Fully-coupled modeling and analysis of the influence of anti-icing bleed air system of engine inlet duct on compressor performance

A fully-coupled method that integrates the compressor, inlet duct and anti-icing bleed air system (AI-BAS) was established to offer a quick prediction of the effects of anti-icing bleeding on compressor performance, facilitating the development of a fully-coupled AI-BAS model and a thermodynamic cycle model for gas turbine engines. While the flow within the inlet duct was solved by 3-D numerical simulation, the AI-BAS was simulated by a reduced-order model and the thermodynamic performance of the compressor was estimated by a parallel-compressor method. Comparison with the results by the full-annular CFD simulation suggested that the proposed fully coupled method can adeptly predict the effects of inflow distortion on compressor performance. In this study, as the increase of anti-icing bleed air ratio, the distortion on AIP and the resulted performance degradation of compressor becomes obvious, especially the surge margin. In the fully coupled modeling with AI-BAS, both the bleed air ratio and temperature of discharged bleed air increase with the compressor pressure ratio. The variation of bleed air ratio reaches nearly 1 %. The compressor's operating point is observed to traverse among lines representing constant bleed air flow ratio, which cannot be captured by the classical bleed air model

Influence of Shock Wave on Loss and Breakdown of Tip-Leakage Vortex in Turbine Rotor with Varying Backpressure

In modern turbine rotors, tip-leakage flow is a common phenomenon that accounts for about 1/3 of the stage loss. Studies show that as the imposed load increases, a shock wave appears in the tip region, which causes a significant interference on the leakage vortex. In the present study, numerical simulations are carried out to investigate the influence of the shock wave on the loss and breakdown of the tip-leakage vortex. The obtained results indicate that with no effective control on the flow, the loss of the leakage vortex has an approximate exponential growth up to about 10 times as the outlet Mach number increases from 0.67 to 1.15 and the corresponding proportion in the total loss increases sharply to 30.2%. It is found that the stagnation position of the breakdown changes with the backpressure and the amplitude of variation along the axial direction is up to 0.13 Cx. It is inferred that the breakdown of the leakage vortex core may be affected by the periodical passing of downstream blade and the induced pressure fluctuation may result in additional vibration in this rotor blade. The leakage vortex is unstable in supersonic flow with a shock wave and it may transfer to a flow with a low-velocity bubble in its core region. It is concluded that the leakage vortex breakdown mainly originates from interferences of the shock wave, while the internal cause of such breakdown is the centrifugal instability of the vortex

A critical GxxxA motif in the γ6 calcium channel subunit mediates its inhibitory effect on Cav3.1 calcium current

The eight members of the calcium channel γ subunit family are integral membrane proteins that regulate the expression and behaviour of voltage and ligand gated ion channels. While a subgroup consisting of γ2, γ3, γ4 and γ8 (the TARPs) modulate AMPA receptor localization and function, the γ1 and γ6 subunits conform to the original description of these proteins as regulators of voltage gated calcium channels. We have previously shown that the γ6 subunit is highly expressed in atrial myocytes and that it is capable of acting as a negative modulator of low voltage activated calcium current. In this study we extend our understanding of γ6 subunit modulation of low voltage activated calcium current. Using engineered chimeric constructs, we demonstrate that the first transmembrane domain (TM1) of γ6 is necessary for its inhibitory effect on Cav3.1 current. Mutational analysis is then used to identify a unique GxxxA motif within TM1 that is required for the function of the subunit strongly suggesting the involvement of helix–helix interactions in its effects. Results from co-immunoprecipitation experiments confirm a physical association of γ6 with the Cav3.1 channel in both HEK cells and atrial myocytes. Single channel analysis reveals that binding of γ6 reduces channel availability for activation. Taken together, the results of this study provide both a molecular and a mechanistic framework for understanding the unique ability of the γ6 calcium channel subunit to modulate low voltage activated (Cav3.1) calcium current density

Regulation of the Putative TRPV1t Salt Taste Receptor by Phosphatidylinositol 4, 5-Bisphosphate

Regulation of the putative amiloride and benzamil (Bz)-insensitive TRPV1t salt taste receptor by phosphatidylinositol 4,5-bisphosphate (PIP2) was studied by monitoring chorda tympani (CT) taste nerve responses to 0.1 M NaCl solutions containing Bz (5 × 10−6 M; a specific ENaC blocker) and resiniferatoxin (RTX; 0–10 × 10−6 M; a specific TRPV1 agonist) in Sprague-Dawley rats and in wildtype (WT) and TRPV1 knockout (KO) mice. In rats and WT mice, RTX elicited a biphasic effect on the NaCl + Bz CT response, increasing the CT response between 0.25 × 10−6 and 1 × 10−6 M. At concentrations >1 × 10−6 M, RTX inhibited the CT response. An increase in PIP2 by topical lingual application of U73122 (a phospholipase C blocker) or diC8-PIP2 (a short chain synthetic PIP2) inhibited the control NaCl + Bz CT response and decreased its sensitivity to RTX. A decrease in PIP2 by topical lingual application of phenylarsine oxide (a phosphoinositide 4 kinase blocker) enhanced the control NaCl + Bz CT response, increased its sensitivity to RTX stimulation, and inhibited the desensitization of the CT response at RTX concentrations >1 × 10−6 M. The ENaC-dependent NaCl CT responses were not altered by changes in PIP2. An increase in PIP2 enhanced CT responses to sweet (0.3 M sucrose) and bitter (0.01 M quinine) stimuli. RTX produced the same increase in the Bz-insensitive Na+response when present in salt solutions containing 0.1 M NaCl + Bz, 0.1 M monosodium glutamate + Bz, 0.1 M NaCl + Bz + 0.005 M SC45647, or 0.1 M NaCl + Bz + 0.01 M quinine. No effect of RTX was observed on CT responses in WT mice and rats in the presence of the TRPV1 blocker N-(3-methoxyphenyl)-4-chlorocinnamide (1 × 10−6 M) or in TRPV1 KO mice. We conclude that PIP2 is a common intracellular effector for sweet, bitter, umami, and TRPV1t-dependent salt taste, although in the last case, PIP2 seems to directly regulate the taste receptor protein itself, i.e., the TRPV1 ion channel or its taste receptor variant, TRPV1t

The K+-H+ Exchanger, Nigericin, Modulates Taste Cell pH and Chorda Tympani Taste Nerve Responses to Acidic Stimuli

The relationship between acidic pH, taste cell pHi, and chorda tympani (CT) nerve responses was investigated before and after incorporating the K+-H+ exchanger, nigericin, in the apical membrane of taste cells. CT responses were recorded in anesthetized rats in vivo, and changes in pHi were monitored in polarized fungiform taste cells in vitro. Under control conditions, stimulating the tongue with 0.15 M potassium phosphate (KP) or 0.15 M sodium phosphate (NaP) buffers of pHs between 8.0 and 4.6, KP or NaP buffers did not elicit a CT response. Post-nigericin (500 × 10−6 M), KP buffers, but not NaP buffers, induced CT responses at pHs ≤ 6.6. The effect of nigericin was reversed by the topical lingual application of carbonyl cyanide 3-chloro-phenylhydrazone, a protonophore. Post-nigericin (150 × 10−6 M), KP buffers induced a greater decrease in taste cell pHi relative to NaP buffers and to NaP and KP buffers under control conditions. A decrease in pHi to about 6.9 induced by KP buffers was sufficient to elicit a CT response. The results suggest that facilitating apical H+ entry via nigericin decreases taste cell pHi and demonstrates directly a strong correlation between pHi and the magnitude of the CT response

Involvement of NADPH-Dependent and cAMP-PKA Sensitive H+ Channels in the Chorda Tympani Nerve Responses to Strong Acids

To investigate if chorda tympani (CT) taste nerve responses to strong (HCl) and weak (CO2 and acetic acid) acidic stimuli are dependent upon NADPH oxidase–linked and cAMP-sensitive proton conductances in taste cell membranes, CT responses were monitored in rats, wild-type (WT) mice, and gp91phox knockout (KO) mice in the absence and presence of blockers (Zn2+ and diethyl pyrocarbonate [DEPC]) or activators (8-(4-chlorophenylthio)-cAMP; 8-CPT-cAMP) of proton channels and activators of the NADPH oxidase enzyme (phorbol 12-myristate 13-acetate [PMA], H2O2, and nitrazepam). Zn2+ and DEPC inhibited and 8-CPT-cAMP, PMA, H2O2, and nitrazepam enhanced the tonic CT responses to HCl without altering responses to CO2 and acetic acid. In KO mice, the tonic HCl CT response was reduced by 64% relative to WT mice. The residual CT response was insensitive to H2O2 but was blocked by Zn2+. Its magnitude was further enhanced by 8-CPT-cAMP treatment, and the enhancement was blocked by 8-CPT-adenosine-3′-5′-cyclic monophospho-rothioate, a protein kinase A (PKA) inhibitor. Under voltage-clamp conditions, before cAMP treatment, rat tonic HCl CT responses demonstrated voltage-dependence only at ±90 mV, suggesting the presence of H+ channels with voltage-dependent conductances. After cAMP treatment, the tonic HCl CT response had a quasi-linear dependence on voltage, suggesting that the cAMP-dependent part of the HCl CT response has a quasi-linear voltage dependence between +60 and −60 mV, only becoming sigmoidal when approaching +90 and −90 mV. The results suggest that CT responses to HCl involve 2 proton entry pathways, an NADPH oxidase–dependent proton channel, and a cAMP-PKA sensitive proton channel