Reentrant transition induced by multiplictative noise in the Time Dependent Ginzburg-Landau model

An effect of multiplicative noise in the time-dependent Ginzburg-Landau model is reported, namely, that noise at a relatively low intensity induces a phase transition towards an ordered state, whereas strong noise plays a destructive role, driving the system back to its disordered state through a reentrant phase transition. The phase diagram is calculated analytically using a mean-field theory and a more sophisticated approach and is compared with the results from extensive numerical simulations.

Stochastic processes induced by dichotomous markov noise: Some exact dynamical results

Stochastic processes defined by a general Langevin equation of motion where the noise is the non-Gaussian dichotomous Markov noise are studied. A non-FokkerPlanck master differential equation is deduced for the probability density of these processes. Two different models are exactly solved. In the second one, a nonequilibrium bimodal distribution induced by the noise is observed for a critical value of its correlation time. Critical slowing down does not appear in this point but in another one.

Sidebranching induced by external noise in solutal dendritic growth

We have studied sidebranching induced by fluctuations in dendritic growth. The amplitude of sidebranching induced by internal (equilibrium) concentration fluctuations in the case of solidification with solutal diffusion is computed. This amplitude turns out to be significantly smaller than values reported in previous experiments. The effects of other possible sources of fluctuations (of an external origin) are examined by introducing nonconserved noise in a phase-field model. This reproduces the characteristics of sidebranching found in experiments. Results also show that sidebranching induced by external noise is qualitatively similar to that of internal noise, and it is only distinguished by its amplitude.

Comments on "On resistor-induced thermal noise in linear circuits"

Correspondència referida a l'article de R. Giannetti, publicat ibid. vol.49 p.87-88

Hydrogen-induced changes in the breakdown voltage of InP HEMTs

In this work, electrical measurements show that the breakdown voltage,BVDG, of InP HEMTs increases following exposure to H2. This BVDG shift is nonrecoverable. The increase in BVDG is found to be due to a decrease in the carrier concentration in the extrinsic portion of the device.We provide evidence that H2 reacts with the exposed InAlAs surface in the extrinsic region next to the gate, changing the underlying carrier concentration. Hall measurements of capped and uncapped HEMT samples show that the decrease in sheet carrier concentration can be attributed to a modification of the exposed InAlAs surface. Consistent with this, XPS experiments on uncapped heterostructures give evidence of As loss from the InAlAs surface upon exposure to hydrogen.

External dichotomous noise: The problem of the mean-first-passage time

A retarded backward equation for a non-Markovian process induced by dichotomous noise (the random telegraphic signal) is deduced. The mean-first-passage time of this process is exactly obtained. The Gaussian white noise and the white shot noise limits are studied. Explicit physical results in first approximation are evaluated.

Coherence and anticoherence resonance tunned by noise

We present numerical evidence and a theoretical analysis of the appearance of anticoherence resonance induced by noise, not predicted in former analysis of coherence resonance. We have found that this phenomenon occurs for very small values of the intensity of the noise acting on an excitable system, and we claim that this is a universal signature of a nonmonotonous relaxational behavior near its oscillatory regime. Moreover, we demonstrate that this new phenomenon is totally compatible with the standard situation of coherence resonance appearing at intermediate values of noise intensity.

Laser-induced forward transfer of liquids: Study of the droplet ejection process

Laser-induced forward transfer (LIFT) is a laser direct-write technique that offers the possibility of printing patterns with a high spatial resolution from a wide range of materials in a solid or liquid state, such as conductors, dielectrics, and biomolecules in solution. This versatility has made LIFT a very promising alternative to lithography-based processes for the rapid prototyping of biomolecule microarrays. Here, we study the transfer process through the LIFT of droplets of a solution suitable for microarray preparation. The laser pulse energy and beam size were systematically varied, and the effect on the transferred droplets was evaluated. Controlled transfers in which the deposited droplets displayed optimal features could be obtained by varying these parameters. In addition, the transferred droplet volume displayed a linear dependence on the laser pulse energy. This dependence allowed determining a threshold energy density value, independent of the laser focusing conditions, which acted as necessary conditions for the transfer to occur. The corresponding sufficient condition was given by a different total energy threshold for each laser beam dimension. The threshold energy density was found to be the dimensional parameter that determined the amount of the transferred liquid per laser pulse, and there was no substantial loss of material due to liquid vaporization during the transfer.

Induced quantum metric fluctuations and the validity of semiclassical gravity

We propose a criterion for the validity of semiclassical gravity (SCG) which is based on the stability of the solutions of SCG with respect to quantum metric fluctuations. We pay special attention to the two-point quantum correlation functions for the metric perturbations, which contain both intrinsic and induced fluctuations. These fluctuations can be described by the Einstein-Langevin equation obtained in the framework of stochastic gravity. Specifically, the Einstein-Langevin equation yields stochastic correlation functions for the metric perturbations which agree, to leading order in the large N limit, with the quantum correlation functions of the theory of gravity interacting with N matter fields. The homogeneous solutions of the Einstein-Langevin equation are equivalent to the solutions of the perturbed semiclassical equation, which describe the evolution of the expectation value of the quantum metric perturbations. The information on the intrinsic fluctuations, which are connected to the initial fluctuations of the metric perturbations, can also be retrieved entirely from the homogeneous solutions. However, the induced metric fluctuations proportional to the noise kernel can only be obtained from the Einstein-Langevin equation (the inhomogeneous term). These equations exhibit runaway solutions with exponential instabilities. A detailed discussion about different methods to deal with these instabilities is given. We illustrate our criterion by showing explicitly that flat space is stable and a description based on SCG is a valid approximation in that case.

Coherence and anticoherence resonance tunned by noise

We present numerical evidence and a theoretical analysis of the appearance of anticoherence resonance induced by noise, not predicted in former analysis of coherence resonance. We have found that this phenomenon occurs for very small values of the intensity of the noise acting on an excitable system, and we claim that this is a universal signature of a nonmonotonous relaxational behavior near its oscillatory regime. Moreover, we demonstrate that this new phenomenon is totally compatible with the standard situation of coherence resonance appearing at intermediate values of noise intensity.

Vanishing Clams on an iberian beach: local consequences and global implication of accelerating loss of shells to tourism

Multi-decadal increase in shell removal by tourists, a process that may accelerate degradation of natural habitats, was quantified via two series of monthly surveys, conducted thirty years apart (1978-1981 and 2008-2010) in one small embayment on the Mediterranean coast of Spain. Over the last three decades, the local tourist arrivals have increased almost three-fold (2.74), while the area has remained unaffected by urban encroachment and commercial fisheries. Concomitantly, abundance of mollusk shells along the shoreline decreased almost three-fold (2.62) and displayed a tight inverse correlation with tourist arrivals. A four-fold increase in tourist arrivals observed globally over the last 30 years has likely induced a comparable worldwide acceleration in shell removal from marine shorelines and exerted multiple negative (but currently unquantifiable) habitat changes that may include increased beach erosion, changes in carbon and calcium cycles, and decline in diversity and abundance of organisms dependent on shell availability.

An update of the mechanisms of resistance to EGFR-tyrosine kinase inhibitors in breast cancer: gefitinib (Iressatrade mark)-induced changes in the expression and nucleo-cytoplasmic trafficking of HER-ligands (Review)

Intrinsic resistance to the epidermal growth factor receptor (EGFR; HER1) tyrosine kinase inhibitor (TKI) gefitinib, and more generally to EGFR TKIs, is a common phenomenon in breast cancer. The availability of molecular criteria for predicting sensitivity to EGFR-TKIs is, therefore, the most relevant issue for their correct use and for planning future research. Though it appears that in non-small-cell lung cancer (NSCLC) response to gefitinib is directly related to the occurrence of specific mutations in the EGFR TK domain, breast cancer patients cannot be selected for treatment with gefitinib on the same basis as such EGFR mutations have beenreported neither in primary breast carcinomas nor in several breast cancer cell lines. Alternatively, there is a generalagreement on the hypothesis that the occurrence of molecular alterations that activate transduction pathways downstreamof EGFR (i.e., MEK1/MEK2 - ERK1/2 MAPK and PI-3'K - AKT growth/survival signaling cascades) significantly affect the response to EGFR TKIs in breast carcinomas. However,there are no studies so far addressing a role of EGF-related ligands as intrinsic breast cancer cell modulators of EGFR TKIefficacy. We recently monitored gene expression profiles andsub-cellular localization of HER-1/-2/-3/-4 related ligands (i.e., EGF, amphiregulin, transforming growth factor-α, ß-cellulin,epiregulin and neuregulins) prior to and after gefitinib treatment in a panel of human breast cancer cell lines. First, gefitinibinduced changes in the endogenous levels of EGF-related ligands correlated with the natural degree of breast cancer cellsensitivity to gefitinib. While breast cancer cells intrinsically resistant to gefitinib (IC50 ≥15 μM) markedly up-regulated(up to 600 times) the expression of genes codifying for HERspecific ligands, a significant down-regulation (up to 106 times)of HER ligand gene transcription was found in breast cancer cells intrinsically sensitive to gefitinib (IC50 ≤1 μM). Second,loss of HER1 function differentially regulated the nuclear trafficking of HER-related ligands. While gefitinib treatment induced an active import and nuclear accumulation of the HER ligand NRG in intrinsically gefitinib-resistant breastcancer cells, an active export and nuclear loss of NRG was observed in intrinsically gefitinib-sensitive breast cancer cells.In summary, through in vitro and pharmacodynamic studies we have learned that, besides mutations in the HER1 gene,oncogenic changes downstream of HER1 are the key players regulating gefitinib efficacy in breast cancer cells. It now appears that pharmacological inhibition of HER1 functionalso leads to striking changes in both the gene expression and the nucleo-cytoplasmic trafficking of HER-specific ligands,and that this response correlates with the intrinsic degree of breast cancer sensitivity to the EGFR TKI gefitinib. Therelevance of this previously unrecognized intracrine feedback to gefitinib warrants further studies as cancer cells could bypassthe antiproliferative effects of HER1-targeted therapeutics without a need for the overexpression and/or activation of other HER family members and/or the activation of HER-driven downstream signaling cascades

Mouse hepatic oval cells require Met-dependent PI3K to impair TGF-β-Induced oxidative stress and apoptosis.

We have previously shown that oval cells harboring a genetically inactivated Met tyrosine kinase (Met−/− oval cells) are more sensitive to TGF-β-induced apoptosis than cells expressing a functional Met (Metflx/flx), demonstrating that the HGF/Met axis plays a pivotal role in oval cell survival. Here, we have examined the mechanism behind this effect and have found that TGF-β induced a mitochondria-dependent apoptotic cell death in Metflx/flx and Met−/− oval cells, associated with a marked increase in levels of the BH3-only proteins Bim and Bmf. Bmf plays a key role during TGF-β-mediated apoptosis since knocking down of BMF significantly diminished the apoptotic response in Met-/- oval cells. TGF-β also induced oxidative stress accompanied by NADPH oxidase 4 (Nox4) mRNA up-regulation and decreased protein levels of antioxidant enzymes. Antioxidants inhibit both TGF-β-induced caspase 3 activity and Bmf up-regulation, revealing an oxidative stress-dependent Bmf regulation by TGF-β. Notably, oxidative stress-related events were strongly amplified in Met−/− oval cells, emphasizing the critical role of Met in promoting survival. Pharmacological inhibition of PI3K did impair HGF-driven protection from TGF-β-induced apoptosis and increased sensitivity of Metflx/flx oval cells to TGF-ß by enhancing oxidative stress, reaching apoptotic indices similar to those obtained in Met−/− oval cells. Interestingly, both PI3K inhibition and/or knockdown itself resulted in caspase-3 activation and loss of viability in Metflx/flx oval cells, whereas no effect was observed in Met−/− oval cells. Altogether, results presented here provide solid evidences that both paracrine and autocrine HGF/Met signaling requires PI3K to promote mouse hepatic oval cell survival against TGF-β-induced oxidative stress and apoptosis.

Dose and time-dependent selective neurotoxicity induced by mephedrone in mice.

Mephedrone is a drug of abuse marketed as 'bath salts'. There are discrepancies concerning its long-term effects. We have investigated the neurotoxicity of mephedrone in mice following different exposition schedules. Schedule 1: four doses of 50 mg/kg. Schedule 2: four doses of 25 mg/kg. Schedule 3: three daily doses of 25 mg/kg, for two consecutive days. All schedules induced, in some animals, an aggressive behavior and hyperthermia as well as a decrease in weight gain. Mephedrone (schedule 1) induced dopaminergic and serotoninergic neurotoxicity that persisted 7 days after exposition. At a lower dose (schedule 2) only a transient dopaminergic injury was found. In the weekend consumption pattern (schedule 3), mephedrone induced dopamine and serotonin transporter loss that was accompanied by a decrease in tyrosine hydroxylase and tryptophan hydroxylase 2 expression one week after exposition. Also, mephedrone induced a depressive-like behavior, as well as a reduction in striatal D2 density, suggesting higher susceptibility to addictive drugs. In cultured cortical neurons, mephedrone induced a concentration-dependent cytotoxic effect. Using repeated doses for 2 days in an elevated ambient temperature we evidenced a loss of frontal cortex dopaminergic and hippocampal serotoninergic neuronal markers that suggest injuries at nerve endings.

Dose and time-dependent selective neurotoxicity induced by mephedrone in mice.

Mephedrone is a drug of abuse marketed as 'bath salts'. There are discrepancies concerning its long-term effects. We have investigated the neurotoxicity of mephedrone in mice following different exposition schedules. Schedule 1: four doses of 50 mg/kg. Schedule 2: four doses of 25 mg/kg. Schedule 3: three daily doses of 25 mg/kg, for two consecutive days. All schedules induced, in some animals, an aggressive behavior and hyperthermia as well as a decrease in weight gain. Mephedrone (schedule 1) induced dopaminergic and serotoninergic neurotoxicity that persisted 7 days after exposition. At a lower dose (schedule 2) only a transient dopaminergic injury was found. In the weekend consumption pattern (schedule 3), mephedrone induced dopamine and serotonin transporter loss that was accompanied by a decrease in tyrosine hydroxylase and tryptophan hydroxylase 2 expression one week after exposition. Also, mephedrone induced a depressive-like behavior, as well as a reduction in striatal D2 density, suggesting higher susceptibility to addictive drugs. In cultured cortical neurons, mephedrone induced a concentration-dependent cytotoxic effect. Using repeated doses for 2 days in an elevated ambient temperature we evidenced a loss of frontal cortex dopaminergic and hippocampal serotoninergic neuronal markers that suggest injuries at nerve endings.