Open weather and climate science in the digital era

The need for open science has been recognized by the communities of meteorology and climate science. While these domains are mature in terms of applying digital technologies, the implementation of open science methodologies is less advanced. In a session on “Weather and Climate Science in the Digital Era” at the 14th IEEE International eScience Conference domain specialists and data and computer scientists discussed the road towards open weather and climate science. Roughly 80 % of the studies presented in the conference session showed the added value of open data and software. These studies included open datasets from disparate sources in their analyses or developed tools and approaches that were made openly available to the research community. Furthermore, shared software is a prerequisite for the studies which presented systems like a model coupling framework or digital collaboration platform. Although these studies showed that sharing code and data is important, the consensus among the participants was that this is not sufficient to achieve open weather and climate science and that there are important issues to address. At the level of technology, the application of the findable, accessible, interoperable, and reusable (FAIR) principles to many datasets used in weathe

Microarray analysis identifies a set of CXCR3 and CCR2 ligand chemokines as early IFNβ-responsive genes in peripheral blood lymphocytes in vitro: an implication for IFNβ-related adverse effects in multiple sclerosis

BACKGROUND: A substantial proportion of multiple sclerosis (MS) patients discontinue interferon-beta (IFNβ) treatment due to various adverse effects, most of which emerge at the early phase after initiation of the treatment and then diminish with time. At present, the molecular mechanism underlying IFNβ-related adverse effects remains largely unknown. The aim of this study is to identify a comprehensive list of early IFNβ-responsive genes (IRGs) in peripheral blood mononuclear cells (PBMC) that may play a key role in induction of adverse effects. METHODS: Total RNA of PBMC exposed to 50 ng/ml recombinant human IFNβ for 3 to 24 hours in vitro was processed for cDNA microarray analysis, followed by quantitative real-time RT-PCR analysis. RESULTS: Among 1,258 genes on the array, IFNβ elevated the expression of 107 and 87 genes, while it reduced the expression of 22 and 23 genes at 3 and 24 hours, respectively. Upregulated IRGs were categorized into conventional IFN-response markers, components of IFN-signaling pathways, chemokines, cytokines, growth factors, and their receptors, regulators of apoptosis, DNA damage, and cell cycle, heat shock proteins, and costimulatory and adhesion molecules. IFNβ markedly upregulated CXCR3 ligand chemokines (SCYB11, SCYB10 and SCYB9) chiefly active on effector T helper type 1 (Th1) T cells, and CCR2 ligand chemokines (SCYA8 and SCYA2) effective on monocytes, whereas it downregulated CXCR2 ligand chemokines (SCYB2, SCYB1 and IL8) primarily active on neutrophils. CONCLUSION: IFNβ immediately induces a burst of gene expression of proinflammatory chemokines in vitro that have potential relevance to IFNβ-related early adverse effects in MS patients in vivo