Observing different phases for the dynamics of entanglement in an ion trap

The evolution of the entanglement between two oscillators coupled to a common thermal environment is non-trivial. The long time limit has three qualitatively different behaviors (phases) depending on parameters such as the temperature of the bath ({\em Phys. Rev. Lett.} \textbf{100}, 220401). The phases include cases with non-vanishing long-term entanglement, others with a final disentangled state, and situations displaying an infinite sequence of events of disappearance and revival of entanglement. We describe an experiment to realize these different scenarios in an ion trap. The motional degrees of freedom of two ions are used to simulate the system while the coupling to an extra (central) ion, which is continuously laser cooled, is the gateway to a decohering reservoir. The scheme proposed allows for the observation and control of motional entanglement dynamics, and is an example of a class of simulations of quantum open systems in the non-Markovian regime.Comment: 5 pages, 5 figure

Decoherence induced by a dynamic spin environment (II): Disentanglement by local system-environment interactions

This article studies the decoherence induced on a system of two qubits by local interactions with a spin chain with nontrivial internal dynamics (governed by an XY Hamiltonian). Special attention is payed to the transition between two limits: one in which both qubits interact with the same site of the chain and another one where they interact with distant sites. The two cases exhibit different behaviours in the weak and strong coupling regimes: when the coupling is weak it is found that decoherence tends to decrease with distance, while for strong coupling the result is the opposite. Also, in the weak coupling case, the long distance limit is rapidly reached, while for strong coupling there is clear evidence of an expected effect: environment-induced interactions between the qubits of the system. A consequence of this is the appearance of quasiperiodic events that can be interpreted as ``sudden deaths'' and ``sudden revivals'' of the entanglement between the qubits, with a time scale related to the distance between them.Comment: 10 pages, 9 figure

Kidney regeneration: common themes from the embryo to the adult

The vertebrate kidney has an inherent ability to regenerate following acute damage. Successful regeneration of the injured kidney requires the rapid replacement of damaged tubular epithelial cells and reconstitution of normal tubular function. Identifying the cells that participate in the regeneration process as well as the molecular mechanisms involved may reveal therapeutic targets for the treatment of kidney disease. Renal regeneration is associated with the expression of genetic pathways that are necessary for kidney organogenesis, suggesting that the regenerating tubular epithelium may be “reprogrammed” to a less-differentiated, progenitor state. This review will highlight data from various vertebrate models supporting the hypothesis that nephrogenic genes are reactivated as part of the process of kidney regeneration following acute kidney injury (AKI). Emphasis will be placed on the reactivation of developmental pathways and how our understanding of the resulting regeneration process may be enhanced by lessons learned in the embryonic kidney.Fil: Cirio, Maria Cecilia. University of Pittsburgh; Estados Unidos. Consejo Nacional de Investigaciones Científicas y Técnicas; ArgentinaFil: de Groh, Eric D.. University of Pittsburgh; Estados UnidosFil: de Caestecker, Mark P.. Vanderbilt University; Estados UnidosFil: Davidson, Alan J.. The University of Auckland; Nueva ZelandaFil: Hukriede, Neil A.. University of Pittsburgh; Estados Unido

Using individual tracking data to validate the predictions of species distribution models

The authors would like to thank the College of Life Sciences of Aberdeen University and Marine Scotland Science which funded CP's PhD project. Skate tagging experiments were undertaken as part of Scottish Government project SP004. We thank Ian Burrett for help in catching the fish and the other fishermen and anglers who returned tags. We thank José Manuel Gonzalez-Irusta for extracting and making available the environmental layers used as environmental covariates in the environmental suitability modelling procedure. We also thank Jason Matthiopoulos for insightful suggestions on habitat utilization metrics as well as Stephen C.F. Palmer, and three anonymous reviewers for useful suggestions to improve the clarity and quality of the manuscript.Peer reviewedPostprintPostprintPostprintPostprintPostprin

Controlled Anisotropic Deformation of Ag Nanoparticles by Si Ion Irradiation

The shape and alignment of silver nanoparticles embedded in a glass matrix is controlled using silicon ion irradiation. Symmetric silver nanoparticles are transformed into anisotropic particles whose larger axis is along the ion beam. Upon irradiation, the surface plasmon resonance of symmetric particles splits into two resonances whose separation depends on the fluence of the ion irradiation. Simulations of the optical absorbance show that the anisotropy is caused by the deformation and alignment of the nanoparticles, and that both properties are controlled with the irradiation fluence.Comment: Submitted to Phys. Rev. Lett. (October 14, 2005

Decreased expression of caveolin 1 in patients with systemic sclerosis: crucial role in the pathogenesis of tissue fibrosis.

OBJECTIVE: Recent studies have implicated caveolin 1 in the regulation of transforming growth factor beta (TGFbeta) downstream signaling. Given the crucial role of TGFbeta in the pathogenesis of systemic sclerosis (SSc), we sought to determine whether caveolin 1 is also involved in the pathogenesis of tissue fibrosis in SSc. We analyzed the expression of CAV1 in affected SSc tissues, studied the effects of lack of expression of CAV1 in vitro and in vivo, and analyzed the effects of restoration of caveolin 1 function on the fibrotic phenotype of SSc fibroblasts in vitro. METHODS: CAV1 expression in tissues was analyzed by immunofluorescence and confocal microscopy. The extent of tissue fibrosis in Cav1-knockout mice was assessed by histologic/histochemical analyses and quantified by hydroxyproline assays. Cav1-null and SSc fibroblast phenotypes and protein production were analyzed by real-time polymerase chain reaction, immunofluorescence, Western blot, and multiplexed enzyme-linked immunosorbent assay techniques. The effects of restoration of caveolin 1 function in SSc fibroblasts in vitro were also examined using a cell-permeable recombinant CAV1 peptide. RESULTS: CAV1 was markedly decreased in the affected lungs and skin of SSc patients. Cav1-knockout mice developed pulmonary and skin fibrosis. Down-regulation of caveolin 1 was maintained in cultured SSc fibroblasts, and restoration of caveolin 1 function in vitro normalized their phenotype and abrogated TGFbeta stimulation through inhibition of Smad3 activation. CONCLUSION: Caveolin 1 appears to participate in the pathogenesis of tissue fibrosis in SSc. Restoration of caveolin 1 function by treatment with a cell-permeable peptide corresponding to the CAV1 scaffolding domain may be a novel therapeutic approach in SSc

Myocardial creatine levels do not influence response to acute oxidative stress in isolated perfused heart

Background: Multiple studies suggest creatine mediates anti-oxidant activity in addition to its established role in cellular energy metabolism. The functional significance for the heart has yet to be established, but antioxidant activity could contribute to the cardioprotective effect of creatine in ischaemia/reperfusion injury. Objectives: To determine whether intracellular creatine levels influence responses to acute reactive oxygen species (ROS) exposure in the intact beating heart. We hypothesised that mice with elevated creatine due to over-expression of the creatine transporter (CrT-OE) would be relatively protected, while mice with creatine-deficiency (GAMT KO) would fare worse. Methods and Results: CrT-OE mice were pre-selected for creatine levels 20–100% above wild-type using in vivo 1 H– MRS. Hearts were perfused in isovolumic Langendorff mode and cardiac function monitored throughout. After 20 min equilibration, hearts were perfused with either H2O2 0.5 mM (30 min), or the anti-neoplastic drug doxorubicin 15 mM (100 min). Protein carbonylation, creatine kinase isoenzyme activities and phospho-PKCd expression were quantified in perfused hearts as markers of oxidative damage and apoptotic signalling. Wild-type hearts responded to ROS challenge with a profound decline in contractile function that was ameliorated by co-administration of catalase or dexrazoxane as positive controls. In contrast, the functional deterioration in CrT-OE and GAMT KO hearts was indistinguishable from wildtype controls, as was the extent of oxidative damage and apoptosis. Exogenous creatine supplementation also failed to protect hearts from doxorubicin-induced dysfunction. Conclusions: Intracellular creatine levels do not influence the response to acute ROS challenge in the intact beating heart, arguing against creatine exerting (patho-)physiologically relevant anti-oxidant activity

CB1 Receptor Antagonism Blocks Stress-Potentiated Reinstatement of Cocaine Seeking in Rats

Rationale Under some conditions, stress, rather than directly triggering cocaine seeking, potentiates reinstatement to other stimuli, including a subthreshold cocaine dose. The mechanisms responsible for stress-potentiated reinstatement are not well defined. Endocannabinoid signaling is increased by stress and regulates synaptic transmission in brain regions implicated in motivated behavior. Objectives The objective of this study was to test the hypothesis that cannabinoid type 1 receptor (CB1R) signaling is required for stress-potentiated reinstatement of cocaine seeking in rats. Methods Following i.v. cocaine self-administration (2 h access/day) and extinction in male rats, footshock stress alone does not reinstate cocaine seeking but reinstatement is observed when footshock is followed by an injection of an otherwise subthreshold dose of cocaine (2.5 mg/kg, i.p.). CB1R involvement was tested by systemic administration of the CB1R antagonist AM251 (0, 1, or 3 mg/kg, i.p.) prior to testing for stress-potentiated reinstatement. Results Stress-potentiated reinstatement was blocked by both 1 and 3 mg/kg AM251. By contrast, AM251 only attenuated food-reinforced lever pressing at the higher dose (i.e., 3 mg/kg) and did not affect locomotor activity at either dose tested. Neither high-dose cocaine-primed reinstatement (10 mg/kg, i.p.) nor footshock stress-triggered reinstatement following long-access cocaine self-administration (6 h access/day) was affected by AM251 pretreatment. Footshock stress increased concentrations of both endocannabinoids, N-arachidonylethanolamine and 2-arachidonoylglycerol, in regions of the prefrontal cortex. Conclusions These findings demonstrate that footshock stress increases prefrontal cortical endocannabinoids and stress-potentiated reinstatement is CB1R-dependent, suggesting that CB1R is a potential therapeutic target for relapse prevention, particularly in individuals whose cocaine use is stress-related