Phonon-mediated vs. Coulombic Back-Action in Quantum Dot circuits

Quantum point contacts (QPCs) are commonly employed to capacitively detect the charge state of coupled quantum dots (QD). An indirect back-action of a biased QPC onto a double QD laterally defined in a GaAs/AlGaAs heterostructure is observed. Energy is emitted by non-equilibrium charge carriers in the leads of the biased QPC. Part of this energy is absorbed by the double QD where it causes charge fluctuations that can be observed under certain conditions in its stability diagram. By investigating the spectrum of the absorbed energy, we identify both acoustic phonons and Coulomb interaction being involved in the back-action, depending on the geometry and coupling constants

An electron jet pump: The Venturi effect of a Fermi liquid

A three-terminal device based on a two-dimensional electron system is investigated in the regime of non-equilibrium transport. Excited electrons scatter with the cold Fermi sea and transfer energy and momentum to other electrons. A geometry analogous to a water jet pump is used to create a jet pump for electrons. Because of its phenomenological similarity we name the observed behavior "electronic Venturi effect".Comment: Journal of Applied Physics Special Topic: Plenary and Invited Papers from the 30th International Conference on the Physics of Semiconductors, Seoul, Korea, 2010; http://link.aip.org/link/?JAP/109/10241

Uncoupling cancer mutations reveals critical timing of p53 loss in sarcomagenesis

It is well accepted that cancer develops following the sequential accumulation of multiple alterations, but how the temporal order of events affects tumor initiation and/or progression remains largely unknown. Here, we describe a mouse model that allows for temporally distinct cancer mutations. By integrating a Flp-inducible allele of K-ras[superscript G12D] with established methods for Cre-mediated p53 deletion, we were able to separately control the mutation of these commonly associated cancer genes in vitro and in vivo. We show that delaying p53 deletion relative to K-ras[superscript G12D] activation reduced tumor burden in a mouse model of soft-tissue sarcoma, suggesting that p53 strongly inhibits very early steps of transformation in the muscle. Furthermore, using in vivo RNA interference, we implicate the p53 target gene p21 as a critical mediator in this process, highlighting cell-cycle arrest as an extremely potent tumor suppressor mechanism.National Institutes of Health (U.S.) (grant 5-U01-CA84306)National Cancer Institute (U.S.) (Cancer Center Support (core) Grant P30-CA14051)Howard Hughes Medical Institute (Investigator)Virginia and D.K. Ludwig Fund for Cancer Research (Scholar

Relaxation of hot electrons in a degenerate two-dimensional electron system: transition to one-dimensional scattering

The energy relaxation channels of hot electrons far from thermal equilibrium in a degenerate two-dimensional electron system are investigated in transport experiments in a mesoscopic three-terminal device. We observe a transition from two dimensions at zero magnetic field to quasi--one-dimensional scattering of the hot electrons in a strong magnetic field. In the two-dimensional case electron-electron scattering is the dominant relaxation mechanism, while the emission of optical phonons becomes more and more important as the magnetic field is increased. The observation of up to 11 optical phonons emitted per hot electron allows us to determine the onset energy of LO phonons in GaAs at cryogenic temperatures with a high precision, \eph=36.0\pm0.1\,meV. Numerical calculations of electron-electron scattering and the emission of optical phonons underline our interpretation in terms of a transition to one-dimensional dynamics.Comment: 15 pages, 9 figure

Investigating Neuroanatomical Features in Top Athletes at the Single Subject Level.

In sport events like Olympic Games or World Championships competitive athletes keep pushing the boundaries of human performance. Compared to team sports, high achievements in many athletic disciplines depend solely on the individual's performance. Contrasting previous research looking for expertise-related differences in brain anatomy at the group level, we aim to demonstrate changes in individual top athlete's brain, which would be averaged out in a group analysis. We compared structural magnetic resonance images (MRI) of three professional track-and-field athletes to age-, gender- and education-matched control subjects. To determine brain features specific to these top athletes, we tested for significant deviations in structural grey matter density between each of the three top athletes and a carefully matched control sample. While total brain volumes were comparable between athletes and controls, we show regional grey matter differences in striatum and thalamus. The demonstrated brain anatomy patterns remained stable and were detected after 2 years with Olympic Games in between. We also found differences in the fusiform gyrus in two top long jumpers. We interpret our findings in reward-related areas as correlates of top athletes' persistency to reach top-level skill performance over years

Quantum interference and phonon-mediated back-action in lateral quantum dot circuits

Spin qubits have been successfully realized in electrostatically defined, lateral few-electron quantum dot circuits. Qubit readout typically involves spin to charge information conversion, followed by a charge measurement made using a nearby biased quantum point contact. It is critical to understand the back-action disturbances resulting from such a measurement approach. Previous studies have indicated that quantum point contact detectors emit phonons which are then absorbed by nearby qubits. We report here the observation of a pronounced back-action effect in multiple dot circuits where the absorption of detector-generated phonons is strongly modified by a quantum interference effect, and show that the phenomenon is well described by a theory incorporating both the quantum point contact and coherent phonon absorption. Our combined experimental and theoretical results suggest strategies to suppress back-action during the qubit readout procedure.Comment: 25 pages, 8 figure

Repression of a Potassium Channel by Nuclear Hormone Receptor and TGF-β Signaling Modulates Insulin Signaling in Caenorhabditis elegans

Transforming growth factor β (TGF-β) signaling acts through Smad proteins to play fundamental roles in cell proliferation, differentiation, apoptosis, and metabolism. The Receptor associated Smads (R-Smads) interact with DNA and other nuclear proteins to regulate target gene transcription. Here, we demonstrate that the Caenorhabditis elegans R-Smad DAF-8 partners with the nuclear hormone receptor NHR-69, a C. elegans ortholog of mammalian hepatocyte nuclear factor 4α HNF4α), to repress the exp-2 potassium channel gene and increase insulin secretion. We find that NHR-69 associates with DAF-8 both in vivo and in vitro. Functionally, daf-8 nhr-69 double mutants show defects in neuropeptide secretion and phenotypes consistent with reduced insulin signaling such as increased expression of the sod-3 and gst-10 genes and a longer life span. Expression of the exp-2 gene, encoding a voltage-gated potassium channel, is synergistically increased in daf-8 nhr-69 mutants compared to single mutants and wild-type worms. In turn, exp-2 acts selectively in the ASI neurons to repress the secretion of the insulin-like peptide DAF-28. Importantly, exp-2 mutation shortens the long life span of daf-8 nhr-69 double mutants, demonstrating that exp-2 is required downstream of DAF-8 and NHR-69. Finally, animals over-expressing NHR-69 specifically in DAF-28–secreting ASI neurons exhibit a lethargic, hypoglycemic phenotype that is rescued by exogenous glucose. We propose a model whereby DAF-8/R-Smad and NHR-69 negatively regulate the transcription of exp-2 to promote neuronal DAF-28 secretion, thus demonstrating a physiological crosstalk between TGF-β and HNF4α-like signaling in C. elegans. NHR-69 and DAF-8 dependent regulation of exp-2 and DAF-28 also provides a novel molecular mechanism that contributes to the previously recognized link between insulin and TGF-β signaling in C. elegans

A newly described strain of Eimeria arloingi (strain A) belongs to the phylogenetic group of ruminant-infecting pathogenic species, which replicate in host endothelial cells in vivo

Coccidiosis caused by Eimeria species is an important disease worldwide, particularly in ruminants and poultry. Eimeria infection can result in significant economic losses due to costs associated with treatment and slower growth rates, or even with mortality of heavily infected individuals. In goat production, a growing industry due to increasing demand for caprine products worldwide, coccidiosis is caused by several Eimeria species with E. arloingi and E. ninakohlyakimovae the most pathogenic. The aims of this study were genetic characterization of a newly isolated European E. arloingi strain (A) and determination of phylogenetic relationships with Eimeria species from other ruminants. Therefore, a DNA sequence of E. arloingi strain (A) containing 2290 consensus nucleotides (the majority of 18S rDNA, complete ITS-1 and 5.8S sequences, and the partial ITS-2) was amplified and phylogenetic relationship determined with the most similar sequences available on GenBank. The phylogenetic tree presented a branch constituted by bovine Eimeria species plus E. arloingi, and another one exclusively populated by ovine Eimeria species. Moreover, E. arloingi, E. bovis and E. zuernii, which all replicate in host intestinal endothelial cells of the lacteals, were found within the same cluster. This study gives new insights into the evolutionary phylogenetic relationships of this newly described caprine Eimeria strain and confirmed its close relationship to other highly pathogenic ruminant Eimeria species characterized by macromeront formation in host endothelial cells of the central lymph capillaries of the small intestine