CFD ANALYSIS OF LAMINAR FORCED CONVECTIVE HEAT TRANSFER FOR TiO2/WATER NANOFLUID IN A SEMI-CIRCULAR CROSS-SECTIONED MICRO-CHANNEL

In this study, forced convection flow and heat transfer characteristics of TiO2/water nanofluid flow with different nanoparticle volume fractions (1.0\%, 2.0\%, 3.0\% and 4.0\%) in semi - circular cross - sectioned micro - channel was numerically investigated. The three - dimensional study was conducted under steady state laminar flow condition where Reynolds number changing from 100 to 1000. CFD model has been generated by using ANSYS FLUENT 15.0 software based on finite volume method. The flow was under hydrodynamically and thermally developing flow condition. Uniform surface heat flux boundary condition was applied at the bottom surface of the micro - channel. The average and local Nusselt number and Darcy friction factor values were obtained using numerical results. Also, the effects of using nanofluid on local values of Nusselt number and Darcy friction factor were investigated. Numerical results indicate that the increasing of nanoparticle volume fraction of nanofluid, the average Nusselt number increases; however, there is no significant variation in average Darcy friction factor

Granzyme B is expressed in mouse mast cells in vivo and in vitro and causes delayed cell death independent of perforin

Mast cells respond to pathogens and allergens by secreting a vast array of preformed and newly synthesized mediators, including enzymes, vasoactive amines, lipid mediators, cytokines and chemokines, thereby affecting innate and adaptive immune responses and pathogenesis. Here, we present evidence that skin-, but not lung-associated primary mast cells as well as in vitro-differentiated bone marrow-derived mast cells (BMMC) express granzyme (gzm) B, but not gzmA or perforin (perf). GzmB is associated with cytoplasmic granules of BMMC and secreted after Fcε-receptor-mediated activation. BMMC from wild type but not gzmB-deficient mice cause cell death in susceptible adherent target cells, indicating that the perf-independent cytotoxicity of BMMC is executed by gzmB. Furthermore, gzmB induces a disorganization of endothelial cell-cell contacts. The data suggest that activated mast cells contribute, via secreted gzmB, to cell death, increased vascular permeability, leukocyte extravasation and subsequent inflammatory processes in affected tissues

Granzyme B is expressed in mouse mast cells in vivo and in vitro and causes delayed cell death independent of perforin

Mast cells respond to pathogens and allergens by secreting a vast array of preformed and newly synthesized mediators, including enzymes, vasoactive amines, lipid mediators, cytokines and chemokines, thereby affecting innate and adaptive immune responses and pathogenesis. Here, we present evidence that skin-, but not lung-associated primary mast cells as well as in vitro-differentiated bone marrow-derived mast cells (BMMC) express granzyme (gzm) B, but not gzmA or perforin (perf). GzmB is associated with cytoplasmic granules of BMMC and secreted after Fcε-receptor-mediated activation. BMMC from wild type but not gzmB-deficient mice cause cell death in susceptible adherent target cells, indicating that the perf-independent cytotoxicity of BMMC is executed by gzmB. Furthermore, gzmB induces a disorganization of endothelial cell-cell contacts. The data suggest that activated mast cells contribute, via secreted gzmB, to cell death, increased vascular permeability, leukocyte extravasation and subsequent inflammatory processes in affected tissues