Analyse af elbilers forbrug

Det er et mål for EU at opnå en kraftig reduktion i udledningen af CO2 fra transportsektoren. Elbiler kan være en af måderne at opnå dele af denne reduktion fordi det er muligt at oplade elbiler med strøm fra vedvarende energikilder så som vindmøller. En væsentlig udfordring med at erstatte brændstofbiler med elbiler er, at elbilerne har en betydelig kortere rækkevidde. Denne artikel anvender GPS data fra 164 elbiler og 447 brændstofbiler til at undersøge om der er forskelle på, hvordan elbiler og brændstofbiler anvendes og hvilke hastigheder de kører med. Herudover anvendes forbrugsdata (CAN bus data) fra elbiler til at vurdere på den faktiske rækkevidde for disse biler. Hovedkonklusionerne er, at ture i elbiler generelt er lidt kortere, at elbiler kører lidt stærkere i byerne, men betydeligt langsommere på motorvejene. For rækkevidden af elbiler konkluderes det, at dette er meget afhængigt af årstiden (temperaturen) og spænder fra 77 km (vinteren) til 130 km (sommeren) for den type af elbiler undersøgt i denne artikel

Hurtigste versus mest brændstoføkonomiske ruter

Der er stort fokus på at forbedre brændstoføkonomien i transportbranchen generelt. I denne artikel anvendes brændstoftallene fra Controller Area Network Bus (CANBus) kombineret med GPS data til at skabe et digitalt vejkort, hvor det er muligt at sammenligne de hurtigste ruter med de mest brændstoføkonomiske ruter. Kortet er baseret på ca. 100 millioner CANBus observationer og ca. 2,1 milliarder GPS observationer. Hovedkonklusionen er, at CANBus data kan anvendes til at estimere brændstofforbruget for en rute. Sammenlignet med estimering af køretider er det mere kompliceret at estimere brændstofforbrug fordi der er eksterne faktorer som påvirker forbruget f.eks. chaufførens kørestil, køretøjs vedligeholdelsesstand og vejret. På websiden daisy.aau.dk/its kan hurtigste, korteste og mest brændstoføkonomiske rute sammenlignes for hele Danmark

Hurtigste versus mest brændstoføkonomiske ruter

Der er stort fokus på at forbedre brændstoføkonomien i transportbranchen generelt. I denne artikel anvendes brændstoftallene fra Controller Area Network Bus (CANBus) kombineret med GPS data til at skabe et digitalt vejkort, hvor det er muligt at sammenligne de hurtigste ruter med de mest brændstoføkonomiske ruter. Kortet er baseret på ca. 100 millioner CANBus observationer og ca. 2,1 milliarder GPS observationer. Hovedkonklusionen er, at CANBus data kan anvendes til at estimere brændstofforbruget for en rute. Sammenlignet med estimering af køretider er det mere kompliceret at estimere brændstofforbrug fordi der er eksterne faktorer som påvirker forbruget f.eks. chaufførens kørestil, køretøjs vedligeholdelsesstand og vejret. På websiden daisy.aau.dk/its kan hurtigste, korteste og mest brændstoføkonomiske rute sammenlignes for hele Danmark

Probenecid Inhibits the Human Bitter Taste Receptor TAS2R16 and Suppresses Bitter Perception of Salicin

Bitter taste stimuli are detected by a diverse family of G protein-coupled receptors (GPCRs) expressed in gustatory cells. Each bitter taste receptor (TAS2R) responds to an array of compounds, many of which are toxic and can be found in nature. For example, human TAS2R16 (hTAS2R16) responds to β-glucosides such as salicin, and hTAS2R38 responds to thiourea-containing molecules such as glucosinolates and phenylthiocarbamide (PTC). While many substances are known to activate TAS2Rs, only one inhibitor that specifically blocks bitter receptor activation has been described. Here, we describe a new inhibitor of bitter taste receptors, p-(dipropylsulfamoyl)benzoic acid (probenecid), that acts on a subset of TAS2Rs and inhibits through a novel, allosteric mechanism of action. Probenecid is an FDA-approved inhibitor of the Multidrug Resistance Protein 1 (MRP1) transporter and is clinically used to treat gout in humans. Probenecid is also commonly used to enhance cellular signals in GPCR calcium mobilization assays. We show that probenecid specifically inhibits the cellular response mediated by the bitter taste receptor hTAS2R16 and provide molecular and pharmacological evidence for direct interaction with this GPCR using a non-competitive (allosteric) mechanism. Through a comprehensive analysis of hTAS2R16 point mutants, we define amino acid residues involved in the probenecid interaction that result in decreased sensitivity to probenecid while maintaining normal responses to salicin. Probenecid inhibits hTAS2R16, hTAS2R38, and hTAS2R43, but does not inhibit the bitter receptor hTAS2R31 or non-TAS2R GPCRs. Additionally, structurally unrelated MRP1 inhibitors, such as indomethacin, fail to inhibit hTAS2R16 function. Finally, we demonstrate that the inhibitory activity of probenecid in cellular experiments translates to inhibition of bitter taste perception of salicin in humans. This work identifies probenecid as a pharmacological tool for understanding the cell biology of bitter taste and as a lead for the development of broad specificity bitter blockers to improve nutrition and medical compliance

Effects of Electrical and Structural Remodeling on Atrial Fibrillation Maintenance: A Simulation Study

Atrial fibrillation, a common cardiac arrhythmia, often progresses unfavourably: in patients with long-term atrial fibrillation, fibrillatory episodes are typically of increased duration and frequency of occurrence relative to healthy controls. This is due to electrical, structural, and contractile remodeling processes. We investigated mechanisms of how electrical and structural remodeling contribute to perpetuation of simulated atrial fibrillation, using a mathematical model of the human atrial action potential incorporated into an anatomically realistic three-dimensional structural model of the human atria. Electrical and structural remodeling both shortened the atrial wavelength - electrical remodeling primarily through a decrease in action potential duration, while structural remodeling primarily slowed conduction. The decrease in wavelength correlates with an increase in the average duration of atrial fibrillation/flutter episodes. The dependence of reentry duration on wavelength was the same for electrical vs. structural remodeling. However, the dynamics during atrial reentry varied between electrical, structural, and combined electrical and structural remodeling in several ways, including: (i) with structural remodeling there were more occurrences of fragmented wavefronts and hence more filaments than during electrical remodeling; (ii) dominant waves anchored around different anatomical obstacles in electrical vs. structural remodeling; (iii) dominant waves were often not anchored in combined electrical and structural remodeling. We conclude that, in simulated atrial fibrillation, the wavelength dependence of reentry duration is similar for electrical and structural remodeling, despite major differences in overall dynamics, including maximal number of filaments, wave fragmentation, restitution properties, and whether dominant waves are anchored to anatomical obstacles or spiralling freely

Finishing the euchromatic sequence of the human genome

The sequence of the human genome encodes the genetic instructions for human physiology, as well as rich information about human evolution. In 2001, the International Human Genome Sequencing Consortium reported a draft sequence of the euchromatic portion of the human genome. Since then, the international collaboration has worked to convert this draft into a genome sequence with high accuracy and nearly complete coverage. Here, we report the result of this finishing process. The current genome sequence (Build 35) contains 2.85 billion nucleotides interrupted by only 341 gaps. It covers ∼99% of the euchromatic genome and is accurate to an error rate of ∼1 event per 100,000 bases. Many of the remaining euchromatic gaps are associated with segmental duplications and will require focused work with new methods. The near-complete sequence, the first for a vertebrate, greatly improves the precision of biological analyses of the human genome including studies of gene number, birth and death. Notably, the human enome seems to encode only 20,000-25,000 protein-coding genes. The genome sequence reported here should serve as a firm foundation for biomedical research in the decades ahead