Confined Dirac Particles in Constant and Tilted Magnetic Field

We study the confinement of charged Dirac particles in 3+1 space-time due to the presence of a constant and tilted magnetic field. We focus on the nature of the solutions of the Dirac equation and on how they depend on the choice of vector potential that gives rise to the magnetic field. In particular, we select a "Landau gauge" such that the momentum is conserved along the direction of the vector potential yielding spinor wavefunctions, which are localized in the plane containing the magnetic field and normal to the vector potential. These wave functions are expressed in terms of the Hermite polynomials. We point out the relevance of these findings to the relativistic quantum Hall effect and compare with the results obtained for a constant magnetic field normal to the plane in 2+1 dimensions.Comment: 10 page

Adenoviral delivery of angiotensin-(1-7) or angiotensin-(1-9) inhibits cardiomyocyte hypertrophy via the mas or angiotensin Type 2 receptor

The counter-regulatory axis of the renin angiotensin system peptide angiotensin-(1-7) [Ang-(1-7)] has been identified as a potential therapeutic target in cardiac remodelling, acting via the mas receptor. Furthermore, we recently reported that an alternative peptide, Ang-(1-9) also counteracts cardiac remodelling via the angiotensin type 2 receptor (AT(2)R). Here, we have engineered adenoviral vectors expressing fusion proteins which release Ang-(1-7) [RAdAng-(1-7)] or Ang-(1-9) [RAdAng-(1-9)] and compared their effects on cardiomyocyte hypertrophy in rat H9c2 cardiomyocytes or primary adult rabbit cardiomyocytes, stimulated with angiotensin II, isoproterenol or arg-vasopressin. RAdAng-(1-7) and RAdAng-(1-9) efficiently transduced cardiomyocytes, expressed fusion proteins and secreted peptides, as demonstrated by western immunoblotting and conditioned media assays. Furthermore, secreted Ang-(1-7) and Ang-(1-9) inhibited cardiomyocyte hypertrophy (Control = 168.7±8.4 µm; AngII = 232.1±10.7 µm; AngII+RAdAng-(1-7) = 186±9.1 µm, RAdAng-(1-9) = 180.5±9 µm; P<0.05) and these effects were selectively reversed by inhibitors of their cognate receptors, the mas antagonist A779 for RAdAng-(1-7) and the AT(2)R antagonist PD123,319 for RAdAng-(1-9). Thus gene transfer of Ang-(1-7) and Ang-(1-9) produces receptor-specific effects equivalent to those observed with addition of exogenous peptides. These data highlight that Ang-(1-7) and Ang-(1-9) can be expressed via gene transfer and inhibit cardiomyocyte hypertrophy via their respective receptors. This supports applications for this approach for sustained peptide delivery to study molecular effects and potential gene therapeutic actions

Electron trapping in graphene quantum dots with magnetic flux

It is known that the appearance of Klein tunneling in graphene makes it hard to keep or localize electrons in a graphene-based quantum dot (GQD). However, a magnetic field can be used to temporarily confine an electron that is traveling into a GQD. The electronic states investigated here are resonances with a finite trapping time, also referred to as quasi-bound states. By subjecting the GDQ to a magnetic flux, we study the scattering phenomenon and the Aharonov-Bohm effect on the lifetime of quasi-bound states existing in a GQD. We demonstrate that the trapping time increases with the magnetic flux sustaining the trapped states for a long time even after the flux is turned off. Furthermore, we discover that the probability density within the GQD is also clearly improved. We demonstrate that the trapping time of an electron inside a GQD can be successfully extended by adjusting the magnetic flux parameters.Comment: 10 pages, 7 figure