Josephson Coupling through a Quantum Dot

We derive, via fourth order perturbation theory, an expression for the Josephson current through a gated interacting quantum dot. We analyze our expression for two different models of the superconductor-dot-superconductor (SDS) system. When the matrix elements connecting dot and leads are featureless constants, we compute the Josephson coupling J_c as a function of the gate voltage and Coulomb interaction. In the diffusive dot limit, we compute the probability distribution P(J_c) of Josephson couplings. In both cases, pi junction behavior (J_c < 0) is possible, and is not simply dependent on the parity of the dot occupancy.Comment: 9 pages; 3 encapsulated PostScript figure

PD-0283: 4D dose accumulation for dose painting by numbers for lung cancer

In conventional radiotherapy of locally advanced lung cancer (LALC) doses levels are homogeneously delivered to the entire PTV, whereat dose escalation is restricted by normal tissue toxicity. Several studies have shown the geometrical correlation between high FDG uptake in a PET scan and tumour recurrence. This is the rationale for FDG-based local dose escalation, e.g. by dose prescription on the voxel values of a PET scan – dose painting by numbers (DPBN). The aim of this study is to investigate the robustness of the DPBN plans against tumour motio

Antiferromagnetic Order of the Ru and Gd in Superconducting RuSr2GdCu2O8

Neutron diffraction has been used to study the magnetic order in RuSr{2}GdCu2O8. The Ru moments order antiferromagnetically at T{N}=136(2)K, coincident with the previously reported onset of ferromagnetism. Neighboring spins are antiparallel in all three directions, with a low T moment of 1.18(6) mu {B} along the c-axis. Our measurements put an upper limit of ~0.1 mu{B} to any net zero-field moment, with fields exceeding ~0.4T needed to induce a measurable magnetization. The Gd ions order independently at T{N}=2.50(2)K with the same spin configuration. PACS numbers: 74.72.Jt, 75.25.+z, 74.25.Ha, 75.30.KzComment: Four pages, Latex, 5 eps figure

Proximity effects and characteristic lengths in ferromagnet-superconductor structures

We present an extensive theoretical investigation of the proximity effects that occur in Ferromagnet/Superconductor ($F/S$) systems. We use a numerical method to solve self consistently the Bogoliubov-de Gennes equations in the continuum. We obtain the pair amplitude and the local density of states (DOS), and use these results to extract the relevant lengths characterizing the leakage of superconductivity into the magnet and to study spin splitting into the superconductor. These phenomena are investigated as a function of parameters such as temperature, magnet polarization, interfacial scattering, sample size and Fermi wavevector mismatch, all of which turn out to have important influence on the results. These comprehensive results should help characterize and analyze future data and are shown to be in agreement with existing experiments.Comment: 24 pages, including 26 figure

Layered ferromagnet-superconductor structures: the π\pi state and proximity effects

We investigate clean mutilayered structures of the SFS and SFSFS type, (where the S layer is intrinsically superconducting and the F layer is ferromagnetic) through numerical solution of the self-consistent Bogoliubov-de Gennes equations for these systems. We obtain results for the pair amplitude, the local density of states, and the local magnetic moment. We find that as a function of the thickness $d_F$ of the magnetic layers separating adjacent superconductors, the ground state energy varies periodically between two stable states. The first state is an ordinary "0-state", in which the order parameter has a phase difference of zero between consecutive S layers, and the second is a "$\pi$-state", where the sign alternates, corresponding to a phase difference of $\pi$ between adjacent S layers. This behavior can be understood from simple arguments. The density of states and the local magnetic moment reflect also this periodicity.Comment: 12 pages, 10 Figure

Spike firing and IPSPs in layer V pyramidal neurons during beta oscillations in rat primary motor cortex (M1) in vitro

Beta frequency oscillations (10-35 Hz) in motor regions of cerebral cortex play an important role in stabilising and suppressing unwanted movements, and become intensified during the pathological akinesia of Parkinson's Disease. We have used a cortical slice preparation of rat brain, combined with concurrent intracellular and field recordings from the primary motor cortex (M1), to explore the cellular basis of the persistent beta frequency (27-30 Hz) oscillations manifest in local field potentials (LFP) in layers II and V of M1 produced by continuous perfusion of kainic acid (100 nM) and carbachol (5 µM). Spontaneous depolarizing GABA-ergic IPSPs in layer V cells, intracellularly dialyzed with KCl and IEM1460 (to block glutamatergic EPSCs), were recorded at -80 mV. IPSPs showed a highly significant (P< 0.01) beta frequency component, which was highly significantly coherent with both the Layer II and V LFP oscillation (which were in antiphase to each other). Both IPSPs and the LFP beta oscillations were abolished by the GABAA antagonist bicuculline. Layer V cells at rest fired spontaneous action potentials at sub-beta frequencies (mean of 7.1+1.2 Hz; n = 27) which were phase-locked to the layer V LFP beta oscillation, preceding the peak of the LFP beta oscillation by some 20 ms. We propose that M1 beta oscillations, in common with other oscillations in other brain regions, can arise from synchronous hyperpolarization of pyramidal cells driven by synaptic inputs from a GABA-ergic interneuronal network (or networks) entrained by recurrent excitation derived from pyramidal cells. This mechanism plays an important role in both the physiology and pathophysiology of control of voluntary movement generation

Dopamine acting at D1-like, D2-like and α1-adrenergic receptors differentially modulates theta and gamma oscillatory activity in primary motor cortex

The loss of dopamine (DA) in Parkinson’s is accompanied by the emergence of exaggerated theta and beta frequency neuronal oscillatory activity in the primary motor cortex (M1) and basal ganglia. DA replacement therapy or deep brain stimulation reduces the power of these oscillations and this is coincident with an improvement in motor performance implying a causal relationship. Here we provide in vitro evidence for the differential modulation of theta and gamma activity in M1 by DA acting at receptors exhibiting conventional and non-conventional DA pharmacology. Recording local field potentials in deep layer V of rat M1, co-application of carbachol (CCh, 5 μM) and kainic acid (KA, 150 nM) elicited simultaneous oscillations at a frequency of 6.49 ± 0.18 Hz (theta, n = 84) and 34.97 ± 0.39 Hz (gamma, n = 84). Bath application of DA resulted in a decrease in gamma power with no change in theta power. However, application of either the D1-like receptor agonist SKF38393 or the D2-like agonist quinpirole increased the power of both theta and gamma suggesting that the DA-mediated inhibition of oscillatory power is by action at other sites other than classical DA receptors. Application of amphetamine, which promotes endogenous amine neurotransmitter release, or the adrenergic α1-selective agonist phenylephrine mimicked the action of DA and reduced gamma power, a result unaffected by prior co-application of D1 and D2 receptor antagonists SCH23390 and sulpiride. Finally, application of the α1-adrenergic receptor antagonist prazosin blocked the action of DA on gamma power suggestive of interaction between α1 and DA receptors. These results show that DA mediates complex actions acting at dopamine D1-like and D2-like receptors, α1 adrenergic receptors and possibly DA/α1 heteromultimeric receptors to differentially modulate theta and gamma activity in M1

Restoring brain function after stroke - bridging the gap between animals and humans

Stroke is the leading cause of complex adult disability in the world. Recovery from stroke is often incomplete, which leaves many people dependent on others for their care. The improvement of long-term outcomes should, therefore, be a clinical and research priority. As a result of advances in our understanding of the biological mechanisms involved in recovery and repair after stroke, therapeutic opportunities to promote recovery through manipulation of poststroke plasticity have never been greater. This work has almost exclusively been carried out in preclinical animal models of stroke with little translation into human studies. The challenge ahead is to develop a mechanistic understanding of recovery from stroke in humans. Advances in neuroimaging techniques now enable us to reconcile behavioural accounts of recovery with molecular and cellular changes. Consequently, clinical trials can be designed in a stratified manner that takes into account when an intervention should be delivered and who is most likely to benefit. This approach is expected to lead to a substantial change in how restorative therapeutic strategies are delivered in patients after stroke