7 research outputs found
Instabilities in the wake of an inclined prolate spheroid
We investigate the instabilities, bifurcations and transition in the wake
behind a 45-degree inclined 6:1 prolate spheroid, through a series of direct
numerical simulations (DNS) over a wide range of Reynolds numbers (Re) from 10
to 3000. We provide a detailed picture of how the originally symmetric and
steady laminar wake at low Re gradually looses its symmetry and turns unsteady
as Re is gradually increased. Several fascinating flow features have first been
revealed and subsequently analysed, e.g. an asymmetric time-averaged flow
field, a surprisingly strong side force etc. As the wake partially becomes
turbulent, we investigate a dominating coherent wake structure, namely a
helical vortex tube, inside of which a helical symmetry alteration scenario was
recovered in the intermediate wake, together with self-similarity in the far
wake.Comment: Book chapter in "Computational Modeling of Bifurcations and
Instabilities in Fluid Dynamics (A. Gelfgat ed.)", Springe
The zebrafish galectins Drgal1-L2 and Drgal3-L1 bind in vitro to the infectious hematopoietic necrosis virus (IHNV) glycoprotein and reduce viral adhesion to fish epithelial cells
Metabolic Plasticity in Resting and Thrombin Activated Platelets
Platelet thrombus formation includes several integrated processes involving aggregation, secretion of granules, release of arachidonic acid and clot retraction, but it is not clear which metabolic fuels are required to support these events. We hypothesized that there is flexibility in the fuels that can be utilized to serve the energetic and metabolic needs for resting and thrombin-dependent platelet aggregation. Using platelets from healthy human donors, we found that there was a rapid thrombin-dependent increase in oxidative phosphorylation which required both glutamine and fatty acids but not glucose. Inhibition of fatty acid oxidation or glutamine utilization could be compensated for by increased glycolytic flux. No evidence for significant mitochondrial dysfunction was found, and ATP/ADP ratios were maintained following the addition of thrombin, indicating the presence of functional and active mitochondrial oxidative phosphorylation during the early stages of aggregation. Interestingly, inhibition of fatty acid oxidation and glutaminolysis alone or in combination is not sufficient to prevent platelet aggregation, due to compensation from glycolysis, whereas inhibitors of glycolysis inhibited aggregation approximately 50%. The combined effects of inhibitors of glycolysis and oxidative phosphorylation were synergistic in the inhibition of platelet aggregation. In summary, both glycolysis and oxidative phosphorylation contribute to platelet metabolism in the resting and activated state, with fatty acid oxidation and to a smaller extent glutaminolysis contributing to the increased energy demand