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In order to predict the pressure drop and the mean void fraction for bubbly flows in packed beds, a new one-dimensional (l-D) model is proposed. The balance equations for both phases are derived from local Eulerian two-fluid equations which are spatially averaged at a mesoscale, that is, at a length-scale large compared with the microscale that characterizes the fixed bed. This model that differs from previous mechanistic models, has been supplemented by closure laws for the liquid-solid and the gas-liquid interactions, those structures account for the flow dynamics at the pore scale. It is first experimentally demonstrated that, in dilute conditions, the bubble-size distribution only depends on the pore size, when the later is smaller than the capillary length scale. It is also shown that the mean-bubble dynamics is similar to that of a slug, with a relative velocity at mesoscale linearly increasing with the liquid superficial velocity. Besides, that relative velocity monotonically increases with the gas flow rate ratio, a behavior that can be attributed to the formation of preferential paths for the gas phase. Concerning the liquid-solid interactions, the two-phase flow pressure drop scaled by its single-phase flow counterpart at the same superficial liquid velocity is predicted to linearly increase with the void fraction, with a prefactor evolving with the Capillary number. These closures prove consistent with available experiments, both in upward and in downward situations. Although these proposals deserve to be further tested over an extended range of flow parameters, this model paves the way to reasonably accurate predictions of bubbly flows in packed beds able to account for refined parameters related with the flow dynamics. [ABSTRACT FROM AUTHOR]

Background The SNRK (sucrose-nonfermenting-related kinase) enzyme is critical for cardiac function. However, the underlying cause for heart failure observed in Snrk cardiac conditional knockout mouse is unknown. Methods and Results Previously, 6-month adult mice knocked out for Snrk in cardiomyocytes (CMs) displayed left ventricular dysfunction. Here, 4-month adult mice, on angiotensin II (Ang II) infusion, show rapid decline in cardiac systolic function, which leads to heart failure and death in 2 weeks. These mice showed increased expression of nuclear factor κ light chain enhancer of activated B cells (NF-κB), inflammatory signaling proteins, proinflammatory proteins in the heart, and fibrosis. Interestingly, under Ang II infusion, mice knocked out for Snrk in endothelial cells did not show significant systolic or diastolic dysfunction. Although an NF-κB inflammation signaling pathway was increased in Snrk knockout endothelial cells, this did not lead to fibrosis or mortality. In hearts of adult mice knocked out for Snrk in CMs, we also observed NF-κB pathway activation in CMs, and an increased presence of Mac2 + macrophages was observed in basal and Ang II-infused states. In vitro analysis of Snrk knockdown HL-1 CMs revealed similar upregulation of the NF-κB signaling proteins and proinflammatory proteins that was exacerbated on Ang II treatment. The Ang II-induced NF-κB pathway-mediated proinflammatory effects were mediated in part through protein kinase B or AKT, wherein AKT inhibition restored the proinflammatory signaling protein levels to baseline in Snrk knockdown HL-1 CMs. Conclusions During heart failure, SNRK acts as a cardiomyocyte-specific repressor of cardiac inflammation and fibrosis.