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R Benzi

Publications and source records attributed to R Benzi.

At least 19 recordsLinked to original sources
PubMed2006

Surface roughness-hydrophobicity coupling in microchannel and nanochannel flows.

An approach based on a lattice version of the Boltzmann kinetic equation for describing multiphase flows in nano- and microcorrugated devices is proposed. We specialize it to describe the wetting-dewetting transition of fluids in the presence of nanoscopic grooves etched on the boundaries. This approach permits us to retain the essential supramolecular details of fluid-solid interactions without surrendering--actually boosting--the computational efficiency of continuum methods. The method is used to analyze the importance of conspiring effects between hydrophobicity and roughness on the global mass flow rate of the microchannel. In particular we show that smart surfaces can be tailored to yield very different mass throughput by changing the bulk pressure. The mesoscopic method is also validated quantitatively against the molecular dynamics results of [Cottin-Bizonne, Nat. Mater. 2, 237 (2003)].

Journal Article↗
PubMed2006

Mesoscopic modeling of a two-phase flow in the presence of boundaries: The contact angle.

We present a mesoscopic model, based on the Boltzmann equation, for the interaction between a solid wall and a nonideal fluid. We present an analytic derivation of the contact angle in terms of the surface tension between the liquid-gas, the liquid-solid, and the gas-solid phases. We study the dependency of the contact angle on the two free parameters of the model, which determine the interaction between the fluid and the boundaries, i.e. the equivalent of the wall density and of the wall-fluid potential in molecular dynamics studies. We compare the analytical results obtained in the hydrodynamical limit for the density profile and for the surface tension expression with the numerical simulations. We compare also our two-phase approach with some exact results obtained by E. Lauga and H. Stone [J. Fluid. Mech. 489, 55 (2003)] and J. Philip [Z. Angew. Math. Phys. 23, 960 (1972)] for a pure hydrodynamical incompressible fluid based on Navier-Stokes equations with boundary conditions made up of alternating slip and no-slip strips. Finally, we show how to overcome some theoretical limitations connected with the discretized Boltzmann scheme proposed by X. Shan and H. Chen [Phys. Rev. E 49, 2941 (1994)] and we discuss the equivalence between the surface tension defined in terms of the mechanical equilibrium and in terms of the Maxwell construction.

Journal Article↗
PubMed2001

Double scaling and intermittency in shear dominated flows.

The nature of intermittency in shear dominated flows changes with respect to homogeneous and isotropic conditions since the process of energy transfer is affected by the turbulent kinetic energy production associated with the Reynolds stresses. For these flows, a new form of refined similarity law is able to describe the increased level of intermittency. Ideally a length scale associated with the mean shear separates the two ranges, i.e., the classical Kolmogorov-like inertial range, below, and the shear dominated range, above. In the present paper we give evidence of the coexistence of the two regimes and we support the conjecture that the statistical properties of the dissipation field are practically insensible to the mean shear. This allows for a theoretical prediction of the scaling exponents of structure functions in the shear dominated range based on the known intermittency corrections for isotropic flows. The prediction is found to closely match the available numerical and experimental data. The analysis shows that the larger anisotropic scales of shear turbulence display universality, and determines the modality by which the dissipation field fixes the properties of turbulent fluctuations in the shear dominated range.

Journal Article↗
PubMed1994

Substrate competition in postischemic myocardium. Effect of substrate availability during reperfusion on metabolic and contractile recovery in isolated rat hearts.

Normal myocardium can derive energy for contraction and relaxation from oxidative metabolism of a variety of substrates. This investigation examined the influence of substrate availability early during reperfusion on the substrate pattern of oxidative metabolism and recovery of contractile function. For this purpose, isovolumically beating isolated rat hearts, perfused retrogradely with erythrocyte-supplemented buffer containing 0.4 mmol/L palmitate and 11 mmol/L glucose, were subjected to 40 minutes of no-flow ischemia. Hearts were reperfused with medium containing selected concentrations of palmitate and glucose. The substrate pattern for oxidative metabolism was determined on the basis of myocardial release of 14CO2 after equilibration of the hearts during the initial 15 minutes of reperfusion with either [1-14C]palmitate or [U-14C]glucose. In continuously perfused control hearts, glucose oxidation was largely inhibited by palmitate. During postischemic reperfusion, oxidation of glucose was increased by 59% (P < .05) and 467% (P <.01) in hearts reperfused after the ischemic period with 11 mmol/L glucose plus 0.4 or 1.2 mmol/L palmitate, respectively. Oxidation of palmitate was concomitantly reduced during reperfusion at low (0.4 mmol/L) but not at high (1.2 mmol/L) palmitate concentration. Compared with hearts reperfused with medium containing 0.4 mmol/L palmitate as sole substrate, hearts reperfused with medium containing 11 mmol/L glucose with 0.4 mmol/L palmitate exhibited lower left ventricular diastolic pressure (69 +/- 5 versus 90 +/- 3 mm Hg [mean +/- SEM], P < .05), less release of creatine kinase (31 +/- 5 versus 59 +/- 7 U/g wet wt, P < .05), and better recovery of left ventricular pressure development (26 +/- 9 versus 6 +/- 4 mm Hg, P < .05). Omission of palmitate or increasing the palmitate concentration to 1.2 mmol/L did not significantly alter postischemic myocardial contracture and enzyme release. The findings support the view that glucose oxidation early during reperfusion may be crucial for functional recovery. The results further indicate that interaction of substrates of oxidative metabolism is altered in severely injured postischemic myocardium. Inhibition of glucose oxidation by fatty acids was partially reversed during reperfusion.

Adenosine Triphosphate↗
PubMed1990

[Physiopathological basis of protection of the ischemic myocardium].

Ischemia initiates a cascade of intracellular events that culminates in the death of the myocyte. Reperfusion of ischemic myocardium is the most efficient way of salvaging jeopardized cells. Additional measures referred to as "myocardial protection" may further reduce ischemic injury, primarily by delaying the progression of cellular damage during ischemia. The pathophysiological aspects of ischemic injury and the possibilities for protection of ischemic myocardium are reviewed. In addition to the "established" methods of myocardial protection, the concept of prevention of "reperfusion injury", presently under experimental investigation, is discussed.

Calcium↗