The quadrant analysis of the intense tangential Reynolds stress in plane turbulent channels is generalized to three-dimensional structures (Qs), with special emphasis on the logarithmic and outer layers. Wall-detached Qs are background stress fluctuations. They are small and isotropically oriented, and their contributions to the mean stress cancel. Wall-attached Qs are larger, and carry most of the mean Reynolds stresses. They form a family of roughly self-similar objects that become increasingly complex away from the wall, resembling the vortex clusters in del Álamo et al. (J. Fluid Mech., vol. 561, 2006, pp. 329–358). Individual Qs have fractal dimensions of the order of $D= 2$, slightly fuller than the clusters. They can be described as ‘sponges of flakes’, while vortex clusters are ‘sponges of strings’. The number of attached Qs decays away from the wall, but the fraction of the stress that they carry is independent of their sizes. A substantial fraction of the stress resides in a few large objects extending beyond the centreline, reminiscent of the very large structures of several authors. The predominant logarithmic-layer structure is a side-by-side pair of a sweep (Q4) and an ejection (Q2), with an associated cluster, and shares dimensions and stresses with the conjectured attached eddies of Townsend (J. Fluid Mech., vol. 11, 1961, pp. 97–120). Those attached eddies tend to be aligned streamwise from each other, located near the side walls between the low- and high-velocity large-scale streaks, but that organization does not extend far enough to explain the very long structures in the centre of the channel.

The minimal simulation boxes of the buffer layer of turbulent channels can be extended to the logarithmic and outer regions, where they contain a segment of streamwise velocity streak, and a vortex cluster. Smaller boxes restrict "healthy" turbulence closer to the wall, to a layer whose thickness scales with the spanwise size of the box. These minimal boxes burst quasiperiodically, and the bursting period for a band of wall distances grows linearly away from the wall, independently of the box size within the limits within which turbulence is well represented.

The nocturnal atmospheric boundary layer (ABL) poses several challenges to standard turbulence and dispersion models, since the stable stratification imposed by the radiative cooling of the ground modifies the flow turbulence in ways that are not yet completely understood. In the present work we perform direct numerical simulation of a turbulent open channel flow with a constant (cooling) heat flux imposed at the ground. This configuration provides a very simplified model for the surface layer at night. As a result of the ground cooling, the Reynolds stresses and the turbulent fluctuations near the ground re-adjust on times of the order of L/u τ , where L is the Obukhov length scale and u τ is the friction velocity. For relatively weak cooling turbulence survives, but when Re L = Lu τ /ν 100 turbulence collapses, a situation that is also observed in the ABL. This criterion, which can be locally measured in the field, is justified in terms of the scale separation between the largest and smallest structures of the dynamic sublayer.

The dynamics of the sublayer and buffer regions of wall-bounded turbulent flows are analysed using autonomous numerical simulations in which the outer flow, and on some occasions specific wavelengths, are masked. The results are compared with a turbulent channel flow at moderate Reynolds number. Special emphasis is put on the largest flow scales. It is argued that in this region there are two kinds of large structures: long and narrow ones which are endogenous to the wall, in the sense of being only slightly modified by the presence or absence of an outer flow, and long and wide structures which extend to the outer flow and which are very different in the two cases. The latter carry little Reynolds stress near the wall in full simulations, and are largely absent from the autonomous ones. The former carry a large fraction of the stresses in the two cases, but are shown to be quasi-linear passive wakes of smaller structures, and they can be damped without modifying the dynamics of other spectral ranges. They can be modelled fairly accurately as being infinitely long, and it is argued that this is why good statistics are obtained in short or even in minimal simulation boxes. It is shown that this organization implies that the scaling of the near-wall streamwise fluctuations is anomalous.

Atrial fibrillation (AF) alters left atrial (LA) hemodynamics, which can lead to thrombosis in the left atrial appendage (LAA), systemic embolism and stroke. A personalized risk-stratification of AF patients for stroke would permit improved balancing of preventive anticoagulation therapies against bleeding risk. We investigated how LA anatomy and function impact LA and LAA hemodynamics, and explored whether patient-specific analysis by computational fluid dynamics (CFD) can predict the risk of LAA thrombosis. We analyzed 4D-CT acquisitions of LA wall motion with an in-house immersed-boundary CFD solver. We considered six patients with diverse atrial function, three with either a LAA thrombus (removed digitally before running the simulations) or a history of transient ischemic attacks (LAAT/TIA-pos), and three without a LAA thrombus or TIA (LAAT/TIA-neg). We found that blood inside the left atrial appendage of LAAT/TIA-pos patients had marked alterations in residence time and kinetic energy when compared with LAAT/TIA-neg patients. In addition, we showed how the LA conduit, reservoir and booster functions distinctly affect LA and LAA hemodynamics. Finally, fixed-wall and moving-wall simulations produced different LA hemodynamics and residence time predictions for each patient. Consequently, fixed-wall simulations risk-stratified our small cohort for LAA thrombosis worse than moving-wall simulations, particularly patients with intermediate LAA residence time. Overall, these results suggest that both wall kinetics and LAA morphology contribute to LAA blood stasis and thrombosis.

The interaction between the wall and the core region of turbulent channels is studied using direct numerical simulations at friction Reynolds number ${\hbox{\it Re}}_{\tau} \approx 630$. In these simulations the near-wall energy cycle is effectively removed, replacing the smooth-walled boundary conditions by prescribed velocity disturbances with non-zero Reynolds stress at the walls. The profiles of the first- and second-order moments of the velocity are similar to those over rough surfaces, and the effect of the boundary condition on the mean velocity profile is described using the equivalent sand roughness. Other effects of the disturbances on the flow are essentially limited to a layer near the wall whose height is proportional to a length scale defined in terms of the additional Reynolds stress. The spectra in this roughness sublayer are dominated by the wavenumber of the velocity disturbances and by its harmonics. The wall forcing extracts energy from the flow, while the normal equilibrium between turbulent energy production and dissipation is restored in the overlap region. It is shown that the structure and the dynamics of the turbulence outside the roughness sublayer remain virtually unchanged, regardless of the nature of the wall. The detached eddies of the core region only depend on the mean shear, which is not modified beyond the roughness sublayer by the wall disturbances. On the other hand, the large scales that are correlated across the whole channel scale with $U_{\hbox{\scriptsize{\it LOG}}}=u_{\tau}\kappa^{-1}\log({\hbox{\it Re}}_\tau)$, both in smooth- and in rough-walled flows. This velocity scale can be interpreted as a measure of the velocity difference across the log layer, and it is used to modify the scaling proposed and validated by del Álamo et al. (J. Fluid Mech., vol. 500, 2004, p. 135) for smooth-walled flows.

Acetaldehyde (Ac), the main metabolite of ethanol oxidation, is a very reactive compound involved in alcohol-induced liver damage. In the present work, we studied the effect of Ac in mitochondria functionality. Mitochondria from Wistar rats were isolated and treated with Ac. Ac decreased respiratory control by 50% which was associated with a decrease in adenosine triphosphate content (28.5%). These results suggested that Ac could be inducing changes in cell redox status. We determined protein oxidation, superoxide dismutase (SOD) activity, and glutathione ratio, indicating that Ac induced an enhanced oxidation of proteins and a decrease in SOD activity (90%) and glutathione/oxidized GSH ratio (36%). The data suggested that Ac-induced oxidative stress mediated by mitochondria dysfunction can lead to cell sensitization and to a second oxidative challenge. We pretreated hepatocytes with Ac followed by treatment with antimycin A, and this experiment revealed a noticeable decrease in cell viability, determined by neutral red assay, in comparison with cells treated with Ac alone. Our data demonstrate that Ac impairs mitochondria functionality generating oxidative stress that sensitizes cells to a second damaging signal contributing to the development of alcoholic liver disease.

The vortex clusters in the turbulent outer region of rough- and smooth-walled channels, and their associated velocity structures, are compared using data from numerical experiments at friction Reynolds numbers Reτ ≤ 674. The results indicate that the roughness of the wall does not affect their properties, particularly the existence of wall-detached and wall-attached populations, and the self-similar size distribution of the latter. The average flow field conditioned to the attached clusters reveals similar conical structures of low streamwise velocity for the rough- and smooth-walled cases, which eventually grow into the global modes previously identified from spectral analysis. We conclude that the vortex clusters of the turbulent outer region either originate away from the wall, or quickly forget their origin, in agreement with Townsend's similarity hypothesis.