Steady Magnetohydrodynamic Micropolar Fluid Flow and Heat and Mass Transfer in Permeable Channel with Thermal Radiation

The present work is devoted to the study of magnetohydrodynamic micropolar fluid flow in a permeable channel with thermal radiation. The Rosseland approximation for thermal radiation is taken into account in the modelling of heat transfer. The governing equations are expressed in non-dimensional form. The Homotopy Perturbation Method (HPM) is briefly introduced and applied to derive the solution of nonlinear equations. The effects of various involved parameters like Reynolds number, microrotation parameter and Prandtl number on flow and heat transfer are discussed. Further, their effects on Nusselt and Sherwood numbers are also investigated from the physical point of view. Analytic solutions of the problem are obtained by HPM and a numerical technique bvp4c package MATLAB is applied to predict the graphs between different parameters.

The ultimate state of turbulent permeable-channel flow

Direct numerical simulations have been performed for heat and momentum transfer in internally heated turbulent shear flow with constant bulk mean velocity and temperature, $u_{b}$ and $\theta _{b}$ , between parallel, isothermal, no-slip and permeable walls. The wall-normal transpiration velocity on the walls $y=\pm h$ is assumed to be proportional to the local pressure fluctuations, i.e. $v=\pm \beta p/\rho$ (Jiménez et al., J. Fluid Mech., vol. 442, 2001, pp. 89–117). The temperature is supposed to be a passive scalar, and the Prandtl number is set to unity. Turbulent heat and momentum transfer in permeable-channel flow for the dimensionless permeability parameter $\beta u_b=0.5$ has been found to exhibit distinct states depending on the Reynolds number $Re_b=2h u_b/\nu$ . At $Re_{b}\lesssim 10^4$ , the classical Blasius law of the friction coefficient and its similarity to the Stanton number, $St\approx c_{f}\sim Re_{b}^{-1/4}$ , are observed, whereas at $Re_{b}\gtrsim 10^4$ , the so-called ultimate scaling, $St\sim Re_b^0$ and $c_{f}\sim Re_b^0$ , is found. The ultimate state is attributed to the appearance of large-scale intense spanwise rolls with the length scale of $O(h)$ arising from the Kelvin–Helmholtz type of shear-layer instability over the permeable walls. The large-scale rolls can induce large-amplitude velocity fluctuations of $O(u_b)$ as in free shear layers, so that the Taylor dissipation law $\epsilon \sim u_{b}^{3}/h$ (or equivalently $c_{f}\sim Re_b^0$ ) holds. In spite of strong turbulence promotion there is no flow separation, and thus large-amplitude temperature fluctuations of $O(\theta _b)$ can also be induced similarly. As a consequence, the ultimate heat transfer is achieved, i.e. a wall heat flux scales with $u_{b}\theta _{b}$ (or equivalently $St\sim Re_b^0$ ) independent of thermal diffusivity, although the heat transfer on the walls is dominated by thermal conduction.

Mathematical model of solute transfer in a permeable channel with effect of variable viscosity

This paper describes a mathematical model of solute transfer in fluid flow across a permeable channel with variable viscosity, with applications to glomerular capillary blood flow. Solute transfer through the glomerular capillary wall is controlled by the difference in transcapillary hydrostatic pressure and the analogous difference in colloid osmotic pressure (Starling’s law). Using appropriate analytical and numerical approaches, the solutions of coupled equations regulating fluid flow and solute transport are found. The current study’s hydrostatic and osmotic pressure curves are qualitatively in excellent agreement with the experimental data. The effects of variable viscosity on velocity profiles, concentration profiles, and total solute clearance are seen to be substantial, and the findings are graphically depicted.

Sacubitril Ameliorates Cardiac Fibrosis Through Inhibiting TRPM7 Channel

Heart failure caused by cardiac fibrosis has become a major challenge of public health worldwide. Cardiomyocyte programmed cell death (PCD) and activation of fibroblasts are crucial pathological features, both of which are associated with aberrant Ca2+ influx. Transient receptor potential cation channel subfamily M member 7 (TRPM7), the major Ca2+ permeable channel, plays a regulatory role in cardiac fibrosis. In this study, we sought to explore the mechanistic details for sacubitril, a component of sacubitril/valsartan, in treating cardiac fibrosis. We demonstrated that sacubitril/valsartan could effectively ameliorate cardiac dysfunction and reduce cardiac fibrosis induced by isoprotereno (ISO) in vivo. We further investigated the anti-fibrotic effect of sacubitril in fibroblasts. LBQ657, the metabolite of sacubitril, could significantly attenuate transforming growth factor-β 1 (TGF-β1) induced cardiac fibrosis by blocking TRPM7 channel, rather than suppressing its protein expression. In addition, LBQ657 reduced hypoxia-induced cardiomyocyte PCD via suppression of Ca2+ influx regulated by TRPM7. These findings suggested that sacubitril ameliorated cardiac fibrosis by acting on both fibroblasts and cardiomyocytes through inhibiting TRPM7 channel.

Role of Pannexin 1 ATP-Permeable Channels in the Regulation of Signaling Pathways during Skeletal Muscle Unloading

Skeletal muscle unloading results in atrophy. We hypothesized that pannexin 1 ATP-permeable channel (PANX1) is involved in the response of muscle to unloading. We tested this hypothesis by blocking PANX1, which regulates efflux of ATP from the cytoplasm. Rats were divided into six groups (eight rats each): non-treated control for 1 and 3 days of the experiments (1C and 3C, respectively), 1 and 3 days of hindlimb suspension (HS) with placebo (1H and 3H, respectively), and 1 and 3 days of HS with PANX1 inhibitor probenecid (PRB; 1HP and 3HP, respectively). When compared with 3C group there was a significant increase in ATP in soleus muscle of 3H and 3HP groups (32 and 51%, respectively, p < 0.05). When compared with 3H group, 3HP group had: (1) lower mRNA expression of E3 ligases MuRF1 and MAFbx (by 50 and 38% respectively, p < 0.05) and MYOG (by 34%, p < 0.05); (2) higher phosphorylation of p70S6k and p90RSK (by 51 and 35% respectively, p < 0.05); (3) lower levels of phosphorylated eEF2 (by 157%, p < 0.05); (4) higher level of phosphorylated GSK3β (by 189%, p < 0.05). In conclusion, PANX1 ATP-permeable channels are involved in the regulation of muscle atrophic processes by modulating expression of E3 ligases, and protein translation and elongation processes during unloading.

Pkd2 Affects Cilia Length and Impacts LR Flow Dynamics and Dand5

The left-right (LR) field recognizes the importance of the mechanism involving the calcium permeable channel Polycystin-2. However, whether the early LR symmetry breaking mechanism is exclusively via Polycystin-2 has not been tested. For that purpose, we need to be able to isolate the effects of decreasing the levels of Pkd2 protein from any eventual effects on flow dynamics. Here we demonstrate that curly-up (cup) homozygous mutants have abnormal flow dynamics. In addition, we performed one cell stage Pkd2 knockdowns and LR organizer specific Pkd2 knockdowns and observed that both techniques resulted in shorter cilia length and abnormal flow dynamics. We conclude that Pkd2 reduction leads to LR defects that cannot be assigned exclusively to its putative role in mediating mechanosensation because indirectly, by modifying cell shape or decreasing cilia length, Pkd2 deficit affects LR flow dynamics.