119 research outputs found

    Bifurcations and chaos in semiconductor superlattices with a tilted magnetic field

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    We study the effects of dissipation on electron transport in a semiconductor superlattice with an applied bias voltage and a magnetic field that is tilted relative to the superlattice axis.In previous work, we showed that although the applied fields are stationary,they act like a THz plane wave, which strongly couples the Bloch and cyclotron motion of electrons within the lowest miniband. As a consequence,the electrons exhibit a unique type of Hamiltonian chaos, which creates an intricate mesh of conduction channels (a stochastic web) in phase space, leading to a large resonant increase in the current flow at critical values of the applied voltage. This phase-space patterning provides a sensitive mechanism for controlling electrical resistance. In this paper, we investigate the effects of dissipation on the electron dynamics by modifying the semiclassical equations of motion to include a linear damping term. We demonstrate that even in the presence of dissipation,deterministic chaos plays an important role in the electron transport process. We identify mechanisms for the onset of chaos and explore the associated sequence of bifurcations in the electron trajectories. When the Bloch and cyclotron frequencies are commensurate, complex multistability phenomena occur in the system. In particular, for fixed values of the control parameters several distinct stable regimes can coexist, each corresponding to different initial conditions. We show that this multistability has clear, experimentally-observable, signatures in the electron transport characteristics.Comment: 14 pages 11 figure

    Theory of Transmission through disordered superlattices

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    We derive a theory for transmission through disordered finite superlattices in which the interface roughness scattering is treated by disorder averaging. This procedure permits efficient calculation of the transmission thr ough samples with large cross-sections. These calculations can be performed utilizing either the Keldysh or the Landauer-B\"uttiker transmission formalisms, both of which yield identical equations. For energies close to the lowest miniband, we demonstrate the accuracy of the computationally efficient Wannier-function approximation. Our calculations indicate that the transmission is strongly affected by interface roughness and that information about scale and size of the imperfections can be obtained from transmission data.Comment: 12 pages, 6 Figures included into the text. Final version with minor changes. Accepted by Physical Review

    A 160-kilobit molecular electronic memory patterned at 10^(11) bits per square centimetre

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    The primary metric for gauging progress in the various semiconductor integrated circuit technologies is the spacing, or pitch, between the most closely spaced wires within a dynamic random access memory (DRAM) circuit. Modern DRAM circuits have 140nm pitch wires and a memory cell size of 0.0408 μm^2. Improving integrated circuit technology will require that these dimensions decrease over time. However, at present a large fraction of the patterning and materials requirements that we expect to need for the construction of new integrated circuit technologies in 2013 have ‘no known solution’. Promising ingredients for advances in integrated circuit technology are nanowires, molecular electronics and defect-tolerant architectures, as demonstrated by reports of single devices and small circuits. Methods of extending these approaches to large-scale, high-density circuitry are largely undeveloped. Here we describe a 160,000-bit molecular electronic memory circuit, fabricated at a density of 10^(11) bits cm^(-2) (pitch 33 nm; memory cell size 0.0011 mm^2), that is, roughly analogous to the dimensions of a DRAM circuit projected to be available by 2020. A monolayer of bistable, [2]rotaxane molecules 10 served as the data storage elements. Although the circuit has large numbers of defects, those defects could be readily identified through electronic testing and isolated using software coding. The working bits were then configured to form a fully functional random access memory circuit for storing and retrieving information

    The Function of Heterodimeric AP-1 Comprised of c-Jun and c-Fos in Activin Mediated Spemann Organizer Gene Expression

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    BACKGROUND:Activator protein-1 (AP-1) is a mediator of BMP or FGF signaling during Xenopus embryogenesis. However, specific role of AP-1 in activin signaling has not been elucidated during vertebrate development. METHODOLOGY/PRINCIPAL FINDINGS:We provide new evidence showing that overexpression of heterodimeric AP-1 comprised of c-jun and c-fos (AP-1(c-Jun/c-Fos)) induces the expression of BMP-antagonizing organizer genes (noggin, chordin and goosecoid) that were normally expressed by high dose of activin. AP-1(c-Jun/c-Fos) enhanced the promoter activities of organizer genes but reduced that of PV.1, a BMP4-response gene. A loss of function study clearly demonstrated that AP-1(c-Jun/c-Fos) is required for the activin-induced organizer and neural gene expression. Moreover, physical interaction of AP-1(c-Jun/c-Fos) and Smad3 cooperatively enhanced the transcriptional activity of goosecoid via direct binding on this promoter. Interestingly, Smad3 mutants at c-Jun binding site failed in regulation of organizer genes, indicating that these physical interactions are specifically necessary for the expression of organizer genes. CONCLUSIONS/SIGNIFICANCE:AP-1(c-Jun/c-Fos) plays a specific role in organizer gene expression in downstream of activin signal during early Xenopus embryogenesis

    The Cytosolic Protein G0S2 Maintains Quiescence in Hematopoietic Stem Cells

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    Bone marrow hematopoietic stem cells (HSCs) balance proliferation and differentiation by integrating complex transcriptional and post-translational mechanisms regulated by cell intrinsic and extrinsic factors. We found that transcripts of G0/G1 switch gene 2 (G0S2) are enriched in lineage− Sca-1+ c-kit+ (LSK) CD150+ CD48− CD41− cells, a population highly enriched for quiescent HSCs, whereas G0S2 expression is suppressed in dividing LSK CD150+ CD48− cells. Gain-of-function analyses using retroviral expression vectors in bone marrow cells showed that G0S2 localizes to the mitochondria, endoplasmic reticulum, and early endosomes in hematopoietic cells. Co-transplantation of bone marrow cells transduced with the control or G0S2 retrovirus led to increased chimerism of G0S2-overexpressing cells in femurs, although their contribution to the blood was reduced. This finding was correlated with increased quiescence in G0S2-overexpressing HSCs (LSK CD150+ CD48−) and progenitor cells (LS−K). Conversely, silencing of endogenous G0S2 expression in bone marrow cells increased blood chimerism upon transplantation and promoted HSC cell division, supporting an inhibitory role for G0S2 in HSC proliferation. A proteomic study revealed that the hydrophobic domain of G0S2 interacts with a domain of nucleolin that is rich in arginine-glycine-glycine repeats, which results in the retention of nucleolin in the cytosol. We showed that this cytosolic retention of nucleolin occurs in resting, but not proliferating, wild-type LSK CD150+ CD48− cells. Collectively, we propose a novel model of HSC quiescence in which elevated G0S2 expression can sequester nucleolin in the cytosol, precluding its pro-proliferation functions in the nucleolus
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