Operating cost based cruise speed reduction for ground delay programs: Effect of scope length

Ground delay programs typically involve the delaying of aircraft that are departing from origin airports within some set distance of a capacity constrained destination airport. Long haul flights are not delayed in this way. A trade-off exists when fixing the distance parameter: increasing the ‘scope’ distributes delay among more aircraft and may reduce airborne holding delay but could also result in unnecessary delay in the (frequently observed) case of early program cancellation. In order to overcome part of this drawback, a fuel based cruise speed reduction strategy aimed at realizing airborne delay, was suggested by the authors in previous publications. By flying slower, at a specific speed, aircraft that are airborne can recover part of their initially assigned delay without incurring extra fuel consumption if the ground delay program is canceled before planned. In this paper, the effect of the scope of the program is assessed when applying this strategy. A case study is presented by analyzing all the ground delay programs that took place at San Francisco, Newark Liberty and Chicago O’Hare International airports during one year. Results show that by the introduction of this technique it is possible to define larger scopes, partially reducing the amount of unrecovered delay.

Effect of wind on operating cost based cruise speed reduction for delay absorption

En route speed reduction can be used for air traffic flow management (ATFM), e.g., delaying aircraft while airborne or realizing metering at an arrival fix. In previous publications, the authors identified the flight conditions that maximize the airborne delay without incurring extra fuel consumption with respect to the nominal (not delayed) flight. In this paper, the effect of wind on this strategy is studied, and the sensitivity to wind forecast errors is also assessed. A case study done in Chicago O’Hare airport (ORD) is presented, showing that wind has a significant effect on the airborne delay that can be realized and that, in some cases, even tailwinds might lead to an increase in the maximum amount of airborne delay. The values of airborne delay are representative enough to suggest that this speed reduction technique might be useful in a real operational scenario. Moreover, the speed reduction strategy is more robust than nominal operations against fuel consumption in the presence of wind forecast uncertainties.

Effect of Short-Chain Fatty Acid Acetate on Colon Cancer

Acetate is a short chain fatty acid produced as a result of fermentation of ingested fibers by the gut microbiota. While it has been shown to reduce cell proliferation in some cancer cell lines1,2, more recent studies on liver3 and brain4 tumours suggest that acetate may actually promote tumour growth. Acetate in the cell is normally converted into acetyl-coA by two enzymes and metabolized; mitochondrial (ACSS1) and cytosolic (ACSS2) acetyl-coA synthetase. In the mitochondria acetyl-coA is utilized in the TCA cycle. In the cytosol it is utilized in lipid synthesis. In this study, the effect of acetate treatment on the growth of HT29 colon cancer cell line and its mechanism of action was assessed. HT29 human colorectal adenocarcinoma cells were treated with 10mM NaAc and cell viability, cellular bioenergetics and gene expression were investigated. Cell viability was assessed 24 hours after treatment using an MTT assay (Sigma, UK, n=8). Cellular oxygen consumption rate (OCR) and extracellular acidification rate (ECAR) was measured by XFe Analyzer (Seahorse Bioscience, USA). After a baseline reading cells were treated and OCR and ECAR measurements were observed for 18 hours (n=4). Total mRNA was isolated 24 hours after treatment using RNeasy kit (Qiagen, USA). Quantitative PCR reactions were performed using Taqman gene expression assays and Taqman Universal PCR Master Mix (ThermoFisher Scientific, UK) on Applied Biosystems 7500 Fast Real-Time PCR System (Life Technologies, USA) and analysed using ΔΔCt method (n=3). Acetate treatment led to a significant reduction in cell viability (15.9%, Figure 1). OCR, an indicator of oxidative phosphorylation, was significantly increased (p<0.0001) while ECAR, an indicator of glycolysis, was significantly reduced (p<0.0001, Figure 2). Gene expression of ACSS1 was increased by 1.7 fold of control (p=0.07) and ACSS2 expression was reduced to 0.6 fold of control (p=0.06, Figure 3). In conclusion, in colon cancer cells acetate supplementation induces cell death and increases oxidative capacity. These changes together with the trending decrease in ACSS2 expression suggest suppression of lipid synthesis pathways. We hypothesize that the reduced tumor growth by acetate is a consequence of the suppression of ACSS2 and lipid synthesis, both effects reported previously to reduce tumor growth3–5. These effects clearly warrant further investigation.