin 2 than to calbindin 1. Thus, characterization of calbindin-D32k in echinoderms provides an important view of the evolution of this protein family and represents a valuable marker to study the nervous system of invertebrates

Untangling the Debate: The Ethics of Human Enhancement

Human enhancement, in which nanotechnology is expected to play a major role, continues to be a highly contentious ethical debate, with experts on both sides calling it the single most important issue facing science and society in this brave, new century. This paper is a broad introduction to the symposium herein that explores a range of perspectives related to that debate. We will discuss what human enhancement is and its apparent contrast to therapy; and we will begin to tease apart the myriad intertwined issues that arise in the debate: (1) freedom & autonomy, (2) health & safety, (3) fairness & equity, (4) societal disruption, and (5) human dignity

Thresholds and Tortoises: Modernist Animality in Pirandello's Fiction

The present study provides a posthumanist reading of Pirandello’s fiction, with the aim of highlighting the author’s specifically modernist take on animality. The first half of the chapter illustrates Pirandello’s awareness of a zoological continuum encompassing human and nonhuman beings; particular emphasis is placed on his innovative dialogue with the nineteenth-century tradition (Balzac), as well as on the typically modernist aspects of his posthumanist gaze – e.g. the sense of a “cosmic” detachment from human events, and the strategic use of thresholds (openings and epilogues) to undermine the anthropocentrism inherent to traditional narrative forms. The second half focuses on a specific case study, i.e. the role assigned to the tortoise in the short stories “Paura d’esser felice” and “La tartaruga”. In both texts, the protagonist’s “becoming-tortoise” (Deleuze and Guattari) is instrumental to Pirandello’s modernist critique of anthropocentrism

Induction of Epithelial Mesenchimal Transition and Vasculogenesis in the Lenses of Dbl Oncogene Transgenic Mice

BACKGROUND: The Dbl family of proteins represents a large group of proto-oncogenes involved in cell growth regulation. The numerous domains that are present in many Dbl family proteins suggest that they act to integrate multiple inputs in complicated signaling networks involving the Rho GTPases. Alterations of the normal function of these proteins lead to pathological processes such as developmental disorders and neoplastic transformation. We generated transgenic mice introducing the cDNA of Dbl oncogene linked to the metallothionein promoter into the germ line of FVB mice and found that onco-Dbl expression in mouse lenses affected proliferation, migration and differentiation of lens epithelial cells. RESULTS: We used high density oligonucleotide microarray to define the transcriptional profile induced by Dbl in the lenses of 2 days, 2 weeks, and 6 weeks old transgenic mice. We observed modulation of genes encoding proteins promoting epithelial-mesenchymal transition (EMT), such as down-regulation of epithelial cell markers and up-regulation of fibroblast markers. Genes encoding proteins involved in the positive regulation of apoptosis were markedly down regulated while anti-apoptotic genes were strongly up-regulated. Finally, several genes encoding proteins involved in the process of angiogenesis were up-regulated. These observations were validated by histological and immunohistochemical examination of the transgenic lenses where vascularization can be readily observed. CONCLUSION: Onco-Dbl expression in mouse lens correlated with modulation of genes involved in the regulation of EMT, apoptosis and vasculogenesis leading to disruption of the lens architecture, epithelial cell proliferation, and aberrant angiogenesis. We conclude that onco-Dbl has a potentially important, previously unreported, capacity to dramatically alter epithelial cell migration, replication, polarization and differentiation and to induce vascularization of an epithelial tissue

KRIT1 Regulates the Homeostasis of Intracellular Reactive Oxygen Species

KRIT1 is a gene responsible for Cerebral Cavernous Malformations (CCM), a major cerebrovascular disease characterized by abnormally enlarged and leaky capillaries that predispose to seizures, focal neurological deficits, and fatal intracerebral hemorrhage. Comprehensive analysis of the KRIT1 gene in CCM patients has suggested that KRIT1 functions need to be severely impaired for pathogenesis. However, the molecular and cellular functions of KRIT1 as well as CCM pathogenesis mechanisms are still research challenges. We found that KRIT1 plays an important role in molecular mechanisms involved in the maintenance of the intracellular Reactive Oxygen Species (ROS) homeostasis to prevent oxidative cellular damage. In particular, we demonstrate that KRIT1 loss/down-regulation is associated with a significant increase in intracellular ROS levels. Conversely, ROS levels in KRIT1−/− cells are significantly and dose-dependently reduced after restoration of KRIT1 expression. Moreover, we show that the modulation of intracellular ROS levels by KRIT1 loss/restoration is strictly correlated with the modulation of the expression of the antioxidant protein SOD2 as well as of the transcriptional factor FoxO1, a master regulator of cell responses to oxidative stress and a modulator of SOD2 levels. Furthermore, we show that the KRIT1-dependent maintenance of low ROS levels facilitates the downregulation of cyclin D1 expression required for cell transition from proliferative growth to quiescence. Finally, we demonstrate that the enhanced ROS levels in KRIT1−/− cells are associated with an increased cell susceptibility to oxidative DNA damage and a marked induction of the DNA damage sensor and repair gene Gadd45α, as well as with a decline of mitochondrial energy metabolism. Taken together, our results point to a new model where KRIT1 limits the accumulation of intracellular oxidants and prevents oxidative stress-mediated cellular dysfunction and DNA damage by enhancing the cell capacity to scavenge intracellular ROS through an antioxidant pathway involving FoxO1 and SOD2, thus providing novel and useful insights into the understanding of KRIT1 molecular and cellular functions