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In an era marked by rapid global changes, the reinforcement and modernization of plant health surveillance systems have become imperative. Sixty-five scientists present here a research agenda for an enhanced and modernized plant health surveillance to anticipate and mitigate disease and pest emergence. Our approach integrates a wide range of scientific fields (from life, social, physical and engineering sciences) and identifies the key knowledge gaps, focusing on anticipation, risk assessment, early detection, and multi-actor collaboration. The research directions we propose are organized around four complementary thematic axes. The first axis is the anticipation of pest emergence, encompassing innovative forecasting, adaptive potential, and the effects of climatic and cropping system changes. The second axis addresses the use of versatile broad-spectrum surveillance tools, including molecular or imaging diagnostics supported by artificial intelligence, and monitoring generic matrices such as air and water. The third axis focuses on surveillance of known pests from new perspectives, i.e., using novel approaches to detect known species but also anticipating and detecting, within a species, the populations or genotypes that pose a higher risk. The fourth axis advocates the management of plant health as a commons through the establishment of multi-actor and cooperative surveillance systems for long-term data-driven alert systems and information dissemination. We stress the importance of integrating data and information from multiple sources through open science databases and metadata, alongside developing methods for interpolating and extrapolating incomplete data. Finally, we advocate an Integrated Health Surveillance approach in the One Health context, favoring tailored and versatile solutions to plant health problems and recognizing the interconnected risks to the health of plants, humans, animals and the environment, including food insecurity, pesticide residues, e

Item does not contain fulltext, PURPOSE: Hereditary spastic paraplegia type 4 is extremely variable in age at onset; the same variant can cause onset at birth or in the eighth decade. We recently discovered that missense variants in SPAST, which influences microtubule dynamics, are associated with earlier onset and more severe disease than truncating variants, but even within the early and late-onset groups there remained significant differences in onset. Given the rarity of the condition, we adapted an extreme phenotype approach to identify genetic modifiers of onset. METHODS: We performed a genome-wide association study on 134 patients bearing truncating pathogenic variants in SPAST, divided into early- and late-onset groups (aged ≤15 and ≥45 years, respectively). A replication cohort of 419 included patients carrying either truncating or missense variants. Finally, age at onset was analyzed in the merged cohort (N = 553). RESULTS: We found 1 signal associated with earlier age at onset (rs10775533, P = 8.73E-6) in 2 independent cohorts and in the merged cohort (N = 553, Mantel-Cox test, P < .0001). Western blotting in lymphocytes of 20 patients showed that this locus tends to upregulate SARS2 expression in earlier-onset patients. CONCLUSION: SARS2 overexpression lowers the age of onset in hereditary spastic paraplegia type 4. Lowering SARS2 or improving mitochondrial function could thus present viable approaches to therapy.

The archetypical heavy-fermion superconductor CeCu2Si2 is known to present two distinct superconducting phases under pressure. In the low-pressure region, the superconductivity is mediated by spin fluctuations while the superconducting phase observed in the high-pressure region could be associated with a first-order valence transition (FOVT). However, the critical end point (CEP) of the FOVT was shown to be located at negative temperature and only a continuous valence change (crossover regime) was so far observed at 14 K, i.e., far above the optimal superconducting temperature (Tc = 2.3 K). Here we present x-ray absorption measurements under pressure and applied magnetic field at the Ce L3 edge at 2.7 K, i.e., close to the optimal Tc. It was expected that the applied magnetic field could shift the CEP to positive temperature with the possibility to observe a FOVT. Our data indicate the valence of Ce increases continuously (crossover regime) from 3.11 at ambient pressure up to 3.20 at 8.5 GPa likewise for any applied magnetic field up to 6 T.

We report muon spin rotation (mu SR) and neutron diffraction on the rare-earth-based magnets (Mo2/3RE1/3)2AlC, also predicted as parent materials for two-dimensional (2D) derivatives, where the rare earth (RE) = Nd, Gd (only mu SR), Tb, Dy, Ho, and Er. By crossing information between the two techniques, we determine the magnetic moment (m), structure, and dynamic properties of all compounds. We find that only for RE = Nd and Gd the moments are frozen on a microsecond timescale. Out of these two, the most promising compound for a potential 2D high m magnet is the Gd variant, since the parent crystals are pristine with m = 6.5 +/- 0.5 mu B, Neel temperature of 29 +/- 1 K, and the magnetic anisotropy between out-of- and in-plane coupling is smaller than 10-8. This result suggests that magnetic ordering in the Gd variant is dominated by in-plane magnetic interactions and should therefore remain stable when exfoliated into 2D sheets., Funding Agencies|Israel Atomic Energy Commission Pazy Foundation grant; Knut and Alice Wallenberg (KAW) FoundationKnut & Alice Wallenberg Foundation; Flag-ERA JTC 2017 project "MORE-MXenes"

The G4C2-repeat expansion in C9orf72 is the most common cause of frontotemporal dementia and of amyotrophic lateral sclerosis. The variability of age at onset and phenotypic presentations is a hallmark of C9orf72 disease. In this study, we aimed to identify modifying factors of disease onset in C9orf72 carriers using a family-based approach, in pairs of C9orf72 carrier relatives with concordant or discordant age at onset. Linkage and association analyses provided converging evidence for a locus on chromosome Xq27.3. The minor allele A of rs1009776 was associated with an earlier onset (P = 1 × 10-5). The association with onset of dementia was replicated in an independent cohort of unrelated C9orf72 patients (P = 0.009). The protective major allele delayed the onset of dementia from 5 to 13 years on average depending on the cohort considered. The same trend was observed in an independent cohort of C9orf72 patients with extreme deviation of the age at onset (P = 0.055). No association of rs1009776 was detected in GRN patients, suggesting that the effect of rs1009776 was restricted to the onset of dementia due to C9orf72. The minor allele A is associated with a higher SLITRK2 expression based on both expression quantitative trait loci (eQTL) databases and in-house expression studies performed on C9orf72 brain tissues. SLITRK2 encodes for a post-synaptic adhesion protein. We further show that synaptic vesicle glycoprotein 2 and synaptophysin, two synaptic vesicle proteins, were decreased in frontal cortex of C9orf72 patients carrying the minor allele. Upregulation of SLITRK2 might be associated with synaptic dysfunctions and drives adverse effects in C9orf72 patients that could be modulated in those carrying the protective allele. How the modulation of SLITRK2 expression affects synaptic functions and influences the disease onset of dementia in C9orf72 carriers will require further investigations. In summary, this study describes an original approach to detect modifier g