We present our timesaving joint RANS/LES approach (we originally developed it for numerical simulations of turbulent premixed combustion) to simulate flameless combustion with separate injection of gas fuel and strong...We present our timesaving joint RANS/LES approach (we originally developed it for numerical simulations of turbulent premixed combustion) to simulate flameless combustion with separate injection of gas fuel and strong exhaust gas recirculation. It is based on successive RANS/LES numerical modeling where part of the information (stationary average fields) is achieved by RANS simulations and part (instantaneous nonstationary image of the process) by LES. The latter is performed using the RANS field of mean dissipation rate to model the sub-grid turbulent viscosity in the context of the Kolmogorov theory of small-scale turbulence. We analyze flameless combustion in the FLOX? combustor where we also simulate non-premixed flame combustion used for preliminary heating of the combustor. Different regimes take place using different systems of air injection. We applied for both regimes the simple assumption of “mixed is burnt”. The main results are the following: 1) RANS simulations demonstrate for used two injection systems respectively more compact flame and distributed flameless combustion. 2)There is agreement between RANS and corresponding LES results: RANS and averaged LES profiles of the velocity and temperature are in reasonable agreement. 3) LES modeling with Kolmogorov independent on time sub-grid viscosity reproduce instantaneous image of the process including the vortex structures. Probably due to using an annular injector system for air the instantaneous field of the temperature demonstrate significant irregularity in the beginning of the burner, which in an animation looks like moving coherent structures. 4) In the joint RANS/LES approach the computer time of the LES sub-problems is much shorter than classic LES modeling due to using time independent subgrid transport coefficients and avoiding long-continued simulations, which are necessary for averaging of instantaneous LES fields. Practically in our simulations time consuming of the LES sub-problem was only several times lager then the RANS one and it makes this approach suitable for industrial applications.展开更多
Background Autophagy is critical for cellular homeostasis.Autophagy related 14(ATG14)is a key regulator of autophagy initiation;however,its role in hepatocyte survival remains poorly understood.This study aimed to inv...Background Autophagy is critical for cellular homeostasis.Autophagy related 14(ATG14)is a key regulator of autophagy initiation;however,its role in hepatocyte survival remains poorly understood.This study aimed to investigate the hepatocyte-specific function of ATG14 in vivo.Methods We generated Atg14 hepatocyte-specific knockout(HepKO)mice using adeno-associated virus to deliver thyroxine-binding globulin gene promoter-driven Cre into Atg14 floxed mice at an adult age and fed control and knockout mice with either normal chow or a Western diet.Blood and tissue samples were collected for biochemical and histological analyses.Results Atg14 HepKO mice develop severe hepatomegaly under normal dietary conditions.ATG14 deficiency leads to hepatic injury,inflammation and fibrosis.Multiple forms of cell death,including apoptosis and pyroptosis,increase significantly.When challenged with a Western diet for 4 weeks,Atg14 HepKO mice exhibit exacerbated hepatic injury,inflammation and fibrosis despite no significant lipid droplet accumulation in the liver.Transcriptomic analysis reveals upregulation of several cell death pathways,including pyroptosis,apoptosis and necroptosis.Further biochemical and microscopic analyses validate the induction of multiple cell death pathways.In addition,NLR family pyrin domain containing 3 inflammasome-mediated pyroptosis is significantly elevated in Atg14 HepKO mouse livers and ATG14-deficient hepatocytes.Conclusion Our data suggest that ATG14 is required for maintaining hepatocyte identity,survival and function and that hepatic ATG14 deficiency may lead to hepatomegaly,tissue injury,inflammation and fibrosis.展开更多
文摘We present our timesaving joint RANS/LES approach (we originally developed it for numerical simulations of turbulent premixed combustion) to simulate flameless combustion with separate injection of gas fuel and strong exhaust gas recirculation. It is based on successive RANS/LES numerical modeling where part of the information (stationary average fields) is achieved by RANS simulations and part (instantaneous nonstationary image of the process) by LES. The latter is performed using the RANS field of mean dissipation rate to model the sub-grid turbulent viscosity in the context of the Kolmogorov theory of small-scale turbulence. We analyze flameless combustion in the FLOX? combustor where we also simulate non-premixed flame combustion used for preliminary heating of the combustor. Different regimes take place using different systems of air injection. We applied for both regimes the simple assumption of “mixed is burnt”. The main results are the following: 1) RANS simulations demonstrate for used two injection systems respectively more compact flame and distributed flameless combustion. 2)There is agreement between RANS and corresponding LES results: RANS and averaged LES profiles of the velocity and temperature are in reasonable agreement. 3) LES modeling with Kolmogorov independent on time sub-grid viscosity reproduce instantaneous image of the process including the vortex structures. Probably due to using an annular injector system for air the instantaneous field of the temperature demonstrate significant irregularity in the beginning of the burner, which in an animation looks like moving coherent structures. 4) In the joint RANS/LES approach the computer time of the LES sub-problems is much shorter than classic LES modeling due to using time independent subgrid transport coefficients and avoiding long-continued simulations, which are necessary for averaging of instantaneous LES fields. Practically in our simulations time consuming of the LES sub-problem was only several times lager then the RANS one and it makes this approach suitable for industrial applications.
基金the National Institute of Diabetes and Digestive and Kidney Diseases(R01DK120689,R01DK121925,P30DK097512)the National Institute on Alcohol Abuse and Alcoholism(R01AA028506),the National Institute on Aging(R21AG072288)the National Cancer Institute(P30CA082709 and P30CA023168),the Walther Cancer Foundation and the Ricks Family Foundation.
文摘Background Autophagy is critical for cellular homeostasis.Autophagy related 14(ATG14)is a key regulator of autophagy initiation;however,its role in hepatocyte survival remains poorly understood.This study aimed to investigate the hepatocyte-specific function of ATG14 in vivo.Methods We generated Atg14 hepatocyte-specific knockout(HepKO)mice using adeno-associated virus to deliver thyroxine-binding globulin gene promoter-driven Cre into Atg14 floxed mice at an adult age and fed control and knockout mice with either normal chow or a Western diet.Blood and tissue samples were collected for biochemical and histological analyses.Results Atg14 HepKO mice develop severe hepatomegaly under normal dietary conditions.ATG14 deficiency leads to hepatic injury,inflammation and fibrosis.Multiple forms of cell death,including apoptosis and pyroptosis,increase significantly.When challenged with a Western diet for 4 weeks,Atg14 HepKO mice exhibit exacerbated hepatic injury,inflammation and fibrosis despite no significant lipid droplet accumulation in the liver.Transcriptomic analysis reveals upregulation of several cell death pathways,including pyroptosis,apoptosis and necroptosis.Further biochemical and microscopic analyses validate the induction of multiple cell death pathways.In addition,NLR family pyrin domain containing 3 inflammasome-mediated pyroptosis is significantly elevated in Atg14 HepKO mouse livers and ATG14-deficient hepatocytes.Conclusion Our data suggest that ATG14 is required for maintaining hepatocyte identity,survival and function and that hepatic ATG14 deficiency may lead to hepatomegaly,tissue injury,inflammation and fibrosis.
