Untersuchungen zum netzgeführten Taktbetrieb einer Betonkerntemperierung

Die verstärkte Einspeisung von Strom aus fluktuierender Erneuerbarer Energieerzeugung stellt unser Energiesystem vor große Herausforderungen. Gebäuden kommt vor diesem Hintergrund eine wichtige Rolle als flexible Verbraucher und Erzeuger zu. Neben dem Nutzerkomfort und der Energieeffizienz von Gebäuden wird zukünftig auch ihr Einfluss auf das Stromnetz zur Optimierungsgröße. In Verbindung mit einer Betonkerntemperierung (BKT) birgt die Gebäudemasse ein erhebliches Lastmanagement-Potenzial. Die in dieser Arbeit entwickelte netzgeführte Taktbetriebsstrategie soll helfen, dieses Potenzial im praktischen Gebäudebetrieb wirkungsvoll und effizient zu nutzen. Grundlage für die Untersuchungen sind die Planungsdaten eines in 2020 fertig- gestellten Nichtwohngebäudes. Anhand dieser wurde in der Simulationsumgebung TRNSYS ein komplexes Gebäude- und Anlagenmodell zur Versorgung einer Bürozone aufgebaut. Im Modell erfolgt die Grundbeheizung sowie die Kühlung der Zone im Sommer über eine mittig in der Betondecke angeordnete BKT. Die Wärme- und Kältebereitstellung für die BKT erfolgt über eine erdreichgekoppelte reversible Wärmepumpe. Die Beladung der BKT in der Referenzvariante erfolgt im Dauerbetrieb über außentemperaturabhängige Heiz-/Kühlkurven nach dem Unknown-But-Bounded-Verfahren (UBB). Darauf aufbauend wird eine netzgeführte Taktstrategie auf Basis des UBB-Taktverfahrens entwickelt. Ziel der Netzführung auf Grundlage eines entwickelten Netzsignals ist die Verschiebung der Beladungszeiten der Betondecke in Zeiten, die im Hinblick auf das elektrische Energiesystem als günstig zu bewerten sind. Die in Frage kommenden Netzreferenzgrößen werden auf Basis von Netzdaten der Jahre 2017 bis 2020 bewertet. Es werden die Auswirkungen der Betriebsstrategie im Hinblick auf thermischen Raumkomfort, Energieeffizienz und -verbrauch sowie den Netzeinfluss der Wärme- und Kälteversorgung der Bürozone untersucht. Im Ergebnis zeigt sich, dass die „Netzdienlichkeit“ des Gesamtsystems durch Anwendung der Netzführung der BKT signifikant erhöht werden kann. Die definierten Komfortanforderungen werden eingehalten, im Hinblick auf Energieeffizienz und -verbrauch sind nur leichte Einbußen zu beobachten

Simulation and analysis of load shifting and energy saving potential of CO2-based demand-controlled ventilation in a sports training center

This paper aims to evaluate and characterize the impact of optimizing the operation of the HVAC system through maintaining dynamic CO2-based Demand-Controlled ventilation (DCV) on the electricity load profile and energy consumption of the sports training center of Leibniz University Hannover. The actual ventilation control scheme, in which the operation of the HVAC system is operated with a two-stage volume flow controller based on indoor CO2 concentration is improved through two steps to avoid overventilation and reduce power consumption. For this purpose, a detailed multi-zone model of the sports center and energy supply system has been developed in TRNSYS. In the first step, a multi-stage control scenario is implemented considering the occupancy schedules and indoor CO2 concentration measurement data. In the second step, based on an indoor CO2 concentration model, a predictive control scenario is developed and applied. Aiming at characterizing the influence of these operation scenarios on the power consumption of the building, the annual electricity load profiles of the simulation cases will be analyzed and compared with the actual load profile of the building based on the technical planning documents and data provided by building management system (BMS). Simulation results show that utilizing predictive CO2-based DCV leads to a reduction of the peak load electricity by almost 2 kW and the base load by 5 kW as well as decreasing the annual energy consumption by 40 %

Candida albicans translocation through the intestinal epithelial barrier is promoted by fungal zinc acquisition and limited by NFκB-mediated barrier protection.

The opportunistic fungal pathogen Candida albicans thrives on human mucosal surfaces as a harmless commensal, but frequently causes infections under certain predisposing conditions. Translocation across the intestinal barrier into the bloodstream by intestine-colonizing C. albicans cells serves as the main source of disseminated candidiasis. However, the host and microbial mechanisms behind this process remain unclear. In this study we identified fungal and host factors specifically involved in infection of intestinal epithelial cells (IECs) using dual-RNA sequencing. Our data suggest that host-cell damage mediated by the peptide toxin candidalysin-encoding gene ECE1 facilitates fungal zinc acquisition. This in turn is crucial for the full virulence potential of C. albicans during infection. IECs in turn exhibit a filamentation- and damage-specific response to C. albicans infection, including NFκB, MAPK, and TNF signaling. NFκB activation by IECs limits candidalysin-mediated host-cell damage and mediates maintenance of the intestinal barrier and cell-cell junctions to further restrict fungal translocation. This is the first study to show that candidalysin-mediated damage is necessary for C. albicans nutrient acquisition during infection and to explain how IECs counteract damage and limit fungal translocation via NFκB-mediated maintenance of the intestinal barrier

Loss of <i>ECE1</i> has no effect on the transcriptional zinc starvation response in medium only.

Fold change in gene expression in C. albicans WT (BWP17) and ece1Δ/Δ strains during incubation in cell culture medium for (A) ZRT101, (B) ZRT2, (C) PRA1, (D) ZRT3, and (E) ZRC1. All values are shown as the mean with standard deviation. (TIF)</p

NFκB activation limits <i>ECE1</i>-dependent damage and paracellular translocation.

(A) Inhibition of NFκB activation using the high affinity NFκB activation inhibitor quinazoline (QNZ) increases the damage potential of C. albicans wildtype, but not for the non-filamentous efg1ΔΔ/cph1ΔΔ strain or the non-damaging ece1Δ/Δ strain towards C2BBe1 cells after 24 h. LDH release was adjusted by subtracting the release from uninfected and untreated host cells. (B) Inhibition of NFκB activation increases fungal translocation of C. albicans after 24 h across intestinal epithelial cells independent of damage potential. (C) Blocking NFκB activation significantly increases the breakdown of barrier integrity after 24 h of the intestinal epithelial cell layer for efg1ΔΔ/cph1ΔΔ and ece1Δ/Δ, with a similar but not significant effect on both WT strains. (D) E-cadherin protein levels normalized to GAPDH and presented relative to levels in untreated C2BBe1 cells. QNZ treatment further increased degradation of E-cadherin during infection with WT (SC5314) and ece1Δ/Δ. (E) Fluorescent labeling of E-cadherin during C. albicans infection with and without QNZ treatment (scale bar = 50 μm). Inhibition of NFκB activation decreased the organization of E-cadherin at IEC borders upon infection with the ece1Δ/Δ and both WT strains. Representative pictures for each strain and treatment condition are shown from 3 biological replicates with median score values in the inset for each strain and condition. All values are shown as the mean with standard deviation. Host-cell damage (A), fungal translocation (B), and barrier integrity (C) data were compared using a one-way ANOVA. Statistical significance for host-cell damage (A) and fungal translocation (B) data was determined with a post-hoc Tukey’s multiple comparisons test, while significance for the barrier integrity (C) data was determined using a post-hoc Šidák’s multiple comparisons test. Statistical significance: **, P ≤ 0.01; ****, P ≤ 0.0001.</p

Detection antibodies for immune signaling proteins.

Detection antibodies for immune signaling proteins.</p

Western blot detection of cell-cell junction proteins for IECs during <i>C</i>. <i>albicans</i> infection and NFκB inhibition.

Confluent, differentiated C2BBe1 cells were infected with WT ece1Δ/Δ, and efg1ΔΔ/cph1ΔΔ C. albicans for 24 h. Samples were either untreated or treated with an NFκB activation inhibitor (QNZ) and the protein content was sampled. (A) Proteins that make up tight and adherens junctions (E-cadherin and claudin-1) were detected with GAPDH serving as a control. (B) Claudin-1 protein levels normalized to GAPDH and presented relative to levels in untreated C2BBe1 cells. QNZ treatment further increased degradation of claudin-1, even during infection with efg1ΔΔ/cph1ΔΔ and ece1Δ/Δ. All values are shown as the mean with standard deviation. (TIF)</p

Loss of <i>ECE1</i> increases the transcriptional zinc starvation response during infection of IECs.

Fold change in gene expression in C. albicans WT (BWP17) and ece1Δ/Δ strains during co-incubation with C2BBe1 cells for (A) ZRT101, (B) ZRT2, (C) PRA1, (D) ZRT3, and (E) ZRC1. Fold changes are calculated as the normalized gene expression at each time point compared to the respective 0 h control samples. (F) Fold change in normalized gene expression of the ece1Δ/Δ strain compared to WT(BWP17) at 24 h in medium only or during infection of IECs. Gene expression was analyzed by q-RT-PCR and is normalized to ACT1 as a housekeeping gene. All values are shown as the mean with standard deviation. All the ratio data from q-RT-PCR experiments were log-transformed before performing a two-tailed, paired t-test. Statistical significance: *, P ≤ 0.05.</p

Western blot detection of immune signaling proteins for IECs infected with WT and <i>ece1</i>Δ/Δ.

(A) Confluent, differentiated C2BBe1 cells were infected with WT (BWP17) and ece1Δ/Δ C. albicans for 6 h and the protein content was sampled. Proteins involved in the damage response of oral epithelial cells were detected with ACT1 serving as a control. n.d. = not determined. (B) Protein levels normalized to actin. For p38, MKP1, EPHA2, EGFR, and AKT the normalized protein level for the phosphorylated protein is presented relative to the total respective protein level. (TIF)</p