Large bubble rupture sparks fast liquid jet

This Letter presents the novel experimental observation of long and narrow jets shooting out in disconnecting large elongated bubbles. We investigate this phenomenon by carrying out experiments with various viscosities, surface tensions, densities and nozzle radii. We propose a universal scaling law for the jet velocity, which unexpectedly involves the bubble height to the power 3/2. This anomalous exponent suggests an energy focusing phenomenon. We demonstrate experimentally that this focusing is purely gravity-driven and independent of the pinch-off singularity

It's Harder to Splash on Soft Solids

Droplets splash when they impact dry, flat substrates above a critical velocity that depends on parameters such as droplet size, viscosity and air pressure. By imaging ethanol drops impacting silicone gels of different stiffnesses we show that substrate stiffness also affects the splashing threshold. Splashing is reduced or even eliminated: droplets on the softest substrates need over 70\% more kinetic energy to splash than they do on rigid substrates. We show that this is due to energy losses caused by deformations of soft substrates during the first few microseconds of impact. We find that solids with Young's moduli $\lesssim 100$kPa reduce splashing, in agreement with simple scaling arguments. Thus materials like soft gels and elastomers can be used as simple coatings for effective splash prevention. Soft substrates also serve as a useful system for testing splash-formation theories and sheet-ejection mechanisms, as they allow the characteristics of ejection sheets to be controlled independently of the bulk impact dynamics of droplets.Comment: 5 pages, 4 figure

Drop splashing after impact onto immiscible pools of different viscosities

Droplet impact onto liquid pools is a canonical scenario relevant to numerous natural phenomena and industrial processes. However, despite their ubiquity, multi-fluid systems with the drop and pool consisting of different liquids are far less well understood. Our hypothesis is that the post-impact dynamics greatly depends on the pool-to-droplet viscosity ratio , which we explore over a range of six orders of magnitude using a combination of experiments and theoretical approaches (mathematical modelling and direct numerical simulation). Our findings indicate that in this scenario the splashing threshold and the composition of the ejecta sheet are controlled by the viscosity ratio. We uncover that increasing the pool viscosity decreases the splashing threshold for high viscosity pools () when the splash comes from the droplet. By contrast, for low viscosity pools, the splash sheet comes from the pool and increasing the pool viscosity increases the splashing threshold. Surprisingly, there are conditions for which no splashing is observed under the conditions attainable in our laboratory. Furthermore, considering the interface velocity together with asymptotic arguments underlying the generation of the ejecta has allowed us to understand meaningful variations in the pressure during impact and rationalise the observed changes in the splashing threshold

Kelvin-Helmholtz instability in the presence of variable viscosity for mudflow resuspension in estuaries

The temporal stability of a parallel shear flow of miscible fluid layers of dif- ferent density and viscosity is investigated through a linear stability analysis and direct numerical simulations. The geometry and rheology of this Newto- nian fluid mixing can be viewed as a simplified model of the behavior of mud- flow at the bottom of estuaries for suspension studies. In this study, focus is on the stability and transition to turbulence of an initially laminar configuration. A parametric analysis is performed by varying the values of three control pa- rameters, namely the viscosity ratio, the Richardson and Reynolds numbers, in the case of initially identical thickness of the velocity, density and viscosity profiles. The range of parameters has been chosen so as to mimic a wide variety of real configurations. This study shows that the Kelvin-Helmholtz instability is controlled by the local Reynolds and Richardson numbers of the inflection point. In addition, at moderate Reynolds number, viscosity strat- ification has a strong influence on the onset of instability, the latter being enhanced at high viscosity ratio, while at high Reynolds number, the influ- ence is less pronounced. In all cases, we show that the thickness of the mixing layer (and thus resuspension) is increased by high viscosity stratification, in particular during the non-linear development of the instability and especially pairing processes. This study suggests that mud viscosity has to be taken into account for resuspension parameterizations because of its impact on the inflec- tion point Reynolds number and the viscosity ratio, which are key parameters for shear instabilities

At clinically relevant concentrations the anaesthetic/amnesic thiopental but not the anticonvulsant phenobarbital interferes with hippocampal sharp wave-ripple complexes

<p>Abstract</p> <p>Background</p> <p>Many sedative agents, including anesthetics, produce explicit memory impairment by largely unknown mechanisms. Sharp-wave ripple (SPW-R) complexes are network activity thought to represent the neuronal substrate for information transfer from the hippocampal to neocortical circuits, contributing to the explicit memory consolidation. In this study we examined and compared the actions of two barbiturates with distinct amnesic actions, the general anesthetic thiopental and the anticonvulsant phenobarbital, on in vitro SPW-R activity.</p> <p>Results</p> <p>Using an in vitro model of SPW-R activity we found that thiopental (50–200 μM) significantly and concentration-dependently reduced the incidence of SPW-R events (it increased the inter-event period by 70–430 %). At the concentration of 25 μM, which clinically produces mild sedation and explicit memory impairment, thiopental significantly reduced the quantity of ripple oscillation (it reduced the number of ripples and the duration of ripple episodes by 20 ± 5%, n = 12, <it>P </it>< 0.01), and suppressed the rhythmicity of SPWs by 43 ± 15% (n = 6, <it>P </it>< 0.05). The drug disrupted the synchrony of SPWs within the CA1 region at 50 μM (by 19 ± 12%; n = 5, <it>P </it>< 0.05). Similar effects of thiopental were observed at higher concentrations. Thiopental did not affect the frequency of ripple oscillation at any of the concentrations tested (10–200 μM). Furthermore, the drug significantly prolonged single SPWs at concentrations ≥50 μM (it increased the half-width and the duration of SPWs by 35–90 %). Thiopental did not affect evoked excitatory synaptic potentials and its results on SPW-R complexes were also observed under blockade of NMDA receptors. Phenobarbital significantly accelerated SPWs at 50 and 100 μM whereas it reduced their rate at 200 and 400 μM. Furthermore, it significantly prolonged SPWs, reduced their synchrony and reduced the quantity of ripples only at the clinically very high concentration of 400 μM, reported to affect memory.</p> <p>Conclusion</p> <p>We hypothesize that thiopental, by interfering with SPW-R activity, through enhancement of the GABA_Areceptor-mediated transmission, affects memory processes which involve hippocampal circuit activation. The quantity but not the frequency of ripple oscillation was affected by the drug.</p

A neural population model of the bi-phasic EEG-power spectrum during general anaesthesia

International audienceThe neuronal mechanisms of general anaesthesia are still poorly understood, though the induction of analgesia, amnesia, immobility and loss of consciousness by anaesthetic agents is well-established in hospital practice. To shed some light onto these mysterious effects, the chapter analyzes mathematically a neural field model describing the neural population dynamics by an integro-differential equation. The power spectrum is derived and compared to experimental results

Obstacles on the way to the clinical visualisation of beta cells: looking for the Aeneas of molecular imaging to navigate between Scylla and Charybdis

For more than a decade, researchers have been trying to develop non-invasive imaging techniques for the in vivo measurement of viable pancreatic beta cells. However, in spite of intense research efforts, only one tracer for positron emission tomography (PET) imaging is currently under clinical evaluation. To many diabetologists it may remain unclear why the imaging world struggles to develop an effective method for non-invasive beta cell imaging (BCI), which could be useful for both research and clinical purposes. Here, we provide a concise overview of the obstacles and challenges encountered on the way to such BCI, in both native and transplanted islets. We discuss the major difficulties posed by the anatomical and cell biological features of pancreatic islets, as well as the chemical and physical limits of the main imaging modalities, with special focus on PET, SPECT and MRI. We conclude by indicating new avenues for future research in the field, based on several remarkable recent results

Effects of the volatile anesthetic enflurane on spontaneous discharge rate and GABA(A)-mediated inhibition of Purkinje cells in rat cerebellar slices

Effects of the volatileanesthetic enflurane on spontaneous discharge rate and GABAA-mediated inhibition of Purkinje cells in rat cerebellar slices.J. Neurophysiol. 77: 2525–2538, 1997. The effects of the volatile anesthetic enflurane on the spontaneous action potential firing and on γ-aminobutyric acid-A (GABAA)-mediated synaptic inhibition of Purkinje cells were investigated in sagittal cerebellar slices. The anesthetic shifted the discharge patterns from continuous spiking toward burst firing and decreased the frequency of extracellularly recorded spontaneous action potentials in a concentration-dependent manner. Half-maximal reduction was observed at a concentration corresponding to 2 MAC (1 MAC induces general anesthesia in 50% of patients and rats). When the GABAA antagonist bicuculline was present, 2 MAC enflurane reduced action potential firing only by 13 ± 8% (mean ± SE). In further experiments, inhibitory postsynaptic currents (IPSCs) were monitored in the whole cell patch-clamp configuration from cells voltage clamped close to −80 mV. At 1 MAC, enflurane attenuated the mean amplitude of IPSCs by 54 ± 3% while simultaneously prolonging the time courses of monoexponential current decays by 413 ± 69%. These effects were similar when presynaptic action potentials were suppressed by 1 μM tetrodotoxin. At 1–2 MAC, enflurane increased GABAA-mediated inhibition of Purkinje cells by 97 ± 20% to 159 ± 38%. During current-clamp recordings, the anesthetic (2 MAC) hyperpolarized the membrane potential by 5.2 ± 1.1 mV in the absence, but only by 1.6 ± 1.2 mV in the presence, of bicuculline. These results suggest that enflurane-induced membrane hyperpolarizations, as well as the reduction of spike rates, were partly caused by an increase in synaptic inhibition. Induction of burst firing was related to other actions of the anesthetic, probably an accelerated activation of an inwardly directed cationic current and a depression of spike after hyperpolarizations