High habitat richness limits the risk of tick-borne encephalitis in Europe: a multi-scale study

The natural transmission cycle of tick-borne encephalitis (TBE) virus is enhanced by complex interactions between ticks and key hosts strongly connected to habitat characteristics. The diversity of wildlife host species and their relative abundance is known to affect transmission of tick-borne diseases (such as, for example, Lyme disease). In the current context of global biodiversity loss, we explored the relationship between the habitat richness index (HRI) and the pattern of human TBE cases in Europe to assess the role of HRI in disease risk mitigation. Methods: We assessed human TBE case distribution across 879 European regions using official epidemiological data reported to the European Surveillance System (TESSy) between 2017 and 2021 from 15 countries. We statistically explored the relationship between TBE presence and a novel variable - the habitat richness index (HRI) - describing the diversity of European ecosystem types. We also validated our findings at local scale using data collected between 2017 and 2021 in 227 municipalities located in Trento and Belluno provinces, two known TBE foci in northern Italy. Findings: Our results showed a significant parabolic effect of HRI on the probability of presence of human TBE cases in the European regions included in our dataset, and a significant, negative effect of HRI on the local presence of TBE in northern Italy. At both spatial scales, TBE risk decreases in areas with higher values of HRI. Interpretation: To our knowledge, no efforts have yet been made to explore the relationship between habitat richness and TBE risk, both in local and in large scale geographical contexts, probably due to the scarcity of high-resolution, large-scale data about the abundance or density of critical host species, such as rodents and ungulates. To overcome this lack o f data, in this study we considered habitat richness as proxy of vertebrate host biodiversity to disentangle its role in driving TBE European occurrence at different spatial scales. The results suggest that biodiversity loss could considerably enhance disease risk for both humans and wildlife, which may influence biodiversity conservation policies within a One Health context approach

Erythropoietin (EPO) increases myelin gene expression in CG4 oligodendrocyte cells through the classical EPO receptor

Erythropoietin (EPO) has protective effects in neurodegenerative and neuroinflammatory diseases, including in animal models of multiple sclerosis, where EPO decreases disease severity. EPO also promotes neurogenesis and is protective in models of toxic demyelination. In this study, we asked whether EPO could promote neurorepair by also inducing remyelination. In addition, we investigated whether the effect of EPO could be mediated by the classical erythropoietic EPO receptor (EPOR), since it is still questioned if EPOR is functional in non-hematopoietic cells. Using CG4 cells, a line of rat oligodendrocyte precursor cells, we found that EPO increases the expression of myelin genes (myelin oligodendrocyte glycoprotein (MOG) and myelin basic protein (MBP)). EPO had no effect in wild-type CG4 cells, which do not express EPOR, whereas it increased MOG and MBP expression in cells engineered to overexpress EPOR (CG4-EPOR). This was reflected in a marked increase in MOG protein levels, as detected by western blot. In these cells, EPO induced by 10-fold the early growth response gene 2 (Egr2), which is required for peripheral myelination. However, Egr2 silencing with a siRNA did not reverse the effect of EPO, indicating that EPO acts through other pathways. In conclusion, EPO induces the expression of myelin genes in oligodendrocytes and this effect requires the presence of EPOR. This study demonstrates that EPOR can mediate neuroreparative effects

Immune or genetic-mediated disruption of CASPR2 causes pain hypersensitivity due to enhanced primary afferent excitability

Human autoantibodies to contactin-associated protein-like 2 (CASPR2) are often associated with neuropathic pain, and CASPR2 mutations have been linked to autism spectrum disorders, in which sensory dysfunction is increasingly recognized. Human CASPR2 autoantibodies, when injected into mice, were peripherally restricted and resulted in mechanical pain-related hypersensitivity in the absence of neural injury. We therefore investigated the mechanism by which CASPR2 modulates nociceptive function. Mice lacking CASPR2 (Cntnap2 ) demonstrated enhanced pain-related hypersensitivity to noxious mechanical stimuli, heat, and algogens. Both primary afferent excitability and subsequent nociceptive transmission within the dorsal horn were increased in Cntnap2 mice. Either immune or genetic-mediated ablation of CASPR2 enhanced the excitability of DRG neurons in a cell-autonomous fashion through regulation of Kv1 channel expression at the soma membrane. This is the first example of passive transfer of an autoimmune peripheral neuropathic pain disorder and demonstrates that CASPR2 has a key role in regulating cell-intrinsic dorsal root ganglion (DRG) neuron excitability

Probabilistic and preferential sampling approaches offer integrated perspectives of Italian forest diversity

Aim: Assessing the performances of different sampling approaches for documenting community diversity may help to identify optimal sampling efforts and strategies, and to enhance conservation and monitoring planning. Here, we used two data sets based on probabilistic and preferential sampling schemes of Italian forest vegetation to analyze the multifaceted performances of the two approaches across three major forest types at a large scale. Location: Italy. Methods: We pooled 804 probabilistic and 16,259 preferential forest plots as samples of vascular plant diversity across the country. We balanced the two data sets in terms of sizes, plot size, geographical position, and vegetation types. For each of the two data sets, 1000 subsets of 201 random plots were compared by calculating the shared and exclusive indicator species, their overlap in the multivariate space, and the areas encompassed by spatially-constrained rarefaction curves. We then calculated an index of performance using the ratio between the additional and total information collected by each sampling approach. The performances were tested and evaluated across the three major forest types. Results: The probabilistic approach performed better in estimating species richness and diversity of species assemblages, but did not detect other components of the regional diversity, such as azonal forests. The preferential approach outperformed the probabilistic approach in detecting forest-specialist species and plant diversity hotspots. Conclusions: Using a novel workflow based on vegetation-plot exclusivities and commonalities, our study suggests probabilistic and preferential sampling approaches are to be used in combination for better conservation and monitor planning purposes to detect multiple aspects of plant community diversity. Our findings can assist the implementation of national conservation planning and large-scale monitoring of biodiversity

Low oxygen tension primes aortic endothelial cells to the reparative effect of tissue-protective cytokines

Erythropoietin (EPO) has both erythropoietic and tissue-protective properties. The EPO analogues carbamylated EPO (CEPO) and pyroglutamate helix B surface peptide (pHBSP) lack the erythropoietic activity of EPO but retain the tissue-protective properties that are mediated by a heterocomplex of EPO receptor (EPOR) and the β common receptor (βCR). We studied the action of EPO and its analogues in a model of wound healing where a bovine aortic endothelial cells (BAECs) monolayer was scratched and the scratch closure was assessed over 24 h under different oxygen concentrations. We related the effects of EPO and its analogues on repair to their effect on BAECs proliferation and migration (evaluated using a micro-Boyden chamber). EPO, CEPO and pHBSP enhanced scratch closure only at lower oxygen (5%), while their effect at atmospheric oxygen (21%) was not significant. The mRNA expression of EPOR was doubled in 5% compared to 21% oxygen, and this was associated with increased EPOR assessed by immunofluorescence and Western blot. By contrast βCR mRNA levels were similar in 5% and 21% oxygen. EPO and its analogues increased both BAECs proliferation and migration, suggesting that both may be involved in the reparative process. The priming effect of low oxygen tension on the action of tissue-protective cytokines may be of relevance to vascular disease, including atherogenesis and restenosis

Diversity of European habitat types is correlated with geography more than climate and human pressure

Habitat richness, that is, the diversity of ecosystem types, is a complex, spatially explicit aspect of biodiversity, which is affected by bioclimatic, geographic, and anthropogenic variables. The distribution of habitat types is a key component for understanding broad-scale biodiversity and for developing conservation strategies. We used data on the distribution of European Union (EU) habitats to answer the following questions: (i) how do bioclimatic, geographic, and anthropogenic variables affect habitat richness? (ii) Which of those factors is the most important? (iii) How do interactions among these variables influence habitat richness and which combinations produce the strongest interactions? The distribution maps of 222 terrestrial habitat types as defined by the Natura 2000 network were used to calculate habitat richness for the 10 km × 10 km EU grid map. We then investigated how environmental variables affect habitat richness, using generalized linear models, generalized additive models, and boosted regression trees. The main factors associated with habitat richness were geographic variables, with negative relationships observed for both latitude and longitude, and a positive relationship for terrain ruggedness. Bioclimatic variables played a secondary role, with habitat richness increasing slightly with annual mean temperature and overall annual precipitation. We also found an interaction between anthropogenic variables, with the combination of increased landscape fragmentation and increased population density strongly decreasing habitat richness. This is the first attempt to disentangle spatial patterns of habitat richness at the continental scale, as a key tool for protecting biodiversity. The number of European habitats is related to geography more than climate and human pressure, reflecting a major component of biogeographical patterns similar to the drivers observed at the species level. The interaction between anthropogenic variables highlights the need for coordinated, continental-scale management plans for biodiversity conservation.Research contributing to this study was funded by the project “Development of a National Plan for Biodiversity Monitoring” (Italian National Institute for Environmental Protection and Research – ISPRA). BIOME Group was partially supported by the H2020 SHOWCASE (Grant agreement No 862480) and by the H2020 COST Action CA17134 ‘Optical synergies for spatiotemporal sensing of scalable ecophysiological traits (SENECO)’

TRY plant trait database - enhanced coverage and open access

Plant traits-the morphological, anatomical, physiological, biochemical and phenological characteristics of plants-determine how plants respond to environmental factors, affect other trophic levels, and influence ecosystem properties and their benefits and detriments to people. Plant trait data thus represent the basis for a vast area of research spanning from evolutionary biology, community and functional ecology, to biodiversity conservation, ecosystem and landscape management, restoration, biogeography and earth system modelling. Since its foundation in 2007, the TRY database of plant traits has grown continuously. It now provides unprecedented data coverage under an open access data policy and is the main plant trait database used by the research community worldwide. Increasingly, the TRY database also supports new frontiers of trait-based plant research, including the identification of data gaps and the subsequent mobilization or measurement of new data. To support this development, in this article we evaluate the extent of the trait data compiled in TRY and analyse emerging patterns of data coverage and representativeness. Best species coverage is achieved for categorical traits-almost complete coverage for 'plant growth form'. However, most traits relevant for ecology and vegetation modelling are characterized by continuous intraspecific variation and trait-environmental relationships. These traits have to be measured on individual plants in their respective environment. Despite unprecedented data coverage, we observe a humbling lack of completeness and representativeness of these continuous traits in many aspects. We, therefore, conclude that reducing data gaps and biases in the TRY database remains a key challenge and requires a coordinated approach to data mobilization and trait measurements. This can only be achieved in collaboration with other initiatives

Immune or Genetic-Mediated Disruption of CASPR2 Causes Pain Hypersensitivity Due to Enhanced Primary Afferent Excitability

Human autoantibodies to contactin-associated protein-like 2 (CASPR2) are often associated with neuropathic pain, and CASPR2 mutations have been linked to autism spectrum disorders, in which sensory dysfunction is increasingly recognized. Human CASPR2 autoantibodies, when injected into mice, were peripherally restricted and resulted in mechanical pain-related hypersensitivity in the absence of neural injury. We therefore investigated the mechanism by which CASPR2 modulates nociceptive function. Mice lacking CASPR2 (Cntnap2-/-) demonstrated enhanced pain-related hypersensitivity to noxious mechanical stimuli, heat, and algogens. Both primary afferent excitability and subsequent nociceptive transmission within the dorsal horn were increased in Cntnap2-/-mice. Either immune or genetic-mediated ablation of CASPR2 enhanced the excitability of DRG neurons in a cell-autonomous fashion through regulation of Kv1 channel expression at the soma membrane. This is the first example of passive transfer of an autoimmune peripheral neuropathic pain disorder and demonstrates that CASPR2 has a key role in regulating cell-intrinsic dorsal root ganglion (DRG) neuron excitability