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We present a computational framework for the calibration of parameters describing cardiovascular models with a focus on the application of growth of abdominal aortic aneurysms (AAA). The growth rate in this sort of pathology is considered a critical parameter in the risk management and is an essential indicator for the assessment of surveillance intervals. Parameters describing growth of AAAs are not measurable directly and need to be estimated from available data often given by medical imaging technologies. Registration procedures often applied in standard workflows of parameter identification to extract the image encoded information are a source of significant systematic error. The concept of surface currents provides means to effectively avoid this source of errors by establishing a mathematical framework to compare surface information, directly accessible from image data. By utilizing this concept it is possible to inversely estimate growth parameters using sophisticated numerical models of AAAs from measurements available as surface information. In this work we present a framework to obtain spatial distributions of parameters governing growth of arterial tissue, and we show how the use of surface currents can significantly improve the results. We further present the application to patient specific follow-up data resulting in a spatial map of volumetric growth rates enabling, for the first time, prediction of further AAA expansion., (Copyright © 2016 John Wiley & Sons, Ltd.)

The gas exchange in adult diving beetles (Coleoptera: Dytiscidae) relies on a subelytral air store, which has to be renewed in regular intervals at the water surface. The dive duration varies from a few minutes to 24 h depending on the species, activity, and temperature. However, some species remain submerged for several weeks. Stygobiont species do not ascend to the surface and gas exchange of these species remains unclear, but it is assumed that they require air filled voids for respiration or they use cutaneous respiration. In this study, we investigate the gas exchange in the running water diving beetle Deronectes aubei, which survive submerged for over 6 weeks. The diffusion distance through the cuticle is too great for cutaneous respiration. Therefore, the dissolved oxygen uptake of submerged beetles was determined and an oxygen uptake via the rich tracheated elytra was observed. Fine structure analyses (SEM and TEM) of the beetles showed tracheated setae mainly on the elytral surface, which acts as tracheal gills. Prevention of the air bubble formation at the tip of the abdomen, which normally act as physical gill in Dytiscidae, resulted in no effect in oxygen uptake in D. aubei, but this was the sole way for a submerged Hydroporus palustris to get oxygen. The setal gas exchange technique explains the restriction of D. aubei to rivers and brooks with high oxygen concentration and it may also be used by subterran living diving beetles, which lack access to atmospheric oxygen. The existence of setal tracheal gills in species in running water which are often found in the hyporheic zone and in stygobiont species supports the known evolution of stygobiont Dytiscidae from species of the hyporheic zone. For species in running water, setal tracheal gills could be seen as an adaptation to avoid drifting downstream by the current.

1. Whole-cell recordings of macroscopic K+ currents were made from acutely dissociated and cultured melanotrophs isolated from the pars intermedia of the adult rat pituitary. 2. In acutely dissociated cells, external capsaicin reversibly decreased the amplitude both of the fast-activating, fast-inactivating potassium current IK(f) and the slowly-activating, slowly-inactivating potassium current IK(s). To simplify the investigation of the mechanism of action of capsaicin experiments were conducted on cultured melanotrophs that express only IK(s). 3. In control cells the activation rate and the amplitude of IK(s) increased with depolarization and the current showed very little inactivation at any voltage during pulses lasting for 100-300 ms. In capsaicin, the decrease of the current amplitude was associated with an increased rate of current decay ('inactivation'). At a given voltage, the extent and the rate of the capsaicin-induced inactivation was proportional to the capsaicin concentration; and, at a given concentration, the extent and rate of the inactivation increased with membrane depolarization. 4. The fit of the Hill equation to data derived from the steady-state block of IK(s) evoked at 10 mV indicated an equilibrium dissociation constant (KD) of 17.4 microM (95% confidence limits 15.8-19.0) and a Hill coefficient of 1.8 (95% Cl 1.5-2.2) suggesting that at least two molecules of capsaicin must bind to the channel to block it. 5. Analysis of the voltage-dependence of the steady-state block in 100 microM capsaicin showed that half-maximal block occurred at -29 +/- 2 mV (n = 10). Two-pulse experiments designed to study the time-dependence of channel block in 100 MicroM capsaicin indicated that the blocking kinetics were well fitted by a single exponential and that the rate of block increased with depolarization. The value for Tblock at 0mV was 24 +/-7ms (n=4).6. Recovery from block in 100 MicroM capsaicin was also well fitted by a single exponential. The recovery time constant ( was 708 +/- 140 ms at - 50 mV, 70 +/- 6 ms at - 70 mV and 19 +/- 1.3 ms at-90 mV (n = 4).7. In 50-100 MicroM capsaicin, the decay of the tail current was biexponential, the values for fast and Tslow being, respectively, less than and greater than the single time constant fitted to the control tail current.Inward and outward K+ currents were equally affected by capsaicin.8. Most of these effects of capsaicin on the IK(S) of melanotrophs can be accounted for by a kinetic scheme in which capsaicin binds to and blocks open K+ channels.

1. The effect of quinidine on the fast-activating, fast-inactivating potassium current (IK(f] in acutely dissociated melanotrophs of the adult rat pituitary was examined. Macroscopic currents were measured by use of the whole-cell configuration of the patch clamp technique. 2. Bath application of quinidine caused a dose-dependent reduction of the peak amplitude of IK(f). The Kd for blockade of IK(f) at 0 mV was estimated to be 41 +/- 5.6 microM. 3. Quinidine elicited a dose-dependent increase of the rate of the decay of IK(f) and this effect was enhanced by membrane depolarization. The possibility that this phenomenon reflects an open channel blocking reaction is discussed. 4. Quinidine also caused a 5 mV hyperpolarizing shift of the steady-state inactivation curve and increased the half-time for recovery from inactivation. Quinidine did not affect the onset of inactivation measured at -30 mV. 5. Internal quinidine did not appear substantially to affect either the peak amplitude or kinetics of IK(f). 6. A study of some structural analogues showed that hydroquinidine and quinacrine had effects similar to those of quinidine. The effect of quinacrine on the amplitude and kinetics of IK(f) was also pH-dependent. Cinchonine, which bears a close structural resemblance to quinidine, was much less effective as a blocker of IK(f).

1. The macroscopic currents induced in cultured rat melanotrophs by exogenous gamma-aminobutyric acid (GABA) were analysed using the patch clamp recording technique. 2. Using various concentrations of intra- and extracellular chloride it was demonstrated that the conductance activated by GABA was chloride selective. Since these currents were blocked with bicuculline and enhanced with chlordiazepoxide the involvement of GABAA receptors similar to those in the CNS is indicated. 3. When chloride was symmetrically distributed across the membrane the voltage/current relationship was linear; pronounced rectification of GABA mediated currents was evident when there was an asymmetrical distribution of chloride. 4. With concentrations of GABA greater than 10 microM a fading of the current was seen during prolonged (5-10 s) applications. This effect appeared to be due to a decline of conductance rather than a shift of the chloride equilibrium potential. 5. Values for the Hill coefficient derived from dose-response curves suggested that the binding of 2 molecules of GABA to the receptor is required for the activation of the chloride channel. 6. There was no indication of a direct, GABAB receptor-mediated change of conductance.