This paper investigates the possibility of improving the fuel efficiency by decreasing the engine speed during the coasting phase of the vehicle. The proposed approach is stimulated by the fact that the engine losses increase with the engine speed. If the engine speed is retained low, the engine losses will be reduced and subsequently the tractive torque will be increased, enabling the vehicle to remain moving for longer duration while coasting. By increasing the time period of the coasting the fuel efficiency can be increased, especially travelling downhill, since it can benefit from the kinematic energy stored in the vehicle to continue coasting for a longer duration. It is already industry standard practice to cut fuel during coasting and refuel at low engine speed. The substantial difference proposed in this paper is the controlled reduction of engine speed during this phase and thus reduction in the engine losses, resulting in improved fuel economy. The simulation model is tested and the results illustrating an improvement to the fuel efficiency through the proposed method are presented. Some results of the experimental tests with a real vehicle through the proposed strategy are also presented in the paper.
The properties of the cell types that are most vulnerable in the Huntington's disease (HD) cortex, the nature of somatic CAG expansion of mHTT in these cells, and their importance in CNS circuitry have not been delineated. Here we have employed serial fluorescence activated nuclear sorting (sFANS), deep molecular profiling, and single nucleus RNA sequencing (snRNAseq) to demonstrate that layer 5a pyramidal neurons are selectively vulnerable in primary motor cortex and other cortical areas. Extensive somatic mHTT-CAG expansion occurs in vulnerable layer 5a pyramidal cells, and in Betz cells, layer 6a, layer 6b neurons that are not lost in HD. Retrograde tracing experiments in the macaque brain identify the vulnerable layer 5a neurons as corticostriatal pyramidal cells. Our data establish that mHTT-CAG expansion is not sufficient for cell loss in the cerebral cortex of HD, and suggest that cortico-striatal disconnection in early-stage HD patients may play an important role in neurodegeneration.
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