Single-parameter non-adiabatic quantized charge pumping

Controlled charge pumping in an AlGaAs/GaAs gated nanowire by single-parameter modulation is studied experimentally and theoretically. Transfer of integral multiples of the elementary charge per modulation cycle is clearly demonstrated. A simple theoretical model shows that such a quantized current can be generated via loading and unloading of a dynamic quasi-bound state. It demonstrates that non-adiabatic blockade of unwanted tunnel events can obliterate the requirement of having at least two phase-shifted periodic signals to realize quantized pumping. The simple configuration without multiple pumping signals might find wide application in metrological experiments and quantum electronics.Comment: 4 pages, 4 figure

Non-adiabatic corrections to elastic scattering of halo nuclei

We derive the formalism for the leading order corrections to the adiabatic approximation to the scattering of composite projectiles. Assuming a two-body projectile of core plus loosely-bound valence particle and a model (the core recoil model) in which the interaction of the valence particle and the target can be neglected, we derive the non-adiabatic correction terms both exactly, using a partial wave analysis, and using the eikonal approximation. Along with the expected energy dependence of the corrections, there is also a strong dependence on the valence-to-core mass ratio and on the strength of the imaginary potential for the core-target interaction, which relates to absorption of the core in its scattering by the target. The strength and diffuseness of the core-target potential also determine the size of the corrections. The first order non-adiabatic corrections were found to be smaller than qualitative estimates would expect. The large absorption associated with the core-target interaction in such halo nuclei as Be11 kills off most of the non-adiabatic corrections. We give an improved estimate for the range of validity of the adiabatic approximation when the valence-target interaction is neglected, which includes the effect of core absorption. Some consideration was given to the validity of the eikonal approximation in our calculations.Comment: 14 pages with 10 figures, REVTeX4, AMS-LaTeX v2.13, submitted to Phys. Rev.

Computational Models of the Notch Network Elucidate Mechanisms of Context-dependent Signaling

The Notch signaling pathway controls numerous cell fate decisions during development and adulthood through diverse mechanisms. Thus, whereas it functions as an oscillator during somitogenesis, it can mediate an all-or-none cell fate switch to influence pattern formation in various tissues during development. Furthermore, while in some contexts continuous Notch signaling is required, in others a transient Notch signal is sufficient to influence cell fate decisions. However, the signaling mechanisms that underlie these diverse behaviors in different cellular contexts have not been understood. Notch1 along with two downstream transcription factors hes1 and RBP-Jk forms an intricate network of positive and negative feedback loops, and we have implemented a systems biology approach to computationally study this gene regulation network. Our results indicate that the system exhibits bistability and is capable of switching states at a critical level of Notch signaling initiated by its ligand Delta in a particular range of parameter values. In this mode, transient activation of Delta is also capable of inducing prolonged high expression of Hes1, mimicking the “ON” state depending on the intensity and duration of the signal. Furthermore, this system is highly sensitive to certain model parameters and can transition from functioning as a bistable switch to an oscillator by tuning a single parameter value. This parameter, the transcriptional repression constant of hes1, can thus qualitatively govern the behavior of the signaling network. In addition, we find that the system is able to dampen and reduce the effects of biological noise that arise from stochastic effects in gene expression for systems that respond quickly to Notch signaling

Particulate air pollution, systemic oxidative stress, inflammation, and atherosclerosis

Air pollution has been associated with significant adverse health effects leading to increased overall morbidity and mortality of worldwide significance. Epidemiological studies have shown that the largest portion of air pollution-related mortality is due to cardiovascular diseases, predominantly those of ischemic nature. Human studies suggest an association with atherosclerosis and increasing experimental animal data support that this association is likely to be causal. While both gasses and particles have been linked to detrimental health effects, more evidence implicates the particulate matter (PM) components as major responsible for a large portion of the proatherogenic effects. Multiple experimental approaches have revealed the ability of PM components to trigger and/or enhance free radical reactions in cells and tissues, both ex vivo as well as in vivo. It appears that exposure to PM leads to the development of systemic prooxidant and proinflammatory effects that may be of great importance in the development of atherosclerotic lesions. This article reviews the epidemiological studies, experimental animal, and cellular data that support the association of air pollutants, especially the particulate components, with systemic oxidative stress, inflammation, and atherosclerosis. It also reviews the use of transcriptomic studies to elucidate molecular pathways of importance in those systemic effects