A numerical simulation is performed for thermal instability and heat transfer of viscoelastic fluids in bounded porous media under the bottom constant heat flux boundary condition. The results for six different combinations of relaxation and retardation times demonstrate the existence of the thermal instability induced flow bifurcation. It is found that the increase of the relaxation time can enhance the heat transfer efficiency by disturbing the fluid flow and facilitating the bifurcation. The increase of the retardation time can stabilize the flow and postpone the bifurcation, leading to simpler flow pattern and lower heat transfer rate.
The effects of two viscoelastic parameters on the thermal convection of a viscoelastic Oldroyd-B fluid in an open-top porous square box with constant heat flux are investigated. The results show that the increase of relaxation time is able to destabilize the fluid flow leading to a higher heat transfer rate, while the increase of retardation time tends to stabilize the flow and suppress the heat transfer. The flow bifurcation appears earlier with the increase of the relaxation time and the decrease of the retardation time, re- suiting in more complicated flow patterns in the porous medium.
The mitochondria play essential roles in both intracellular calcium and reactive oxygen species signaling.As a newly discovered universal and fundamental mitochondrial phenomenon,superoxide flashes reflect transient bursts of superoxide production in the matrix of single mitochondria.Whether and how the superoxide flash activity is regulated by mitochondrial calcium remain largely unknown.Here we demonstrate that elevating mitochondrial calcium either by the calcium ionophore ionomycin or by increasing the bathing calcium in permeabilized HeLa cells increases superoxide flash incidence,and inhibition of the mitochondrial calcium uniporter activity abolishes the flash response.Quantitatively,the superoxide flash incidence is correlated to the steady-state mitochondrial calcium elevation with 1.7-fold increase per 1.0?F/F0 of Rhod-2 signal.In contrast,large mitochondrial calcium transients(e.g.,peak△F/F0~2.8,duration^2 min)in the absence of steady-state elevations failed to alter the flash activity.These results indicate that physiological levels of sustained,but not transient,mitochondrial calcium elevation acts as a potent regulator of superoxide flashes,but its mechanism of action likely involves a multi-step,slow-onset process.
In cardiac myocytes,the sarcoplasmic reticulum(SR)is the main storage organelle of free Ca^(2+).The concentration of free Ca^(2+)in the SR is 0.5–1.0 mmol/L and is 2–3 orders of magnitude greater than that in the cytosol.The SR is composed of interconnected cisternae(junctional SR,i.e.,JSR)and tubules(free SR network,i.e.,FSR)that extend throughout the cytosol[1].Ca^(2+)is released from the JSR into the cytosol via Ca^(2+)release units(CRUs,
Jinghui LiWenjun XieXi ChenYunlong HuoHeping ChengWenchang Tan
