No abstract

Laminar diffusion flames present an elementary configuration for investigating soot formation and validating kinetic models before these are transferred to turbulent combustors. In the present article, we present a joint experimental and modelling investigation of soot formation in a laminar co-flow burner. The diffusion flames are analysed with the aid of laser diagnostic techniques, including elastic light scattering (ELS), planar laser-induced fluorescence of OH (OH-PLIF) and line-of-sight attenuation (LOSA), to measure the spatial distribution of soot, gas phase species and the line-of-sight integrated soot volume fraction (ISVF), respectively. The experimental dataset is supplemented by location-specific TEM images of thermophoretically sampled soot particles. The simulation of the sooting flames is carried out with a recently developed discretisation method for the population balance equation (Liu and Rigopoulos, 2019, Combust. Flame 205, 506-521) that accomplishes an accurate prediction of the particle size distribution, coupled with an in-house CFD code. By minimising numerical errors, we ensure that the discrepancies on the modelling side are mainly due to kinetics and are able to carry out an investigation of alternative models. We include a complete set of soot kinetics for PAH-based nucleation and condensation, HACA-based surface growth and oxidation as well as size-dependent coagulation and aggregation, and consider three different gas phase reaction mechanisms (ABF, BBP and KM2). Based on predictions of the gas phase composition and particle size distribution of soot, modelled counterparts of the laser diagnostic signals are computed and compared with the experimental measurements. The approach of directly predicting signals circumvents the difficulties of explicitly representing the OH concentration in terms of the measured OH-PLIF data and avoids using 'hybrid' modelled and measured values to approximate the OH concentration. Moreover, the LOSA signal is directly converted to the line-of-sight ISVF instead of a measure of local soot volume fraction to avoid tomographic inversion errors. Lastly, the predicted ELS signal is computed in terms of the particle size distribution resolved by the population balance model, thus circumventing the approximation of an integral soot property using a presumed size distribution. While we cannot obtain quantitative agreement between experiments and simulations, the accuracy of the numerical approach and the direct prediction of experimental signals allow us to conduct sensitivity analyses of key empirical parameters and investigate the importance of the PAH chemistry and its influence on the competition between nucleation, condensation and surface growth.

“Two-regime-surge” is a special instability behavior of compressors, which was investigated in this paper. When the compressor operates at medium rotor speed, mild surge happens first, where the transient pressure signals show sinusoidal form with Helmholtz frequency of the compressor system. Reducing the mass flow rate, the mild surge vanishes and gets replaced by the local stall. Further reducing the mass flow rate, deep surge breaks out suddenly. During two-regime-surge, two distinct surge patterns exit and vastly narrow stable flow range, which highlights the characteristics of two-regime-surge. It is found that the impeller leading-edge stall is a necessary part of the mild surge, while the diffuser rotating stall incepts the deep surge. At higher speeds, the mild surge oscillation prompts the early occurrence of the diffuser stall so that the mild surge transforms and the deep surge happens in advance. As a result, both regimes of mild surge and deep surge are going to merge, and the stable flow range at high rotational speed is greatly narrowed. Impeller casing treatment is considered as an effective method for flow range extension because the impeller leading-edge stall is removed and the mild surge is avoided as well.

Ischemia-reperfusion injury (IRI) is an inevitable and serious clinical problem in donations after heart death (DCD) liver transplantation. Excessive sterile inflammation plays a fateful role in liver IRI. Hypothermic oxygenated perfusion (HOPE), as an emerging organ preservation technology, has a better preservation effect than cold storage (CS) for reducing liver IRI, in which regulating inflammation is one of the main mechanisms. HECTD3, a new E3 ubiquitin ligase, and TRAF3 have an essential role in inflammation. However, little is known about HECTD3 and TRAF3 in HOPE-regulated liver IRI. Here, we aimed to investigate the effects of HOPE on liver IRI in a DCD rat model and explore the roles of HECTD3 and TRAF3 in its pathogenesis. We found that HOPE significantly improved liver damage, including hepatocyte and liver sinusoidal endothelial cell injury, and reduced DCD liver inflammation. Mechanistically, both the DOC and HECT domains of HECTD3 directly interacted with TRAF3, and the catalytic Cys (C832) in the HECT domain promoted the K63-linked polyubiquitination of TRAF3 at Lys138. Further, the ubiquitinated TRAF3 at Lys138 increased oxidative stress and activated the NF-κB inflammation pathway to induce liver IRI in BRL-3A cells under hypoxia/reoxygenation conditions. Finally, we confirmed that the expression of HECTD3 and TRAF3 was obviously increased in human DCD liver transplantation specimens. Overall, these findings demonstrated that HOPE can protect against DCD liver transplantation-induced-liver IRI by reducing inflammation via HECTD3-mediated TRAF3 K63-linked polyubiquitination. Therefore, HOPE regulating the HECTD3/TRAF3 pathway is a novel target for improving IRI in DCD liver transplantation.

Hepatic ischemia–reperfusion (IR) injury is a clinical issue that can result in poor outcome and lacks effective therapies at present. Mild hypothermia (32–35°C) is a physiotherapy that has been reported to significantly alleviate IR injury, while its protective effects are attributed to multiple mechanisms, one of which may be the regulation of fatty acid β-oxidation (FAO). The aim of the present study was to investigate the role and underlying mechanisms of FAO in the protective effects of mild hypothermia. We used male mice to establish the experimental models as previously described. In brief, before exposure to in situ ischemia for 1 h and reperfusion for 6 h, mice received pretreatment with mild hypothermia for 2 h and etomoxir (inhibitor of FAO) or leptin (activator of FAO) for 1 h, respectively. Then, tissue and blood samples were collected to evaluate the liver injury, oxidative stress, and changes in hepatic FAO. We found that mild hypothermia significantly reduced the hepatic enzyme levels and the score of hepatic pathological injury, hepatocyte apoptosis, oxidative stress, and mitochondrial injury. In addition, the expression of the rate-limiting enzyme (CPT1a) of hepatic FAO was downregulated almost twofold by IR, while this inhibition could be significantly reversed by mild hypothermia. Experiments with leptin and etomoxir confirmed that activation of FAO could also reduce the hepatic enzyme levels and the score of hepatic pathological injury, hepatocyte apoptosis, oxidative stress, and mitochondrial injury induced by IR, which had the similar effects to mild hypothermia, while inhibition of FAO had negative effects. Furthermore, mild hypothermia and leptin could promote the phosphorylation of JAK2/STAT3 and upregulate the ratio of BCL-2/BAX to suppress hepatocyte apoptosis. Thus, we concluded that FAO played an important role in hepatic IR injury and mild hypothermia attenuated hepatic IR injury mainly via the regulation of JAK2/STAT3-CPT1a-dependent FAO.