Search

This paper presents a numerical simulation analysis of the flow and combustion characteristics of a fuel-rich LOX (liquid oxygen)/kerosene gas generator in an ATR (air turbo rocket) engine, examining the effects of local parameters on the combustion flow field and performance. The analysis considers variations in unit injector mixing ratios and unit mass flow rates. The results indicate that as the mixing ratio in the inner-ring injectors increases (while the mixing ratio in the middle-ring injectors decreases), the oxygen concentration area near the axis zone and the 50% radius zone of the gas generator expands. Conversely, the kerosene concentration area near the axis zone decreases while gradually increasing near the 50% radius zone. In the flow direction section, there is an inverse relationship between the variation trend of local temperature and the oxygen concentration in the local area. As the oxygen concentration increases, the temperature decreases. The temperature distribution across the cross-section of the gas generator exhibits a circular pattern. When the mixing ratio (or mass flow rates) of the unit injector are perfectly balanced, the temperature distribution becomes highly uniform. A larger disparity in flow rate between the inner ring injector and the middle ring injector leads to a lower combustion efficiency. This effect differs from the effect of the mixing ratio difference between the two injector rings. Increasing the mixing ratio in the inner-ring injectors (or decreasing the mixing ratio in the middle-ring injectors) initially leads to a rise in combustion efficiency, followed by a subsequent decline. The maximum combustion efficiency of 89.10% is achieved when the mixing ratio is set to Km-1 = 0.7 and Km-2 = 2.79, respectively. Increasing the flow rate in the inner-ring injectors (or decreasing the flow rate in the middle-ring injectors) initially leads to an improvement in combustion efficiency, followed by a subsequent reduction. The maximum combustion efficiency of 86.13% is achieved when the mass flow rate is set to m-1 = m-2 = 0.1 kg/s. [ABSTRACT FROM AUTHOR]

Copyright of Transactions of Nanjing University of Aeronautics & Astronautics is the property of Editorial Department of Journal of Nanjing University of Aeronautics & Astronautics and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

It is an obstacle to precisely manipulate a doped heteroatom into a desired position in a metal nanocluster. Herein, we overcome this difficulty to obtain Pt1Au37(SCH2PhtBu)24 and Pt2Au36(SCH2PhtBu)24 nanoclusters via controllably doping Pt atoms into the kernels of Au38(SCH2PhtBu)24. We reveal that asymmetrical doping of one Pt atom into either of the cores of Au38(SCH2PhtBu)24 elevates the relative energy of the HOMO (highest occupied molecular orbital) accompanied by one valence electron loss of Pt1Au37(SCH2PhtBu)24, compared to Au38(SCH2PhtBu)24 with 14 electrons, while symmetrical doping of two Pt atoms into the cores of Au38(SCH2PhtBu)24 narrows the HOMO–LUMO gap (LUMO: lowest unoccupied molecular orbital) of Pt2Au36(SCH2PhtBu)24 with two valence electrons less. Consequently, Pt1Au37(SCH2PhtBu)24 shows an electron‐spin‐induced high activity for CO2 electroreduction, whereas Pt2Au36(SCH2PhtBu)24 is least efficient and Au38(SCH2PhtBu)24 has a decent performance. [ABSTRACT FROM AUTHOR]

Regulatory T (Treg) cells are critical in preventing aberrant immune responses. Posttranscriptional control of gene expression by microRNA (miRNA) has recently emerged as an essential genetic element for Treg cell function. Here, we report that mice with Treg cell–specific ablation of miR-142 (hereafter Foxp3CremiR-142fl/fl mice) developed a fatal systemic autoimmune disorder due to a breakdown in peripheral T-cell tolerance. Foxp3CremiR-142fl/fl mice displayed a significant decrease in the abundance and suppressive capacity of Treg cells. Expression profiling of miR-142–deficient Treg cells revealed an up-regulation of multiple genes in the interferon gamma (IFNγ) signaling network. We identified several of these IFNγ-associated genes as direct miR-142-3p targets and observed excessive IFNγ production and signaling in miR-142–deficient Treg cells. Ifng ablation rescued the Treg cell homeostatic defect and alleviated development of autoimmunity in Foxp3CremiR-142fl/fl mice. Thus, our findings implicate miR-142 as an indispensable regulator of Treg cell homeostasis that exerts its function by attenuating IFNγ responses. This study identifies microRNA-142 as a central regulator of the development, homeostasis and function of regulatory T cells. Mechanistically, the miR-142-3p isoform controls regulatory T cell homeostasis and immune tolerance by attenuating IFNγ responses. [ABSTRACT FROM AUTHOR]

The evolution behavior of anode gas during aluminum electrolysis has been a hot spot of research for energy saving and process control. In the present work, the bubble evolution behavior during aluminum electrolysis was investigated using a lab-scale see-though cell. The bubble evolution characters on an 11 cm2 (bottom surface area) flat anode, an 11 cm2 slotted anode, and a 50 cm2 flat anode were investigated with statistical analysis, respectively. The results showed that bubbles tended to generate and adhere to certain regions on the anode surface due to the heterogeneity of the carbon material, and the adhering regions moved when current density was increased. The anode slot lowered the actual current density on the anode significantly by reducing the anode bubble coverage. Influenced by the group effect of bubbles, the 50 cm2 flat anode behavior constituted a lower bubble coverage rate, lower average bubble size, and lower actual current density than the 11 cm2 flat anode. [ABSTRACT FROM AUTHOR]

It has been established that the primary form of neuron death following hypoxic ischemic brain damage is apoptosis. Imbalances in the expression of genes in the B-cell lymphoma 2 (Bcl-2) family located in the mitochondrion, and in the expression of their encoded proteins, are key events in the mitochondrial apoptotic pathway, which lead to damage of cellular structure and function. The present study aimed to explore the regulatory effect of retinoic acid receptor α (RAR-α) on the apoptosis of PC12 cells induced by oxygen-glucose deprivation (OGD) in the retinoic acid signaling pathway. Recombinant adenovirus RAR-α small interfering RNA (Ad-siRAR-α) was used to transduce PC12 cells, and the efficiency of RAR-α expression inhibition was detected by semi-quantitative reverse transcription polymerase chain reaction (RT-PCR). An empty adenovirus vector was transfected in PC12 cells, which were used as the control. Flow cytometry with Annexin V-propidium iodide (PI) and fluorescence probe JC-1 staining was used to detect the apoptosis rate and mitochondrial transmembrane potential (MMP), respectively, of PC12 cells after transduction with Ad-siRAR-α. Furthermore, the expression levels of key genes in the RAR-α and mitochondrial apoptotic pathway, Bcl-2 and Bcl-2-associated protein (Bax) were analyzed by RT-quantitative (q)PCR and western blot analysis. RAR-α mRNA expression was observed to be decreased in PC12 cells following OGD-induced injury, and this decrease can be reversed by 4 µmol/l ATRA treatment. After 36 h transfection with Ad-siRAR-α, RAR-α gene expression was significantly inhibited compared with the control (P<0.05). The results of Annexin V-PI, fluorescence probe JC-1 staining and flow cytometry demonstrated that the apoptosis rate significantly increased and MMP significantly decreased in OGD-induced PC12 cells following transduction with Ad-siRAR-α compared with the control (both P<0.05). RT-qPCR and western blot analysis indicated that Bax expression was significantly increased and Bcl-2 expression was significantly decreased in PC12 cells transduced with Ad-siRAR-α after OGD-induced injury at the mRNA and protein level (P<0.05). In conclusion, Ad-siRAR-α transduction could promote apoptosis in OGD-induced PC12 cells. This suggests that the expression of Bax and Bcl-2 in the mitochondrial apoptosis signaling pathway is, at least in part, mediated by RAR-α expression, thereby indicating that RAR-α expression exerts an anti-apoptotic effect on OGD-damaged PC12 cells. [ABSTRACT FROM AUTHOR]