Biodiversity data supports research on human infectious diseases: Global trends, challenges, and opportunities.

The unprecedented generation of large volumes of biodiversity data is consistently contributing to a wide range of disciplines, including disease ecology. Emerging infectious diseases are usually zoonoses caused by multi-host pathogens. Therefore, their understanding may require the access to biodiversity data related to the ecology and the occurrence of the species involved. Nevertheless, despite several data-mobilization initiatives, the usage of biodiversity data for research into disease dynamics has not yet been fully leveraged. To explore current contribution, trends, and to identify limitations, we characterized biodiversity data usage in scientific publications related to human health, contrasting patterns of studies citing the Global Biodiversity Information Facility (GBIF) with those obtaining data from other sources. We found that the studies mainly obtained data from scientific literature and other not aggregated or standardized sources. Most of the studies explored pathogen species and, particularly those with GBIF-mediated data, tended to explore and reuse data of multiple species (>2). Data sources varied according to the taxa and epidemiological roles of the species involved. Biodiversity data repositories were mainly used for species related to hosts, reservoirs, and vectors, and barely used as a source of pathogens data, which was usually obtained from human and animal-health related institutions. While both GBIF- and not GBIF-mediated data studies explored similar diseases and topics, they presented discipline biases and different analytical approaches. Research on emerging infectious diseases may require the access to geographical and ecological data of multiple species. The One Health challenge requires interdisciplinary collaboration and data sharing, which is facilitated by aggregated repositories and platforms. The contribution of biodiversity data to understand infectious disease dynamics should be acknowledged, strengthened, and promoted.

Data integration enables global biodiversity synthesis.

The accessibility of global biodiversity information has surged in the past two decades, notably through widespread funding initiatives for museum specimen digitization and emergence of large-scale public participation in community science. Effective use of these data requires the integration of disconnected datasets, but the scientific impacts of consolidated biodiversity data networks have not yet been quantified. To determine whether data integration enables novel research, we carried out a quantitative text analysis and bibliographic synthesis of >4,000 studies published from 2003 to 2019 that use data mediated by the world's largest biodiversity data network, the Global Biodiversity Information Facility (GBIF). Data available through GBIF increased 12-fold since 2007, a trend matched by global data use with roughly two publications using GBIF-mediated data per day in 2019. Data-use patterns were diverse by authorship, geographic extent, taxonomic group, and dataset type. Despite facilitating global authorship, legacies of colonial science remain. Studies involving species distribution modeling were most prevalent (31% of literature surveyed) but recently shifted in focus from theory to application. Topic prevalence was stable across the 17-y period for some research areas (e.g., macroecology), yet other topics proportionately declined (e.g., taxonomy) or increased (e.g., species interactions, disease). Although centered on biological subfields, GBIF-enabled research extends surprisingly across all major scientific disciplines. Biodiversity data mobilization through global data aggregation has enabled basic and applied research use at temporal, spatial, and taxonomic scales otherwise not possible, launching biodiversity sciences into a new era.

Connecting data and expertise: a new alliance for biodiversity knowledge.

There has been major progress over the last two decades in digitising historical knowledge of biodiversity and in making biodiversity data freely and openly accessible. Interlocking efforts bring together international partnerships and networks, national, regional and institutional projects and investments and countless individual contributors, spanning diverse biological and environmental research domains, government agencies and non-governmental organisations, citizen science and commercial enterprise. However, current efforts remain inefficient and inadequate to address the global need for accurate data on the world's species and on changing patterns and trends in biodiversity. Significant challenges include imbalances in regional engagement in biodiversity informatics activity, uneven progress in data mobilisation and sharing, the lack of stable persistent identifiers for data records, redundant and incompatible processes for cleaning and interpreting data and the absence of functional mechanisms for knowledgeable experts to curate and improve data. Recognising the need for greater alignment between efforts at all scales, the Global Biodiversity Information Facility (GBIF) convened the second Global Biodiversity Informatics Conference (GBIC2) in July 2018 to propose a coordination mechanism for developing shared roadmaps for biodiversity informatics. GBIC2 attendees reached consensus on the need for a global alliance for biodiversity knowledge, learning from examples such as the Global Alliance for Genomics and Health (GA4GH) and the open software communities under the Apache Software Foundation. These initiatives provide models for multiple stakeholders with decentralised funding and independent governance to combine resources and develop sustainable solutions that address common needs. This paper summarises the GBIC2 discussions and presents a set of 23 complementary ambitions to be addressed by the global community in the context of the proposed alliance. The authors call on all who are responsible for describing and monitoring natural systems, all who depend on biodiversity data for research, policy or sustainable environmental management and all who are involved in developing biodiversity informatics solutions to register interest at https://biodiversityinformatics.org/ and to participate in the next steps to establishing a collaborative alliance. The supplementary materials include brochures in a number of languages (English, Arabic, Spanish, Basque, French, Japanese, Dutch, Portuguese, Russian, Traditional Chinese and Simplified Chinese). These summarise the need for an alliance for biodiversity knowledge and call for collaboration in its establishment.

Lysine deacetylase inhibition prevents diabetes by chromatin-independent immunoregulation and ß-cell protection.

Type 1 diabetes is due to destruction of pancreatic ß-cells. Lysine deacetylase inhibitors (KDACi) protect ß-cells from inflammatory destruction in vitro and are promising immunomodulators. Here we demonstrate that the clinically well-tolerated KDACi vorinostat and givinostat revert diabetes in the nonobese diabetic (NOD) mouse model of type 1 diabetes and counteract inflammatory target cell damage by a mechanism of action consistent with transcription factor--rather than global chromatin--hyperacetylation. Weaning NOD mice received low doses of vorinostat and givinostat in their drinking water until 100-120 d of age. Diabetes incidence was reduced by 38% and 45%, respectively, there was a 15% increase in the percentage of islets without infiltration, and pancreatic insulin content increased by 200%. Vorinostat treatment increased the frequency of functional regulatory T-cell subsets and their transcription factors Gata3 and FoxP3 in parallel to a decrease in inflammatory dendritic cell subsets and their cytokines IL-6, IL-12, and TNF-α. KDACi also inhibited LPS-induced Cox-2 expression in peritoneal macrophages from C57BL/6 and NOD mice. In insulin-producing ß-cells, givinostat did not upregulate expression of the anti-inflammatory genes Socs1-3 or sirtuin-1 but reduced levels of IL-1ß + IFN-γ-induced proinflammatory Il1a, Il1b, Tnfα, Fas, Cxcl2, and reduced cytokine-induced ERK phosphorylation. Further, NF-κB genomic iNos promoter binding was reduced by 50%, and NF-κB-dependent mRNA expression was blocked. These effects were associated with NF-κB subunit p65 hyperacetylation. Taken together, these data provide a rationale for clinical trials of safety and efficacy of KDACi in patients with autoimmune disease such as type 1 diabetes.