Large-amplitude plasma wave generation by laser beating in inhomogeneous magnetized plasmas.

Large-amplitude plasma wave is known to accelerate electrons to high energies. The electron energy gain mainly depends on plasma wave amplitude. In this paper, we investigate the excitation of large-amplitude plasma waves by laser beat-wave in an inhomogeneous plasma. The idea behind this work is to employ linear and radial plasma density profiles to enhance the plasma wave amplitude. PIC simulations are used to validate the numerical solution of the nonlinear wave equation in cylindrical dimensions through the finite difference method. Furthermore, the effects of the quadratic-radial plasma density profiles and magnetic field on the plasma wave excitation are investigated. The study shows that compared to the linear density profile of plasma, the plasma wave amplitude in the case of a linear-radial density profile is far more pronounced. For the linear-radial density profile, the plasma wave amplitude remains steady over greater distances of propagation compared to the linear density profile, resulting in reduced immediate damping effects. It can also be seen that the plasma wave amplitude is higher for the quadratic-radial than for the linear-radial density profiles. The effect of a longitudinal magnetic field on plasma wave amplitude is investigated. It can be seen that the plasma wave amplitude is increased by applying a magnetic field. This study may provide a way to enhance the plasma wave field for accelerating the electrons in laser-plasma accelerators.

In silico study of the impact of oxidation on pyruvate transmission across the hVDAC1 protein channel.

The overexpression of voltage dependent anion channels (VDACs), particularly VDAC1, in cancer cells compared to normal cells, plays a crucial role in cancer cell metabolism, apoptosis regulation, and energy homeostasis. In this study, we used molecular dynamics (MD) simulations to investigate the effect of a low level of VDAC1 oxidation (induced e.g., by cold atmospheric plasma (CAP)) on the pyruvate (Pyr) uptake by VDAC1. Inhibiting Pyr uptake through VDAC1 can suppress cancer cell proliferation. Our primary target was to study the translocation of Pyr across the native and oxidized forms of hVDAC1, the human VDAC1. Specifically, we employed MD simulations to analyze the hVDAC1 structure by modifying certain cysteine residues to cysteic acids and methionine residues to methionine sulfoxides, which allowed us to investigate the effect of oxidation. Our results showed that the free energy barrier for Pyr translocation through the native and oxidized channel was approximately 4.3 ± 0.7 kJ mol-1 and 10.8 ± 1.8 kJ mol-1, respectively. An increase in barrier results in a decrease in rate of Pyr permeation through the oxidized channel. Thus, our results indicate that low levels of CAP oxidation reduce Pyr translocation, resulting in decreased cancer cell proliferation. Therefore, low levels of oxidation are likely sufficient to treat cancer cells given the inhibition of Pyr uptake.