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  1. Electric Aircraft have the potential to revolutionize short-distance air travel with lower operating costs and simplified maintenance. However, due to the long lead-time associated with procuring batteries and the maintenance challenges of replacing and repairing batteries in electric aircraft, there are still unanswered questions related to the true long-term operating costs of electric aircraft. This research examines using a load-sharing system in electric aircraft to optimally tune battery degradation in a multi-battery system such that the battery life of a single battery is extended. The active optimization of energy drawn from multiple battery packs means that each battery pack reaches its optimal replacement point at the same time; thereby simplifying the maintenance procedure and reducing cost. This work uses lithium iron phosphate batteries experimentally characterized and simulated in OpenModelica for a flight load profile. Adaptive agents control the load on the battery according to factors such as state of charge, and state of health, to respond to potential faults. The findings in this work show the potential for adaptive agents to selectively draw more power from a healthy battery to extend the lifespan of a degraded battery such that the remaining useful life of both batteries reaches zero at the same time. Simulations show that dual battery replacement can be facilitated using the proposed method when the in-service battery has a remaining useful life of greater than 0.5; assuming that the replacement battery it is paired with has a remaining useful life of 1.0. Limitations of the proposed method are discussed within this work. 
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    Free, publicly-accessible full text available January 4, 2025
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  3. Misregulation of the signaling axis formed by the receptor tyrosine kinase (RTK) EphA2 and its ligand, ephrinA1, causes aberrant cell-cell contacts that contribute to metastasis. Solid tumors are characterized by an acidic extracellular medium. We intend to take advantage of this tumor feature to design new molecules that specifically target tumors. We created a novel pH-dependent transmembrane peptide, TYPE7, by altering the sequence of the transmembrane domain of EphA2. TYPE7 is highly soluble and interacts with the surface of lipid membranes at neutral pH, while acidity triggers transmembrane insertion. TYPE7 binds to endogenous EphA2 and reduces Akt phosphorylation and cell migration as effectively as ephrinA1. Interestingly, we found large differences in juxtamembrane tyrosine phosphorylation and the extent of EphA2 clustering when comparing TYPE7 with activation by ephrinA1. This work shows that it is possible to design new pH-triggered membrane peptides to activate RTK and gain insights on its activation mechanism. 
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