Capillary interactions between dynamically forced particles adsorbed at a planar interface and on a bubble.

We investigate the dynamic interfacial deformation induced by micrometric particles exerting a periodic force on a planar interface or on a bubble, and the resulting lateral capillary interactions. Assuming that the deformation of the interface is small, neglecting the effect of viscosity, and assuming point particles, we derive analytical formulas for the dynamic deformation of the interface. For the case of a planar interface the dynamic point force simply generates capillary waves, while for the case of a bubble it excites shape oscillations, with a dominat deformation mode that depends on the bubble radius for a given forcing frequency. We evaluate the lateral capillary force acting between two particles, by superimposing the deformations induced by two point forces. We find that the lateral capillary forces experienced by dynamically forced particles are non monotonic and can be repulsive. The results are applicable to micrometric particles driven by different dynamic forcing mechanisms such as magnetic, electric or acoustic fields.

Reply to "Comment on 'Locomotion of a microorganism in weakly viscoelastic liquids' ".

In the present reply we show that the comments casting doubts on the results of our recent paper [M. De Corato et al., Phys. Rev. E 92, 053008 (2015)PLEEE81539-375510.1103/PhysRevE.92.053008] are based on a misinterpretation of the second-order fluid constitutive equation. Nevertheless, we show that, by considering alternative constitutive equations for the viscoelastic stress, we recover, to first-order in the Deborah number, the same results already obtained by De Corato et al. [Phys. Rev. E 92, 053008 (2015)PLEEE81539-375510.1103/PhysRevE.92.053008], thus dissipating any possible doubt about their validity.

Locomotion of a microorganism in weakly viscoelastic liquids.

In the present work we study the motion of microorganisms swimming by an axisymmetric distribution of surface tangential velocity in a weakly viscoelastic fluid. The second-order fluid constitutive equation is used to model the suspending fluid, while the well-known "squirmer model" [M. J. Lighthill, Comm. Pure Appl. Math. 5, 109 (1952); J. R. Blake, J. Fluid Mech. 46, 199 (1971)] is employed to describe the organism propulsion mechanism. A regular perturbation expansion up to first order in the Deborah number is performed, and the generalized reciprocity theorem from Stokes flow theory is then used, to derive analytical formulas for the squirmer velocity. Results show that "neutral" squirmers are unaffected by viscoelasticity, whereas "pullers" and "pushers" are slowed down and hastened, respectively. The power dissipated by the swimming microorganism and the "swimming efficiency" are also analytically quantified.

Hydrodynamics and Brownian motions of a spheroid near a rigid wall.

In this work, we study in detail the hydrodynamics and the Brownian motions of a spheroidal particle suspended in a Newtonian fluid near a flat rigid wall. We employ 3D Finite Element Method (FEM) simulations to compute how the mobility tensor of the spheroid varies with both the particle-wall separation distance and the particle orientation. We then study the Brownian motion of the spheroid by means of a discretized Langevin equation. We specifically focus on the additional drift terms arising from the position and orientational dependence of the mobility matrix. In this respect, we also propose a numerically convenient approximation of the orientational divergence of the mobility matrix that is required in the solution of the Langevin equation. Our results illustrate that both hydrodynamics and Brownian motions of a spheroidal particle near a confining wall display novel features from those of a sphere in the same type of confinement.

Effect of nitric oxide on lymphocytes from sporadic amyotrophic lateral sclerosis patients: toxic or protective role?

Markers of oxidative and nitrosative stress have been found in spinal cord, cortex, cerebrospinal fluid and plasma of patients affected by amyotrophic lateral sclerosis (ALS), a fatal disorder characterised by progressive motor neuron degeneration. In this study, we investigated the effect of the NO-releasing agent, diethylamine NONOate (NONO), on lymphocytes from patients affected by the sporadic form of ALS (SALS) and controls by flow cytometry. In the same experimental conditions we investigated the expression of the antioxidant proteins, Bcl-2 and SOD1. Incubation with NONO induced cell damage in control lymphocytes but did not further damage the already affected untreated SALS lymphocytes. The incubation with NONO induced a time-dependent decrease of Bcl-2 and SOD1 in control lymphocytes. Surprisingly, in SALS lymphocytes the NONO treatment increased the expression of these proteins, which in basal conditions was depressed compared to control lymphocytes.

A randomized phase III study: comparison between intravenous and intraarterial ACNU administration in newly diagnosed primary glioblastomas.

BACKGROUND: In this randomized phase III study, the effectiveness as well as the side-effects of intraarterial [i.a.] (17 patients) versus intravenous [i.v.] (16 patients) ACNU [Nimustine] administration in newly diagnosed glioblastoma, were compared. PATIENTS AND METHODS: All patients undenwent extensive surgical resection, and both groups were homogeneous for the other known risk factors. Thirty-three patients with glioblastoma were treated with ACNU at the dose of 80-100 mg/m2. Treatment was repeated every 5-8 weeks for a minimum of 2 and maximum of 14 cycles. Total survival time (TST) and to time to progression were chosen as outcome variables. RESULTS AND CONCLUSION: No significant differences in systemic and hematological toxicity between the i.a. and iv. ACNU administration routes were detected. In both groups, tolerance of the procedure was excellent. Analysis of the main outcome measured showed no significant differences between i.a. and i.v. ACNU administration: time to progression was 6 months for i.a. ACNU and 4 months for i.v. ACNU and total survival time was 17 months for i.a. ACNU and 20 months for i.v. ACNU. In spite of ACNU dose incrementation, obtained through i.a. route administration, and subsequent higher concentration in the tumor bed, no improvement could be achieved in effectiveness.