资源环境科技发展态势分析平台

There are concerns that recent climate change is altering the frequency and magnitude of river floods in an unprecedented way(1). Historical studies have identified flood-rich periods in the past half millennium in various regions of Europe(2). However, because of the low temporal resolution of existing datasets and the relatively low number of series, it has remained unclear whether Europe is currently in a flood-rich period from a long-term perspective. Here we analyse how recent decades compare with the flood history of Europe, using a new database composed of more than 100 high-resolution (sub-annual) historical flood series based on documentary evidence covering all major regions of Europe. We show that the past three decades were among the most flood-rich periods in Europe in the past 500 years, and that this period differs from other flood-rich periods in terms of its extent, air temperatures and flood seasonality. We identified nine flood-rich periods and associated regions. Among the periods richest in floods are 1560-1580 (western and central Europe), 1760-1800 (most of Europe), 1840-1870 (western and southern Europe) and 1990-2016 (western and central Europe). In most parts of Europe, previous flood-rich periods occurred during cooler-than-usual phases, but the current flood-rich period has been much warmer. Flood seasonality is also more pronounced in the recent period. For example, during previous flood and interflood periods, 41 per cent and 42 per cent of central European floods occurred in summer, respectively, compared with 55 per cent of floods in the recent period. The exceptional nature of the present-day flood-rich period calls for process-based tools for flood-risk assessment that capture the physical mechanisms involved, and management strategies that can incorporate the recent changes in risk.

Analysis of thousands of historical documents recording floods in Europe shows that flooding characteristics in recent decades are unlike those of previous centuries.

Fine-scale satellite data are used to quantify forest harvest rates in 26 European countries, finding an increase in harvested forest area of 49% and an increase in biomass loss of 69% between 2011-2015 and 2016-2018.

Genetic variations underlying susceptibility to complex autoimmune and allergic diseases are concentrated within noncoding regulatory elements termed enhancers(1). The functions of a large majority of disease-associated enhancers are unknown, in part owing to their distance from the genes they regulate, a lack of understanding of the cell types in which they operate, and our inability to recapitulate the biology of immune diseases in vitro. Here, using shared synteny to guide loss-of-function analysis of homologues of human enhancers in mice, we show that the prominent autoimmune and allergic disease risk locus at chromosome 11q13.5(2-7) contains a distal enhancer that is functional in CD4(+) regulatory T (T-reg) cells and required for T-reg-mediated suppression of colitis. The enhancer recruits the transcription factors STAT5 and NF-kappa B to mediate signal-driven expression of Lrrc32, which encodes the protein glycoprotein A repetitions predominant (GARP). Whereas disruption of the Lrrc32 gene results in early lethality, mice lacking the enhancer are viable but lack GARP expression in Foxp3(+) T-reg cells, which are unable to control colitis in a cell-transfer model of the disease. In human T-reg cells, the enhancer forms conformational interactions with the promoter of LRRC32 and enhancer risk variants are associated with reduced histone acetylation and GARP expression. Finally, functional fine-mapping of 11q13.5 using CRISPR-activation (CRISPRa) identifies a CRISPRa-responsive element in the vicinity of risk variant rs11236797 capable of driving GARP expression. These findings provide a mechanistic basis for association of the 11q13.5 risk locus with immune-mediated diseases and identify GARP as a potential target in their therapy.

Shared synteny guides loss-of-function analysis of human enhancer homologues in mice, identifying a distal enhancer at the autoimmune and allergic disease risk locus at chromosome 11q13.5 whose function in regulatory T cells provides a mechanistic basis for its role in disease.

Using lipid residues absorbed in potsherds, the ages of pottery from various archaeological sites are determined and validated using sites for which the dates are well known from other methods.