Row-switched states in two-dimensional underdamped Josephson junction arrays

When magnetic flux moves across layered or granular superconductor structures, the passage of vortices can take place along channels which develop finite voltage, while the rest of the material remains in the zero-voltage state. We present analytical studies of an example of such mixed dynamics: the row-switched (RS) states in underdamped two-dimensional Josephson arrays, driven by a uniform DC current under external magnetic field but neglecting self-fields. The governing equations are cast into a compact differential-algebraic system which describes the dynamics of an assembly of Josephson oscillators coupled through the mesh current. We carry out a formal perturbation expansion, and obtain the DC and AC spatial distributions of the junction phases and induced circulating currents. We also estimate the interval of the driving current in which a given RS state is stable. All these analytical predictions compare well with our numerics. We then combine these results to deduce the parameter region (in the damping coefficient versus magnetic field plane) where RS states can exist.Comment: latex, 48 pages, 15 figs using psfi

Minimization of phonon-tunneling dissipation in mechanical resonators

Micro- and nanoscale mechanical resonators have recently emerged as ubiquitous devices for use in advanced technological applications, for example in mobile communications and inertial sensors, and as novel tools for fundamental scientific endeavors. Their performance is in many cases limited by the deleterious effects of mechanical damping. Here, we report a significant advancement towards understanding and controlling support-induced losses in generic mechanical resonators. We begin by introducing an efficient numerical solver, based on the "phonon-tunneling" approach, capable of predicting the design-limited damping of high-quality mechanical resonators. Further, through careful device engineering, we isolate support-induced losses and perform the first rigorous experimental test of the strong geometric dependence of this loss mechanism. Our results are in excellent agreement with theory, demonstrating the predictive power of our approach. In combination with recent progress on complementary dissipation mechanisms, our phonon-tunneling solver represents a major step towards accurate prediction of the mechanical quality factor.Comment: 12 pages, 4 figure

VEGF Induces More Severe Cerebrovascular Dysplasia in Eng+/− than in Alk1+/− Mice

Brain arteriovenous malformations (BAVMs) are an important cause of intracranial hemorrhage (ICH) in young adults. A small percent of BAVMs is due to hereditary hemorrhagic telangiectasia 1 and 2 (HHT1 and 2), which are caused by mutations in two genes involved in transforming growth factor-β signaling: endoglin (Eng), and activin-like kinase 1 (Alk1). The BAVM phenotype has incomplete penetrance in HHT patients, and the mechanism is unknown. We tested the hypothesis that a “response-to-injury” triggers abnormal vascular (dysplasia) development, using Eng and Alk1 haploinsufficient mice. Adeno-associated virus (AAV) expressing vascular endothelial growth factor (VEGF) was used to mimic the injury conditions. VEGF overexpression caused a similar degree of angiogenesis in the brain of all groups, except that the cortex of Alk1+/− mice had a 33% higher capillary density than other groups. There were different levels of cerebrovascular dysplasia observed in haploinsufficient mice (Eng+/− > Alk1+/−), which simulates the relative penetrance of BAVM in HHT patients (HHT1 > HHT2). Few dysplastic capillaries were observed in AAV-LacZ-injected mice. Our data indicate that both angiogenic stimulation and genetic alteration are necessary for the development of vascular dysplasia, suggesting that anti-angiogenic therapies might be adapted to slow the progression of the disease and decrease the risk of spontaneous ICH

Moving glass theory of driven lattices with disorder

We study periodic structures, such as vortex lattices, moving in a random potential. As predicted in [T. Giamarchi, P. Le Doussal Phys. Rev. Lett. 76 3408 (1996)] the periodicity in the direction transverse to motion leads to a new class of driven systems: the Moving Glasses. We analyse using several RG techniques the properties at T=0 and $T>0$: (i) decay of translational long range order (ii) particles flow along static channels (iii) the channel pattern is highly correlated (iv) barriers to transverse motion. We demonstrate the existence of the ``transverse critical force'' at T=0. A ``static random force'' is shown to be generated by motion. Displacements grow logarithmically in $d=3$ and algebraically in $d=2$. The persistence of quasi long range translational order in $d=3$ at weak disorder, or large velocity leads to predict a topologically ordered ``Moving Bragg Glass''. This state continues the static Bragg glass and is stable at $T>0$, with non linear transverse response and linear asymptotic behavior. In $d=2$, or in $d=3$ at intermediate disorder, another moving glass exist (the Moving Transverse Glass) with smectic quasi order in the transverse direction. A phase diagram in $T$ force and disorder for static and moving structures is proposed. For correlated disorder we predict a ``moving Bose glass'' state with anisotropic transverse Meissner effect and transverse pinning. We discuss experimental consequences such as anomalous Hall effect in Wigner crystal and transverse critical current in vortex lattice.Comment: 74 pages, 27 figures, RevTe

Loss of Akt activity increases circulating soluble endoglin release in preeclampsia:identification of inter-dependency between Akt-1 and heme oxygenase-1

Aims - Endothelial dysfunction is a hallmark of preeclampsia. Desensitization of the phosphoinositide 3-kinase (PI3K)/Akt pathway underlies endothelial dysfunction and haeme oxygenase-1 (HO-1) is decreased in preeclampsia. To identify therapeutic targets, we sought to assess whether these two regulators act to suppress soluble endoglin (sEng), an antagonist of transforming growth factor-ß (TGF-ß) signalling, which is known to be elevated in preeclampsia. Methods and results - Vascular endothelial growth factor-A (VEGF-A), fibroblast growth factor (FGF-2), angiopoietin-1 (Ang-1), and insulin, which all activate the PI3K/Akt pathway, inhibited the release of sEng from endothelial cells. Inhibition of the PI3K/Akt pathway, by overexpression of phosphatase and tensin homolog (PTEN) or a dominant-negative isoform of Akt (Aktdn) induced sEng release from endothelial cells and prevented the inhibitory effect of VEGF-A. Conversely, overexpression of a constitutively active Akt (Aktmyr) inhibited PTEN and cytokine-induced sEng release. Systemic delivery of Aktmyr to mice significantly reduced circulating sEng, whereas Aktdn promoted sEng release. Phosphorylation of Akt was reduced in preeclamptic placenta and this correlated with the elevated level of circulating sEng. Knock-down of Akt using siRNA prevented HO-1-mediated inhibition of sEng release and reduced HO-1 expression. Furthermore, HO-1 null mice have reduced phosphorylated Akt in their organs and overexpression of Aktmyr failed to suppress the elevated levels of sEng detected in HO-1 null mice, indicating that HO-1 is required for the Akt-mediated inhibition of sEng. Conclusion - The loss of PI3K/Akt and/or HO-1 activity promotes sEng release and positive manipulation of these pathways offers a strategy to circumvent endothelial dysfunction

Superconducting and Quantum-Effect Devices

Contains reports on nine research projects and a list of publications.National Science Foundation Fellowship MIP 88-58764Advanced Research Projects Agency/Consortium for Superconducting Electronics Contract MDA972-90-C-0021National Science Foundation Grant DMR 91-08748National Science Foundation Fellowship ProgramU.S. Air Force - Office of Scientific Research Grant F49620-92-J-0064National Science Foundation Grant DMR 94-0202