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Contemporary drought impact assessments have been constrained due to data availability, leading to an incomplete representation of impact trends. To address this, we present a novel method for the comprehensive and near-real-time monitoring of drought socio-economic impacts based on media reports. We tested its application using the case of the exceptional 2018/19 German drought. By employing text mining techniques, 4839 impact statements were identified, relating to livestock, agriculture, forestry, fires, recreation, energy and transport sectors. An accuracy of 95.6% was obtained for their automatic classification. Furthermore, high levels of performance in terms of spatial and temporal precision were found when validating our results against independent data (e.g. soil moisture, average precipitation, population interest in droughts, crop yield and forest fire statistics). The findings highlight the applicability of media data for rapidly and accurately monitoring the propagation of drought consequences over time and space. We anticipate our method to be used as a starting point for an impact-based early warning system.
Aims: 1-Methyl-4-phenyl-tetrahydropyridine (MPTP) is among the most widely used neurotoxins for inducing experimental parkinsonism. MPTP causes parkinsonian symptoms in mice, primates, and humans by killing a subpopulation of dopaminergic neurons. Extrapolations of data obtained using MPTP-based parkinsonism models to human disease are common; however, the precise mechanism by which MPTP is converted into its active neurotoxic metabolite, 1-methyl-4-phenyl-pyridinium (MPP+), has not been fully elucidated. In this study, we aimed to address two unanswered questions related to MPTP toxicology: (1) Why are MPTP-converting astrocytes largely spared from toxicity? (2) How does MPP+ reach the extracellular space? Results: In MPTP-treated astrocytes, we discovered that the membrane-impermeable MPP+, which is generally assumed to be formed inside astrocytes, is almost exclusively detected outside of these cells. Instead of a transporter-mediated export, we found that the intermediate, 1-methyl-4-phenyl-2,3-dihydropyridinium (MPDP+), and/or its uncharged conjugate base passively diffused across cell membranes and that MPP+ was formed predominately by the extracellular oxidation of MPDP+ into MPP+. This nonenzymatic extracellular conversion of MPDP+ was promoted by O-2, a more alkaline pH, and dopamine autoxidation products. Innovation and Conclusion: Our data indicate that MPTP metabolism is compartmentalized between intracellular and extracellular environments, explain the absence of toxicity in MPTP-converting astrocytes, and provide a rationale for the preferential formation of MPP+ in the extracellular space. The mechanism of transporter-independent extracellular MPP+ formation described here indicates that extracellular genesis of MPP+ from MPDP is a necessary prerequisite for the selective uptake of this toxin by catecholaminergic neurons.