Catchment size is an important factor in mapping long-term flood behaviour

From an analysis of 3,738 river gauging stationsof catchments ranging from 5 to 100,000 km2, Blöschl et al. constructed a map that depicts trends of annual maximum discharges across Europe for the 1960-2010 period. On that map Hungary, one of the most flood-prone countries in Europe, appears with nearly unanimously decreasing flood discharges which is in stark contrast with the reality of worsening floods on the Danube over the past 50-60 years in Hungary, costing €58 million in flood defence in 2013 alone, a year with record-breaking flood. The contradiction arises due to differences in scale for the drainage area between the Danube (i.e., over 100,000 km2 in Hungary) and the ones employed for the preparation of the map

Catchment size is an important factor in mapping long-term flood behaviour

From an analysis of 3,738 river gauging stationsof catchments ranging from 5 to 100,000 km2, Blöschl et al. constructed a map that depicts trends of annual maximum discharges across Europe for the 1960-2010 period. On that map Hungary, one of the most flood-prone countries in Europe, appears with nearly unanimously decreasing flood discharges which is in stark contrast with the reality of worsening floods on the Danube over the past 50-60 years in Hungary, costing €58 million in flood defence in 2013 alone, a year with record-breaking flood. The contradiction arises due to differences in scale for the drainage area between the Danube (i.e., over 100,000 km2 in Hungary) and the ones employed for the preparation of the map

Coupling one-dimensional arterial blood flow to three-dimensional tissue perfusion models for in silico trials of acute ischaemic stroke

An acute ischaemic stroke is due to the sudden blockage of an intracranial blood vessel by an embolized thrombus. In the context of setting up in silico trials for the treatment of acute ischaemic stroke, the effect of a stroke on perfusion and metabolism of brain tissue should be modelled to predict final infarcted brain tissue. This requires coupling of blood flow and tissue perfusion models. A one-dimensional intracranial blood flow model and a method to couple this to a brain tissue perfusion model for patient-specific simulations is presented. Image-based patient-specific data on the anatomy of the circle of Willis are combined with literature data and models for vessel anatomy not visible in the images, to create an extended model for each patient from the larger vessels down to the pial surface. The coupling between arterial blood flow and tissue perfusion occurs at the pial surface through the estimation of perfusion territories. The coupling method is able to accurately estimate perfusion territories. Finally, we argue that blood flow can be approximated as steady-state flow at the interface between arterial blood flow and tissue perfusion to reduce the cost of organ-scale simulations

A simplified mesoscale 3D model for characterizing fibrinolysis under flow conditions

One of the routine clinical treatments to eliminate ischemic stroke thrombi is injecting a biochemical product into the patient’s bloodstream, which breaks down the thrombi’s fibrin fibers: intravenous or intravascular thrombolysis. However, this procedure is not without risk for the patient; the worst circumstances can cause a brain hemorrhage or embolism that can be fatal. Improvement in patient management drastically reduced these risks, and patients who benefited from thrombolysis soon after the onset of the stroke have a significantly better 3-month prognosis, but treatment success is highly variable. The causes of this variability remain unclear, and it is likely that some fundamental aspects still require thorough investigations. For that reason, we conducted in vitro flow-driven fibrinolysis experiments to study pure fibrin thrombi breakdown in controlled conditions and observed that the lysis front evolved non-linearly in time. To understand these results, we developed an analytical 1D lysis model in which the thrombus is considered a porous medium. The lytic cascade is reduced to a second-order reaction involving fibrin and a surrogate pro-fibrinolytic agent. The model was able to reproduce the observed lysis evolution under the assumptions of constant fluid velocity and lysis occurring only at the front. For adding complexity, such as clot heterogeneity or complex flow conditions, we propose a 3-dimensional mesoscopic numerical model of blood flow and fibrinolysis, which validates the analytical model’s results. Such a numerical model could help us better understand the spatial evolution of the thrombi breakdown, extract the most relevant physiological parameters to lysis efficiency, and possibly explain the failure of the clinical treatment. These findings suggest that even though real-world fibrinolysis is a complex biological process, a simplified model can recover the main features of lysis evolution.</p