Demand-driven data acquisition for large scale fleets

Automakers manage vast fleets of connected vehicles and face an ever-increasing demand for their sensor readings. This demand originates from many stakeholders, each potentially requiring different sensors from different vehicles. Currently, this demand remains largely unfulfilled due to a lack of systems that can handle such diverse demands efficiently. Vehicles are usually passive participants in data acquisition, each continuously reading and transmitting the same static set of sensors. However, in a multi-tenant setup with diverse data demands, each vehicle potentially needs to provide different data instead. We present a system that performs such vehicle-specific minimization of data acquisition by mapping individual data demands to individual vehicles. We collect personal data only after prior consent and fulfill the requirements of the GDPR. Non-personal data can be collected by directly addressing individual vehicles. The system consists of a software component natively integrated with a major automaker’s vehicle platform and a cloud platform brokering access to acquired data. Sensor readings are either provided via near real-time streaming or as recorded trip files that provide specific consistency guarantees. A performance evaluation with over 200,000 simulated vehicles has shown that our system can increase server capacity on-demand and process streaming data within 269 ms on average during peak load. The resulting architecture can be used by other automakers or operators of large sensor networks. Native vehicle integration is not mandatory; the architecture can also be used with retrofitted hardware such as OBD readers. © 2021 by the authors. Licensee MDPI, Basel, Switzerland

A new coherent states approach to semiclassics which gives Scott's correction

We introduce new coherent states and use them to prove semi-classical estimates for Schr\"odinger operators with regular potentials. This can be further applied to the Thomas-Fermi potential yielding a new proof of the Scott correction for molecules.Comment: A misprint in the definition of new coherent states correcte

Not all roads lead to the immune system: the genetic basis of multiple sclerosis severity

Multiple sclerosis is a leading cause of neurological disability in adults. Heterogeneity in multiple sclerosis clinical presentation has posed a major challenge for identifying genetic variants associated with disease outcomes. To overcome this challenge, we used prospectively ascertained clinical outcomes data from the largest international multiple sclerosis registry, MSBase. We assembled a cohort of deeply phenotyped individuals of European ancestry with relapse-onset multiple sclerosis. We used unbiased genome-wide association study and machine learning approaches to assess the genetic contribution to longitudinally defined multiple sclerosis severity phenotypes in 1813 individuals. Our primary analyses did not identify any genetic variants of moderate to large effect sizes that met genome-wide significance thresholds. The strongest signal was associated with rs7289446 (β = −0.4882, P = 2.73 × 10−7), intronic to SEZ6L on chromosome 22. However, we demonstrate that clinical outcomes in relapse-onset multiple sclerosis are associated with multiple genetic loci of small effect sizes. Using a machine learning approach incorporating over 62 000 variants together with clinical and demographic variables available at multiple sclerosis disease onset, we could predict severity with an area under the receiver operator curve of 0.84 (95% CI 0.79–0.88). Our machine learning algorithm achieved positive predictive value for outcome assignation of 80% and negative predictive value of 88%. This outperformed our machine learning algorithm that contained clinical and demographic variables alone (area under the receiver operator curve 0.54, 95% CI 0.48–0.60). Secondary, sex-stratified analyses identified two genetic loci that met genome-wide significance thresholds. One in females (rs10967273; βfemale = 0.8289, P = 3.52 × 10−8), the other in males (rs698805; βmale = −1.5395, P = 4.35 × 10−8), providing some evidence for sex dimorphism in multiple sclerosis severity. Tissue enrichment and pathway analyses identified an overrepresentation of genes expressed in CNS compartments generally, and specifically in the cerebellum (P = 0.023). These involved mitochondrial function, synaptic plasticity, oligodendroglial biology, cellular senescence, calcium and G-protein receptor signalling pathways. We further identified six variants with strong evidence for regulating clinical outcomes, the strongest signal again intronic to SEZ6L (adjusted hazard ratio 0.72, P = 4.85 × 10−4). Here we report a milestone in our progress towards understanding the clinical heterogeneity of multiple sclerosis outcomes, implicating functionally distinct mechanisms to multiple sclerosis risk. Importantly, we demonstrate that machine learning using common single nucleotide variant clusters, together with clinical variables readily available at diagnosis can improve prognostic capabilities at diagnosis, and with further validation has the potential to translate to meaningful clinical practice change.</p