36 research outputs found
Regulatory Changes in Power Systems Explored with Explainable Artificial Intelligence
A stable supply of electrical energy is essential for the functioning of our
society. Therefore, the electrical power grid's operation and energy and
balancing markets are subject to strict regulations. As the external technical,
economic, or social influences on the power grid change, these regulations must
also be constantly adapted. However, whether these regulatory changes lead to
the intended results is not easy to assess. Could eXplainable Artificial
Intelligence (XAI) models distinguish regulatory settings and support the
understanding of the effects of these changes? In this article, we explore two
examples of regulatory changes in the German energy markets for bulk
electricity and for reserve power. We explore the splitting of the
German-Austrian bidding zone and changes in the pricing schemes of the German
balancing energy market. We find that boosted tree models and feedforward
neural networks before and after a regulatory change differ in their respective
parametrizations. Using Shapley additive explanations, we reveal model
differences, e.g. in terms of feature importances, and identify key features of
these distinct models. With this study, we demonstrate how XAI can be applied
to investigate system changes in power systems.Comment: 7 pages, 3 figure
Selbstverständlich europäisch!? 2020
SELBSTVERSTĂNDLICH EUROPĂISCH!? 2020
Selbstverständlich europäisch!? 2020 / Hillje, Johannes (CC BY-NC-ND) ( -
Kinetics of Ethylene and Ethylene Oxide in Subcellular Fractions of Lungs and Livers of Male B6C3F1 Mice and Male Fischer 344 Rats and of Human Livers
Ethylene (ET) is metabolized in mammals to the carcinogenic ethylene oxide (EO). Although both gases are of high industrial relevance, only limited data exist on the toxicokinetics of ET in mice and of EO in humans. Metabolism of ET is related to cytochrome P450-dependent mono-oxygenase (CYP) and of EO to epoxide hydrolase (EH) and glutathione S-transferase (GST). Kinetics of ET metabolism to EO and of elimination of EO were investigated in headspace vessels containing incubations of subcellular fractions of mouse, rat, or human liver or of mouse or rat lung. CYP-associated metabolism of ET and GST-related metabolism of EO were found in microsomes and cytosol, respectively, of each species. EH-related metabolism of EO was not detectable in hepatic microsomes of rats and mice but obeyed saturation kinetics in hepatic microsomes of humans. In ET-exposed liver microsomes, metabolism of ET to EO followed Michaelis-Menten-like kinetics. Mean values of Vmax [nmol/(min¡mg protein)] and of the apparent Michaelis constant (Km [mmol/l ET in microsomal suspension]) were 0.567 and 0.0093 (mouse), 0.401 and 0.031 (rat), and 0.219 and 0.013 (human). In lung microsomes, Vmax values were 0.073 (mouse) and 0.055 (rat). During ET exposure, the rate of EO production decreased rapidly. By modeling a suicide inhibition mechanism, rate constants for CYP-mediated catalysis and CYP inactivation were estimated. In liver cytosol, mean GST activities to EO expressed as Vmax/Km [Οl/(min¡mg protein)] were 27.90 (mouse), 5.30 (rat), and 1.14 (human). The parameters are most relevant for reducing uncertainties in the risk assessment of ET and EO
Selbstverständlich europäisch!? 2021
SELBSTVERSTĂNDLICH EUROPĂISCH!? 2021
Selbstverständlich europäisch!? 2021 / Hillje, Johannes (CC BY-NC-ND) ( -
Fingolimod induces neuroprotective factors in human astrocytes.
Background
Fingolimod (FTY720) is the first sphingosine-1-phosphate (S1P) receptor modulator approved for the treatment of multiple sclerosis. The phosphorylated active metabolite FTY720-phosphate (FTY-P) interferes with lymphocyte trafficking. In addition, it accumulates in the CNS and reduces brain atrophy in multiple sclerosis (MS), and neuroprotective effects are hypothesized.
Methods
Human primary astrocytes as well as human astrocytoma cells were stimulated with FTY-P or S1P. We analyzed gene expression by a genome-wide microarray and validated induced candidate genes by quantitative PCR (qPCR) and ELISA. To identify the S1P-receptor subtypes involved, we applied a membrane-impermeable S1P analog (dihydro-S1P), receptor subtype specific agonists and antagonists, as well as RNAi silencing.
Results
FTY-P induced leukemia inhibitory factor (LIF), interleukin 11 (IL11), and heparin-binding EGF-like growth factor (HBEGF) mRNA, as well as secretion of LIF and IL11 protein. In order to mimic an inflammatory milieu as observed in active MS lesions, we combined FTY-P application with tumor necrosis factor (TNF). In the presence of this key inflammatory cytokine, FTY-P synergistically induced LIF, HBEGF, and IL11 mRNA, as well as secretion of LIF and IL11 protein. TNF itself induced inflammatory, B-cell promoting, and antiviral factors (CXCL10, BAFF, MX1, and OAS2). Their induction was blocked by FTY-P. After continuous exposure of cells to FTY-P or S1P for up to 7 days, the extent of induction of neurotrophic factors and the suppression of TNF-induced inflammatory genes declined but was still detectable. The induction of neurotrophic factors was mediated via surface S1P receptors 1 (S1PR1) and 3 (S1PR3).
Conclusions
We identified effects of FTY-P on astrocytes, namely induction of neurotrophic mediators (LIF, HBEGF, and IL11) and inhibition of TNF-induced inflammatory genes (CXCL10, BAFF, MX1, and OAS2). This supports the view that a part of the effects of fingolimod may be mediated via astrocytes