Growing Open Science with the Combined Potential of Citizen Science and Auto Science

In this paper, we present our ideas on how to best support researchers in every phase of the research process when dealing with their research data. We propose a Research Data Portal as the central data infrastructure. With the help of this portal, a researcher can easily manage and update his or her research data, share it with collaborators, and reach out to the public. We further propose a Citizen Science Portal, which includes some new and innovative concepts and methods. In this portal, Citizen Science and Auto Science concepts are applied, and support to bring together the best of both worlds is provided. Citizen Science promises to entail the individual (scientists and hobby scientists) to help with research. Auto Science is meant to help analyze research data, e.g., to help publish the data and to help improve its quality, by applying methods from artificial intelligence

ExoClock project: an open platform for monitoring the ephemerides of Ariel targets with contributions from the public

The Ariel mission will observe spectroscopically around 1000 exoplanets to further characterise their atmospheres. For the mission to be as efficient as possible, a good knowledge of the planets’ ephemerides is needed before its launch in 2028. While ephemerides for some planets are being refined on a per-case basis, an organised effort to collectively verify or update them when necessary does not exist. In this study, we introduce the ExoClock project, an open, integrated and interactive platform with the purpose of producing a confirmed list of ephemerides for the planets that will be observed by Ariel. The project has been developed in a manner to make the best use of all available resources: observations reported in the literature, observations from space instruments and, mainly, observations from ground-based telescopes, including both professional and amateur observatories. To facilitate inexperienced observers and at the same time achieve homogeneity in the results, we created data collection and validation protocols, educational material and easy to use interfaces, open to everyone. ExoClock was launched in September 2019 and now counts over 140 participants from more than 15 countries around the world. In this release, we report the results of observations obtained until the 15h of April 2020 for 120 Ariel candidate targets. In total, 632 observations were used to either verify or update the ephemerides of 84 planets. Additionally, we developed the Exoplanet Characterisation Catalogue (ECC), a catalogue built in a consistent way to assist the ephemeris refinement process. So far, the collaborative open framework of the ExoClock project has proven to be highly efficient in coordinating scientific efforts involving diverse audiences. Therefore, we believe that it is a paradigm that can be applied in the future for other research purposes, too

The balance between the intronic miR-342 and its host gene Evl determines hematopoietic cell fate decision

Protein-coding and non-coding genes like miRNAs tightly control hematopoietic differentiation programs. Although miRNAs are frequently located within introns of protein-coding genes, the molecular interplay between intronic miRNAs and their host genes is unclear. By genomic integration site mapping of gamma-retroviral vectors in genetically corrected peripheral blood from gene therapy patients, we identified the EVL/MIR342 gene locus as a hotspot for therapeutic vector insertions indicating its accessibility and expression in human hematopoietic stem and progenitor cells. We therefore asked if and how EVL and its intronic miRNA-342 regulate hematopoiesis. Here we demonstrate that overexpression (OE) of Evl in murine primary Lin- Sca1+ cKit+ cells drives lymphopoiesis whereas miR-342 OE increases myeloid colony formation in vitro and in vivo, going along with a profound upregulation of canonical pathways essential for B-cell development or myelopoietic functions upon Evl or miR-342 OE, respectively. Strikingly, miR-342 counteracts its host gene by targeting lymphoid signaling pathways, resulting in reduced pre-B-cell output. Moreover, EVL overexpression is associated with lymphoid leukemia in patients. In summary, our data show that one common gene locus regulates distinct hematopoietic differentiation programs depending on the gene product expressed, and that the balance between both may determine hematopoietic cell fate decision

The balance between the intronic miR-342 and its host gene Evl determines hematopoietic cell fate decision

Protein-coding and non-coding genes like miRNAs tightly control hematopoietic differentiation programs. Although miRNAs are frequently located within introns of protein-coding genes, the molecular interplay between intronic miRNAs and their host genes is unclear. By genomic integration site mapping of gamma-retroviral vectors in genetically corrected peripheral blood from gene therapy patients, we identified the EVL/MIR342 gene locus as a hotspot for therapeutic vector insertions indicating its accessibility and expression in human hematopoietic stem and progenitor cells. We therefore asked if and how EVL and its intronic miRNA-342 regulate hematopoiesis. Here we demonstrate that overexpression (OE) of Evl in murine primary Li