Goal- and Object-Oriented Models of the Aerodynamic Coefficients

Nowadays, aeronautics discovers new ways of flights near the critical regimes, unconventional aircraft forms, utilizing the micro–electro-mechanical technologies in flow and aircraft control, adaptive and morphing structures, using the structures and controls based on the biological principles, developing highly flexible structures, etc. Before deployment, these new technologies and solutions must be evaluated, tested in wide aerodynamic, flight dynamic simulations that require improved and new type of aerodynamic coefficient models. The chapter overviews the applicable models of the aerodynamic coefficients, introduces some new models and demonstrates how the different models can be applied in different goal- and object-oriented solutions. The following will be shortly explained: (i) how the aerodynamic forces and moments are generating, (ii) how the linear, nonlinear, steady, and nonsteady aerodynamic coefficient structures and forms might be modeled, and (iii) how to harmonize the model with the goal and object of investigations

Rapidly inducible changes in phosphatidylinositol 4,5-bisphosphate levels influence multiple regulatory functions of the lipid in intact living cells

Rapamycin (rapa)-induced heterodimerization of the FRB domain of the mammalian target of rapa and FKBP12 was used to translocate a phosphoinositide 5-phosphatase (5-ptase) enzyme to the plasma membrane (PM) to evoke rapid changes in phosphatidylinositol 4,5-bisphosphate (PtdIns(4,5)P2) levels. Rapa-induced PM recruitment of a truncated type IV 5-ptase containing only the 5-ptase domain fused to FKBP12 rapidly decreased PM PtdIns(4,5)P2 as monitored by the PLCδ1PH-GFP fusion construct. This decrease was paralleled by rapid termination of the ATP-induced Ca2+ signal and the prompt inactivation of menthol-activated transient receptor potential melastatin 8 (TRPM8) channels. Depletion of PM PtdIns(4,5)P2 was associated with a complete blockade of transferrin uptake and inhibition of epidermal growth factor internalization. None of these changes were observed upon rapa-induced translocation of an mRFP-FKBP12 fusion protein that was used as a control. These data demonstrate that rapid inducible depletion of PM PtdIns(4,5)P2 is a powerful tool to study the multiple regulatory roles of this phospholipid and to study differential sensitivities of various processes to PtdIns(4,5)P2 depletion

A Pilot Study into Bio-Behavioural Measurements on Air Traffic Controllers in Remote Tower Operations

What is the impact of shifting to remote tower operations on the Air Traffic Controller? In the joint HungaroControl-Netherlands Aerospace Centre NLR pilot project an assessment of bio-behaviour on three air traffic controllers was made in a remote tower and conventional tower. The research is motivated by HungaroControl’s plans in shifting to remote tower operations at Budapest airport in the upcoming years. This pilot project is considered a feasibility study to investigate if an eye tracker and a heart rate sensor can be used to derive workload, the controllers’ division of attention over information elements, and scanning strategies in two such different environments. Given the limited number of participants and challenges in measuring workload in the two different operational environments conclusions, can only be drawn with care. Nevertheless, preliminary results suggest that there might be an increase in workload in the remote tower environment, and thus further research is needed to clarify at what extend Air Traffic Controllers’ workload could be different, what are the root causes of the increase and how that could be handled. Also the pilot study has given confidence that useful bio-behavioural measures can be obtained for comparison between the remote tower and the conventional tower, and to extend the research to a larger group of controllers

Small aircraft infrared radiation measurements supporting the engine airframe aero-thermal integration

© 2018 Budapest University of Technology and Economics. All rights reserved. The large, EU Supported ESPOSA (Efficient Systems and propulsion for Small Aircraft) project has developed new small gas turbines for small aircraft. One of the important tasks was the engine - airframe aero-thermal radiation integration that included task of minimizing the infrared radiation of the small aircraft, too. This paper discusses the factors influencing on the aircraft infrared radiation, its possible simulation and measurements and introduces the results of small aircraft infrared radiation measurements. The temperature of aircraft hot parts heated by engines were determined for validation of methodology developed and applied to engine - aircraft thermal integration

Structural insights on TRPV5 gating by endogenous modulators.

TRPV5 is a transient receptor potential channel involved in calcium reabsorption. Here we investigate the interaction of two endogenous modulators with TRPV5. Both phosphatidylinositol 4,5-bisphosphate (PI(4,5)P2) and calmodulin (CaM) have been shown to directly bind to TRPV5 and activate or inactivate the channel, respectively. Using cryo-electron microscopy (cryo-EM), we determined TRPV5 structures in the presence of dioctanoyl PI(4,5)P2 and CaM. The PI(4,5)P2 structure reveals a binding site between the N-linker, S4-S5 linker and S6 helix of TRPV5. These interactions with PI(4,5)P2 induce conformational rearrangements in the lower gate, opening the channel. The CaM structure reveals two TRPV5 C-terminal peptides anchoring a single CaM molecule and that calcium inhibition is mediated through a cation-π interaction between Lys116 on the C-lobe of calcium-activated CaM and Trp583 at the intracellular gate of TRPV5. Overall, this investigation provides insight into the endogenous modulation of TRPV5, which has the potential to guide drug discovery

Activation of native TRPC1/C5/C6 channels by endothelin-1 is mediated by both PIP3 and PIP2 in rabbit coronary artery myocytes

We investigate activation mechanisms of native TRPC1/C5/C6 channels (termed TRPC1 channels) by stimulation of endothelin-1 (ET-1) receptor subtypes in freshly dispersed rabbit coronary artery myocytes using single channel recording and immunoprecipitation techniques. ET-1 evoked non-selective cation channel currents with a unitary conductance of 2.6 pS which were not inhibited by either ET(A) or ET(B) receptor antagonists, respectively BQ-123 and BQ788, when administered separately. However, in the presence of both antagonists, ET-1-evoked channel activity was abolished indicating that both ET(A) and ET(B) receptor stimulation activate this conductance. Stimulation of both ET(A) and ET(B) receptors evoked channel activity which was inhibited by the protein kinase C (PKC) inhibitor chelerythrine and by anti-TRPC1 antibodies indicating that activation of both receptor subtypes causes TRPC1 channel activation by a PKC-dependent mechanism. ET(A) receptor-mediated TRPC1 channel activity was selectively inhibited by phosphoinositol-3-kinase (PI-3-kinase) inhibitors wortmannin (50 nm) and PI-828 and by antibodies raised against phosphoinositol-3,4,5-trisphosphate (PIP(3)), the product of PI-3-kinase-mediated phosphorylation of phosphatidylinositol 4,5-bisphosphate (PIP(2)). Moreover, exogenous application of diC8-PIP(3) stimulated PKC-dependent TRPC1 channel activity. These results indicate that stimulation of ET(A) receptors evokes PKC-dependent TRPC1 channel activity through activation of PI-3-kinase and generation of PIP(3). In contrast, ET(B) receptor-mediated TRPC1 channel activity was inhibited by the PI-phospholipase C (PI-PLC) inhibitor U73122. 1-Oleoyl-2-acetyl-sn-glycerol (OAG), an analogue of diacylglycerol (DAG), which is a product of PI-PLC, also activated PKC-dependent TRPC1 channel activity. OAG-induced TRPC1 channel activity was inhibited by anti-phosphoinositol-4,5-bisphosphate (PIP(2)) antibodies and high concentrations of wortmannin (20 μm) which depleted tissue PIP(2) levels. In addition exogenous application of diC8-PIP(2) activated PKC-dependent TRPC1 channel activity. These data indicate that stimulation of ET(B) receptors evokes PKC-dependent TRPC1 activity through PI-PLC-mediated generation of DAG and requires a permissive role of PIP(2). In conclusion, we provide the first evidence that stimulation of ET(A) and ET(B) receptors activate native PKC-dependent TRPC1 channels through two distinct phospholipids pathways involving a novel action of PIP(3), in addition to PIP(2), in rabbit coronary artery myocytes