Influence of the accommodation coefficient on nonlinear bubble oscillations

This paper numerically investigates the effect of mass transfer processes on spherical single bubble dynamics using the Hertz–Langmuir–Knudsen approximation for the mass flux across the interface. Bubble behavior, with and without mass transfer, is studied for different values of pressure wave amplitude and frequency, as well as initial bubble radius. Whereas mass transfer processes do not seem to play a significant role on the bubble response for pressure amplitudes smaller than 0.9 atm, they appear to have an important effect when the amplitude is greater than or equal to 1 atm. For the later case, where the minimum liquid pressure reaches values around its vapor pressure, the importance of mass transfer depends on frequency. For frequencies in the 10^3–10^5 Hz range and initial bubble radii of the order of tens of microns, bubble implosions with and with no mass transfer are significantly different; smaller radii display a lower sensitivity. In this regime, accurate model predictions must, therefore, carefully select the correct value of the accommodation coefficient. For frequencies greater than 10^5 Hz, as a first approximation mass transfer can be ignored

Physics of beer tapping

The popular bar prank known in colloquial English as beer tapping consists in hitting the top of a beer bottle with a solid object, usually another bottle, to trigger the foaming over of the former within a few seconds. Despite the trick being known for long time, to the best of our knowledge, the phenomenon still lacks scientific explanation. Although it seems natural to think that shock-induced cavitation enhances the diffusion of CO$_2$ from the supersaturated bulk liquid into the bubbles by breaking them up, the subtle mechanism by which this happens remains unknown. Here we show that the overall foaming-over process can be divided into three stages where different physical phenomena take place in different time-scales, namely: bubble-collapse (or cavitation) stage, diffusion-driven stage and buoyancy-driven stage. In the bubble-collapse stage, the impact generates a train of expansion-compression waves in the liquid that leads to the fragmentation of pre-existing gas cavities. Upon bubble fragmentation, the sudden increase of the interface-area-to-volume ratio enhances mass transfer significantly, which makes the bubble volume grow by a large factor until CO$_2$ is locally depleted. At that point buoyancy takes over, making the bubble clouds rise and eventually form buoyant vortex rings whose volume grows fast due to the feedback between the buoyancy-induced rising speed and the advection-enhanced CO$_2$ transport from the bulk liquid to the bubble. The physics behind this explosive process might also be connected to some geological phenomena.Comment: 7 pages, 4 figures, 4 movies Accepted in Physical Review Letter

Direct numerical simulations of capillary wave turbulence

This work presents Direct Numerical Simulations of capillary wave turbulence solving the full 3D Navier Stokes equations of a two-phase flow. When the interface is locally forced at large scales, a statistical stationary state appears after few forcing periods. Smaller wave scales are generated by nonlinear interactions, and the wave height spectrum is found to obey a power law in both wave number and frequency in good agreement with weak turbulence theory. By estimating the mean energy flux from the dissipated power, the Kolmogorov-Zakharov constant is evaluated and found to be compatible with the exact theoretical value. The time scale separation between linear, nonlinear interaction and dissipative times is also observed. These numerical results confirm the validity of weak turbulence approach to quantify out-of equilibrium wave statistics.Comment: Physical Review Letters (2014) in pres

Investigation of a New Model for Bubbly Cavitating Flow

A new model for bubbly, cavitating flow is validated and used to study the shock-induced oscillations of bubble clouds arising in shockwave lithotripsy and other applications. Compared to previous models based on volume and phase averaging, the new model extends the range of void fractions that can be reliably simulated and, for appropriately low void fractions, reproduces the results of the polydisperse phase-averaged model with much smaller computational expense

Incomplete Distal Renal Tubular Acidosis and Kidney Stones.

Renal tubular acidosis (RTA) is comprised of a diverse group of congenital or acquired diseases with the common denominator of defective renal acid excretion with protean manifestation, but in adults, recurrent kidney stones and nephrocalcinosis are mainly found in presentation. Calcium phosphate (CaP) stones and nephrocalcinosis are frequently encountered in distal hypokalemic RTA type I. Alkaline urinary pH, hypocitraturia, and, less frequently, hypercalciuria are the tripartite lithogenic factors in distal RTA (dRTA) predisposing to CaP stone formation; the latter 2 are also commonly encountered in other causes of urolithiasis. Although the full blown syndrome is easily diagnosed by conventional clinical criteria, an attenuated forme fruste called incomplete dRTA typically evades clinical testing and is only uncovered by provocative acid-loading challenges. Stone formers (SFs) that cannot acidify urine of pH < 5.3 during acid loading are considered to have incomplete dRTA. However, urinary acidification capacity is not a dichotomous but rather a continuous trait, so incomplete dRTA is not a distinct entity but may be one end of a spectrum. Recent findings suggest that incomplete dRTA can be attributed to heterozygous carriers of hypofunctional V-ATPase. The value of incomplete dRTA diagnosis by provocative testing and genotyping candidate genes is a valuable research tool, but it remains unclear at the moment whether they alter clinical practice and needs further clarification. No randomized controlled trials have been performed in SFs with dRTA or CaP stones, and until such data are available, treatment of CaP stones are centered on reversing the biochemical abnormalities encountered in the metabolic workup. SFs with type I dRTA should receive alkali therapy, preferentially in the form of K-citrate delivered judiciously to treat the chronic acid retention that drives both stone formation and bone disease

Steady-state Function of the Ubiquitous Mammalian Na/H Exchanger (NHE1) in Relation to Dimer Coupling Models with 2Na/2H Stoichiometry

We describe the steady-state function of the ubiquitous mammalian Na/H exchanger (NHE)1 isoform in voltage-clamped Chinese hamster ovary cells, as well as other cells, using oscillating pH-sensitive microelectrodes to quantify proton fluxes via extracellular pH gradients. Giant excised patches could not be used as gigaseal formation disrupts NHE activity within the patch. We first analyzed forward transport at an extracellular pH of 8.2 with no cytoplasmic Na (i.e., nearly zero-trans). The extracellular Na concentration dependence is sigmoidal at a cytoplasmic pH of 6.8 with a Hill coefficient of 1.8. In contrast, at a cytoplasmic pH of 6.0, the Hill coefficient is <1, and Na dependence often appears biphasic. Results are similar for mouse skin fibroblasts and for an opossum kidney cell line that expresses the NHE3 isoform, whereas NHE1−/− skin fibroblasts generate no proton fluxes in equivalent experiments. As proton flux is decreased by increasing cytoplasmic pH, the half-maximal concentration (K1/2) of extracellular Na decreases less than expected for simple consecutive ion exchange models. The K1/2 for cytoplasmic protons decreases with increasing extracellular Na, opposite to predictions of consecutive exchange models. For reverse transport, which is robust at a cytoplasmic pH of 7.6, the K1/2 for extracellular protons decreases only a factor of 0.4 when maximal activity is decreased fivefold by reducing cytoplasmic Na. With 140 mM of extracellular Na and no cytoplasmic Na, the K1/2 for cytoplasmic protons is 50 nM (pH 7.3; Hill coefficient, 1.5), and activity decreases only 25% with extracellular acidification from 8.5 to 7.2. Most data can be reconstructed with two very different coupled dimer models. In one model, monomers operate independently at low cytoplasmic pH but couple to translocate two ions in “parallel” at alkaline pH. In the second “serial” model, each monomer transports two ions, and translocation by one monomer allosterically promotes translocation by the paired monomer in opposite direction. We conclude that a large fraction of mammalian Na/H activity may occur with a 2Na/2H stoichiometry

Thiazides induce glucose intolerance through inhibition of mitochondrial carbonic anhydrase 5b in β-cells

Thiazides are associated with glucose intolerance and new onset diabetes mellitus, but the molecular mechanisms remain elusive. The aim of this study was to decipher the molecular basis of thiazide-induced glucose intolerance. In mice, hydrochlorothiazide induced a pathological glucose tolerance, characterized by reduced first phase insulin secretion but normal insulin sensitivity. In vitro, thiazides inhibited glucose- and sulfonylurea-stimulated insulin secretion in islets and the murine β-cell line Min6 at pharmacologically relevant concentrations. Inhibition of insulin secretion by thiazides was CO2 /HCO3- -dependent, not additive to unselective carbonic anhydrase (CA) inhibition with acetazolamide and independent of extracellular potassium. In contrast, insulin secretion was unaltered in islets of mice lacking the known molecular thiazide targets NCC (SLC12A3) or NDCBE (SLC4A8). CA expression profiling with subsequent knock-down of individual CA isoforms suggested mitochondrial CA5b as molecular target. In support of these findings, thiazides significantly attenuated Krebs cycle anaplerosis through reduction of mitochondrial oxalacetate synthesis. CA5b KO mice were resistant to thiazide-induced glucose intolerance, and insulin secretion of islets isolated from CA5b KO mice was unaffected by thiazides. In summary, our study reveals attenuated insulin secretion due to inhibition of the mitochondrial CA5b isoform in β-cells as molecular mechanism of thiazide-induced glucose intolerance