RESUMEN
Deviations between High Voltage (HV) current measurements and the corresponding real values provoke serious problems in the power trains of Electric Vehicle (EVs). Examples for these problems have inaccurate performance coordinations and unnecessary power limitations during driving or charging. The main reason for the deviations are time delays. By correcting these delays with accurate Time Delay Estimation (TDE), our data shows that we can reduce the measurement deviations from 25% of the maximum current to below 5%. In this paper, we present three different approaches for TDE. We evaluate all approaches with real data from power trains of EVs. To enable an execution on automotive Electronic Control Unit (ECUs), the focus of our evaluation lies not only on the accuracy of the TDE, but also on the computational efficiency. The proposed Linear Regression (LR) approach suffers even from small noise and offsets in the measurement data and is unsuited for our purpose. A better alternative is the Variance Minimization (VM) approach. It is not only more noise-resistant but also very efficient after the first execution. Another interesting approach are Adaptive Filter (AFs), introduced by Emadzadeh et al. Unfortunately, AFs do not reach the accuracy and efficiency of VM in our experiments. Thus, we recommend VM for TDE of HV current signals in the power train of EVs and present an additional optimization to enable its execution on ECUs.
RESUMEN
Specific and reciprocal interactions with the bone marrow microenvironment (BMM) govern the course of hematological malignancies. Matrix metalloproteinase-9 (MMP-9), secreted by leukemia cells, facilitates tumor progression via remodeling of the extracellular matrix (ECM) of the BMM. Hypothesizing that leukemias may instruct the BMM to degrade the ECM, we show, that MMP-9-deficiency in the BMM prolongs survival of mice with BCR-ABL1-induced B-cell acute lymphoblastic leukemia (B-ALL) compared with controls and reduces leukemia-initiating cells. MMP-9-deficiency in the BMM leads to reduced degradation of proteins of the ECM and reduced invasion of B-ALL. Using various in vivo and in vitro assays, as well as recipient mice deficient for the receptor for tumor necrosis factor (TNF) α (TNFR1) we demonstrate that B-ALL cells induce MMP-9-expression in mesenchymal stem cells (MSC) and possibly other cells of the BMM via a release of TNFα. MMP-9-expression in MSC is mediated by activation of nuclear factor kappa B (NF-κB) downstream of TNFR1. Consistently, knockdown of TNF-α in B-ALL-initiating cells or pharmacological inhibition of MMP-9 led to significant prolongation of survival in mice with B-ALL. In summary, leukemia cell-derived Tnfα induced MMP-9-expression by the BMM promoting B-ALL progression. Inhibition of MMP-9 may act as an adjunct to existing therapies.