The noise spectra of a biased quantum dot

The noise spectra associated with correlations of the current through a single level quantum dot, and with the charge fluctuations on the dot, are calculated for a finite bias voltage. The results turn out to be sensitive to the asymmetry of the dot's coupling to the two leads. At zero temperature, both spectra exhibit two or four steps (as a function of the frequency), depending on whether the resonant level lies outside or within the range between the chemical potentials on the two leads. In addition, the low frequency shot-noise exhibits dips in the charge noise and dips, peaks, and discontinuities in the derivative of the current noise. In spite of some smearing, several of these features persist at finite temperatures, where a dip can also turn into a peak

Investigation of the feasibility of sterile assembly of silver-zinc batteries

Electrical performance, bioassays, and packaging concepts evaluated in sterile assembly of silver zinc batterie

Noise spectra of an interacting quantum dot

We study the noise spectra of a many-level quantum dot coupled to two electron reservoirs, when interactions are taken into account only on the dot within the Hartree-Fock approximation. The dependence of the noise spectra on the interaction strength, the coupling to the leads, and the chemical potential is derived. For zero bias and zero temperature, we find that as a function of the (external) frequency, the noise exhibits steps and dips at frequencies reflecting the internal structure of the energy levels on the dot. Modifications due to a finite bias and finite temperatures are investigated for a non-interacting two-level dot. Possible relations to experiments are pointed out.Comment: Added reference

B cells in the aging immune system: time to consider B-1 cells

The investigation of immune senescence has uncovered many changes in B cell development, maintenance, and function with increasing age. However, most of these studies have focused on conventional B cell subsets in the spleen. The B-1 cell subset is an essential arm of the innate immune system, which in general has been understudied in terms of immune senescence. Here, we review what is currently known about B cells during aging and go on to describe why B-1 cell biology is an important component of the aging immune system in the context of diseases that most affect the aged population

Vertical Structure of Stationary Accretion Disks with a Large-Scale Magnetic Field

In earlier works we pointed out that the disk's surface layers are non-turbulent and thus highly conducting (or non-diffusive) because the hydrodynamic and/or magnetorotational (MRI) instabilities are suppressed high in the disk where the magnetic and radiation pressures are larger than the plasma thermal pressure. Here, we calculate the vertical profiles of the {\it stationary} accretion flows (with radial and azimuthal components), and the profiles of the large-scale, magnetic field taking into account the turbulent viscosity and diffusivity and the fact that the turbulence vanishes at the surface of the disk. Also, here we require that the radial accretion speed be zero at the disk's surface and we assume that the ratio of the turbulent viscosity to the turbulent magnetic diffusivity is of order unity. Thus at the disk's surface there are three boundary conditions. As a result, for a fixed dimensionless viscosity $\alpha$-value, we find that there is a definite relation between the ratio ${\cal R}$ of the accretion power going into magnetic disk winds to the viscous power dissipation and the midplane plasma-$\beta$, which is the ratio of the plasma to magnetic pressure in the disk. For a specific disk model with ${\cal R}$ of order unity we find that the critical value required for a stationary solution is $\beta_c \approx 2.4r/(\alpha h)$, where $h$ the disk's half thickness. For weaker magnetic fields, $\beta > \beta_c$, we argue that the poloidal field will advect outward while for $\beta< \beta_c$ it will advect inward. Alternatively, if the disk wind is negligible (${\cal R} \ll 1$), there are stationary solutions with $\beta \gg \beta_c$.Comment: 5 pages, 3 figure

Degeneration and impaired regeneration of gray matter oligodendrocytes in amyotrophic lateral sclerosis.

Oligodendrocytes associate with axons to establish myelin and provide metabolic support to neurons. In the spinal cord of amyotrophic lateral sclerosis (ALS) mice, oligodendrocytes downregulate transporters that transfer glycolytic substrates to neurons and oligodendrocyte progenitors (NG2(+) cells) exhibit enhanced proliferation and differentiation, although the cause of these changes in oligodendroglia is unknown. We found extensive degeneration of gray matter oligodendrocytes in the spinal cord of SOD1 (G93A) ALS mice prior to disease onset. Although new oligodendrocytes were formed, they failed to mature, resulting in progressive demyelination. Oligodendrocyte dysfunction was also prevalent in human ALS, as gray matter demyelination and reactive changes in NG2(+) cells were observed in motor cortex and spinal cord of ALS patients. Selective removal of mutant SOD1 from oligodendroglia substantially delayed disease onset and prolonged survival in ALS mice, suggesting that ALS-linked genes enhance the vulnerability of motor neurons and accelerate disease by directly impairing the function of oligodendrocytes