98 research outputs found

    Normal-Superfluid Interface Scattering For Polarized Fermion Gases

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    We argue that, for the recent experiments with imbalanced fermion gases, a temperature difference may occur between the normal (N) and the gapped superfluid (SF) phase. Using the mean-field formalism, we study particle scattering off the N-SF interface from the deep BCS to the unitary regime. We show that the thermal conductivity across the interface drops exponentially fast with increasing h/kBTh/k_B T, where hh is the chemical potential imbalance. This implies a blocking of thermal equilibration between the N and the SF phase. We also provide a possible mechanism for the creation of gap oscillations (FFLO-like states) as seen in recent studies on these systems.Comment: 4 pages, 3 figure

    Trading interactions for topology in scale-free networks

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    Scale-free networks with topology-dependent interactions are studied. It is shown that the universality classes of critical behavior, which conventionally depend only on topology, can also be explored by tuning the interactions. A mapping, γ=(γμ)/(1μ)\gamma' = (\gamma - \mu)/(1-\mu), describes how a shift of the standard exponent γ\gamma of the degree distribution P(q)P(q) can absorb the effect of degree-dependent pair interactions Jij(qiqj)μJ_{ij} \propto (q_iq_j)^{-\mu}. Replica technique, cavity method and Monte Carlo simulation support the physical picture suggested by Landau theory for the critical exponents and by the Bethe-Peierls approximation for the critical temperature. The equivalence of topology and interaction holds for equilibrium and non-equilibrium systems, and is illustrated with interdisciplinary applications.Comment: 4 pages, 5 figure

    Ising model for distribution networks

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    An elementary Ising spin model is proposed for demonstrating cascading failures (break-downs, blackouts, collapses, avalanches, ...) that can occur in realistic networks for distribution and delivery by suppliers to consumers. A ferromagnetic Hamiltonian with quenched random fields results from policies that maximize the gap between demand and delivery. Such policies can arise in a competitive market where firms artificially create new demand, or in a solidary environment where too high a demand cannot reasonably be met. Network failure in the context of a policy of solidarity is possible when an initially active state becomes metastable and decays to a stable inactive state. We explore the characteristics of the demand and delivery, as well as the topological properties, which make the distribution network susceptible of failure. An effective temperature is defined, which governs the strength of the activity fluctuations which can induce a collapse. Numerical results, obtained by Monte Carlo simulations of the model on (mainly) scale-free networks, are supplemented with analytic mean-field approximations to the geometrical random field fluctuations and the thermal spin fluctuations. The role of hubs versus poorly connected nodes in initiating the breakdown of network activity is illustrated and related to model parameters

    Formation, dynamics and stability of coreless vortex dipoles in phase-separated binary condensates

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    We study the motion of the Gaussian obstacle potential created by blue detuned laser beam through a phase-separated binary condensate in pancake-shaped traps. For the velocity of the obstacle above a critical velocity, we observe the generation of vortex dipoles in the outer component which can penetrate the inner component. This is equivalent to finite, although small, transport of outer component across the inner component. In the inner component, the same method can lead to the formation of coreless vortex dipoles.Comment: 12 pages, 9 figure

    Differential affinity of FLIP and procaspase 8 for FADD’s DED binding surfaces regulates DISC assembly

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    Death receptor activation triggers recruitment of FADD, which via its death effector domain (DED) engages the DEDs of procaspase 8 and its inhibitor FLIP to form death-inducing signalling complexes (DISCs). The DEDs of FADD, FLIP and procaspase 8 interact with one another using two binding surfaces defined by α1/α4 and α2/α5 helices, respectively. Here we report that FLIP has preferential affinity for the α1/α4 surface of FADD, whereas procaspase 8 has preferential affinity for FADD's α2/α5 surface. These relative affinities contribute to FLIP being recruited to the DISC at comparable levels to procaspase 8 despite lower cellular expression. Additional studies, including assessment of DISC stoichiometry and functional assays, suggest that following death receptor recruitment, the FADD DED preferentially engages FLIP using its α1/α4 surface and procaspase 8 using its α2/α5 surface; these tripartite intermediates then interact via the α1/α4 surface of FLIP DED1 and the α2/α5 surface of procaspase 8 DED2

    Clinical responses to EGFR-tyrosine kinase inhibitor retreatment in non-small cell lung cancer patients who benefited from prior effective gefitinib therapy: a retrospective analysis

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    <p>Abstract</p> <p>Background</p> <p>Gefitinib was the first epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) approved for the treatment of advanced non-small cell lung cancer (NSCLC). Few treatment options are available for NSCLC patients who have responded to gefitinib treatment and demonstrated tumor progression. The present study was conducted to evaluate the efficacy and toxicity of the 2<sup>nd </sup>EGFR-TKI administration.</p> <p>Methods</p> <p>We retrospectively analyzed 11 patients who had obtained a partial response (PR) or stable disease (SD) with gefitinib treatment and were re-treated with EGFR-TKI after failure of the initial gefitinib treatment.</p> <p>Results</p> <p>Three patients (27%) were treated with gefitinib as the 2<sup>nd </sup>EGFR-TKI, and 8 patients (73%) received erlotinib. Only one patient (9%) showed PR, 7 (64%) achieved SD, and 3 (27%) had progressive disease. The disease control rate was 73% (95% CI, 43% - 91%) and the median progression-free survival was 3.4 months (95% CI, 2 - 5.2). The median overall survival from the beginning of the 2<sup>nd </sup>EGFR-TKI and from diagnosis were 7.3 months (95% CI, 2.7 - 13) and 36.7 months (95% CI, 23.6 - 43.9), respectively. No statistical differences in PFS or OS were observed between gefitinib and erlotinib as the 2<sup>nd </sup>EGFR-TKI (PFS, P = 0.23 and OS, P = 0.052). The toxicities associated with the 2<sup>nd </sup>EGFR-TKI were generally acceptable and comparable to those observed for the initial gefitinib therapy.</p> <p>Conclusions</p> <p>Our results indicate that a 2<sup>nd </sup>EGFR-TKI treatment can be an effective treatment option for gefitinib responders.</p

    Clinical responses to EGFR-tyrosine kinase inhibitor retreatment in non-small cell lung cancer patients who benefited from prior effective gefitinib therapy: a retrospective analysis

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    <p>Abstract</p> <p>Background</p> <p>Gefitinib was the first epidermal growth factor receptor-tyrosine kinase inhibitor (EGFR-TKI) approved for the treatment of advanced non-small cell lung cancer (NSCLC). Few treatment options are available for NSCLC patients who have responded to gefitinib treatment and demonstrated tumor progression. The present study was conducted to evaluate the efficacy and toxicity of the 2<sup>nd </sup>EGFR-TKI administration.</p> <p>Methods</p> <p>We retrospectively analyzed 11 patients who had obtained a partial response (PR) or stable disease (SD) with gefitinib treatment and were re-treated with EGFR-TKI after failure of the initial gefitinib treatment.</p> <p>Results</p> <p>Three patients (27%) were treated with gefitinib as the 2<sup>nd </sup>EGFR-TKI, and 8 patients (73%) received erlotinib. Only one patient (9%) showed PR, 7 (64%) achieved SD, and 3 (27%) had progressive disease. The disease control rate was 73% (95% CI, 43% - 91%) and the median progression-free survival was 3.4 months (95% CI, 2 - 5.2). The median overall survival from the beginning of the 2<sup>nd </sup>EGFR-TKI and from diagnosis were 7.3 months (95% CI, 2.7 - 13) and 36.7 months (95% CI, 23.6 - 43.9), respectively. No statistical differences in PFS or OS were observed between gefitinib and erlotinib as the 2<sup>nd </sup>EGFR-TKI (PFS, P = 0.23 and OS, P = 0.052). The toxicities associated with the 2<sup>nd </sup>EGFR-TKI were generally acceptable and comparable to those observed for the initial gefitinib therapy.</p> <p>Conclusions</p> <p>Our results indicate that a 2<sup>nd </sup>EGFR-TKI treatment can be an effective treatment option for gefitinib responders.</p

    EGFR-targeting drugs in combination with cytotoxic agents: from bench to bedside, a contrasted reality

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    The clinical experience recently reported with epidermal growth factor receptor (EGFR)-targeting drugs confirms the synergistic interactions observed between these compounds and conventional cytotoxic agents, which were previously established at the preclinical stage. There are, however, examples of major gaps between the bench and the bedside. Particularly demonstrative is the failure of the tyrosine kinase inhibitors (TKIs) (gefitinib and erlotinib) combined with chemotherapy in pretreated nonsmall cell lung cancer patients. These discrepancies can be due to several factors such as the methodology used to evaluate TKI plus cytotoxic agent combinations in preclinical models and the insufficient consideration given to the importance of the drug sequences for the tested combinations. Recent advances in understanding the biologic basis of acquired resistance to these agents have great potential to improve their clinical effectiveness. The purpose of this review is to critically examine the experimental conditions of the preclinical background for anti-EGFR drug–cytotoxic agent combinations and to attempt to explain the gap between clinical observations and preclinical data
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