Coupled Fluctuations near Critical Wetting

Recent work on the complete wetting transition has emphasized the role played by the coupling of fluctuations of the order parameter at the wall and at the depinning fluid interface. Extending this approach to the wetting transition itself we predict a novel crossover effect associated with the decoupling of fluctuations as the temperature is lowered towards the transition temperature T_W. Using this we are able to reanalyse recent Monte-Carlo simulation studies and extract a value \omega(T_W)=0.8 at T_W=0.9T_C in very good agreement with long standing theoretical predictions.Comment: 4 pages, LaTex, 1 postscript figur

My father, myself, and my muscles:associations between muscle dysmorphia, narcissism and relationship with father among exercising males

Research has yet to examine the associations between muscle dysmorphia (MD), narcissism and relationship with father in a male population. This study aimed to address this. We hypothesized that a negatively experienced relationship with the father for males will lead to an increase in MD symptoms due to undermined self-esteem that stems from a lack of the father as a positive masculine role model. A total of 503 exercising males (Mage = 28.5, SD = 9.6 years) completed self-report measures of MD, narcissism, and relationship with father. Our hypothesized indirect effect model found a negative indirect effect of relationship with father on MD symptoms via vulnerable narcissism, but not via grandiose narcissism. Analysis of individual path coefficients also revealed that a poor relationship with father impacts the development of vulnerable narcissism, but not grandiose narcissism. These findings alert practitioners to the fact that some individuals' MD symptoms may be an attempt to protect the fragile self-esteem central to vulnerable narcissism. Practitioners should consider exploring individuals' feelings and perceptions about their fathers in the treatment of MD. Moreover, future research should build on these findings and explore the observed associations in a longitudinal design to assess the causal model.publishedVersio

A point mutation in the hair cell nicotinic cholinergic receptor prolongs cochlear inhibition and enhances noise protection

The transduction of sound in the auditory periphery, the cochlea, is inhibited by efferent cholinergic neurons projecting from the brainstem and synapsing directly on mechanosensory hair cells. One fundamental question in auditory neuroscience is what role(s) this feedback plays in our ability to hear. In the present study, we have engineered a genetically modified mouse model in which the magnitude and duration of efferent cholinergic effects are increased, and we assess the consequences of this manipulation on cochlear function. We generated the Chrna9L9′T of knockin mice with a threonine for leucine change (L9′T) at position 9′ of the second transmembrane domain of the α9 nicotinic cholinergic subunit, rendering α9-containing receptors that were hypersensitive to acetylcholine and had slower desensitization kinetics. The Chrna9L9′T allele produced a 3-fold prolongation of efferent synaptic currents in vitro. In vivo, Chrna9L9′T mice had baseline elevation of cochlear thresholds and efferent-mediated inhibition of cochlear responses was dramatically enhanced and lengthened: both effects were reversed by strychnine blockade of the α9α10 hair cell nicotinic receptor. Importantly, relative to their wild-type littermates, Chrna9L9′T/L9′T mice showed less permanent hearing loss following exposure to intense noise. Thus, a point mutation designed to alter α9α10 receptor gating has provided an animal model in which not only is efferent inhibition more powerful, but also one in which sound-induced hearing loss can be restrained, indicating the ability of efferent feedback to ameliorate sound trauma.Fil: Taranda, Julian. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr. Héctor N. Torres"; Argentina. Tufts University School of Medicine; Estados UnidosFil: Maison, Stéphane F.. Massachusetts Eye and Ear Infirmary; Estados UnidosFil: Ballestero, Jimena Andrea. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr. Héctor N. Torres"; ArgentinaFil: Katz, Eleonora. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr. Héctor N. Torres"; ArgentinaFil: Savino, Jessica. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr. Héctor N. Torres"; ArgentinaFil: Vetter, Douglas E.. Tufts University School of Medicine; Estados UnidosFil: Boulter, Jim. University of California at Los Angeles; Estados UnidosFil: Liberman, M. Charles. Massachusetts Eye and Ear Infirmary; Estados UnidosFil: Fuchs, Paul A.. The Johns Hopkins University School of Medicine; Estados UnidosFil: Elgoyhen, Ana Belen. Consejo Nacional de Investigaciones Científicas y Técnicas. Instituto de Investigaciones en Ingeniería Genética y Biología Molecular "Dr. Héctor N. Torres"; Argentina. Universidad de Buenos Aires. Facultad de Medicina. Departamento de Farmacología; Argentin

Influence of Active Recovery on Cardiovascular Function During Ice Hockey

Background: Ice hockey is a popular sport comprised of high-intensity repeated bouts of activity. Light activity, as opposed to passive rest, has been shown to improve power output in repeated sprinting and could potentially help to offset venous pooling, poor perfusion, and the risk of an ischemic event. The objective of our study was, thus, to examine the efficacy of low-intensity lower body activity following a simulated hockey shift for altering hemodynamic function. Methods: In a cross-over design, 15 healthy hockey players (23 ± 1 years, 54 ± 3 mL/kg/min) performed two simulated hockey shifts. In both conditions, players skated up to 85 % of age-predicted heart rate maximum, followed by either passive recovery or active recovery while hemodynamic measures were tracked for up to 180 s of rest. Results: Light active recovery within the confines of an ice hockey bench, while wearing skates and protective gear, was effective for augmenting cardiac output (an average of 2.5 ± 0.2 L/min, p = 0.03) at 45, 50, and 120 s. These alterations were driven by a sustained elevation in heart rate (12 bpm, p = 0.05) combined with a physiological relevant but non-significant (11.6 mL, p = 0.06) increase in stroke volume. Conclusions: Standing and pacing between shifts offers a realistic in-game solution to help slow the precipitous drop in cardiac output (heart rate and stroke volume) that typically occurs with passive rest. Prolonging the duration of an elevated cardiac output further into recovery may be beneficial for promoting recovery of the working skeletal muscles and also avoiding venous pooling and reduced myocardial perfusion. Key Points: Evidence that light activity in the form of standing/pacing is effective for maintaining cardiac output, and thus venous return Increased cardiac output and venous return may help reduce the chances of poor perfusion (ischemia) and could also promote recovery for performance This is a simple, low-risk, intervention demonstrated for the first time to work within the confines of a player’s bench while wearing hockey gea

Surface induced disorder in body-centered cubic alloys

We present Monte Carlo simulations of surface induced disordering in a model of a binary alloy on a bcc lattice which undergoes a first order bulk transition from the ordered DO3 phase to the disordered A2 phase. The data are analyzed in terms of an effective interface Hamiltonian for a system with several order parameters in the framework of the linear renormalization approach due to Brezin, Halperin and Leibler. We show that the model provides a good description of the system in the vicinity of the interface. In particular, we recover the logarithmic divergence of the thickness of the disordered layer as the bulk transition is approached, we calculate the critical behavior of the maxima of the layer susceptibilities, and demonstrate that it is in reasonable agreement with the simulation data. Directly at the (110) surface, the theory predicts that all order parameters vanish continuously at the surface with a nonuniversal, but common critical exponent. However, we find different exponents for the order parameter of the DO3 phase and the order parameter of the B2 phase. Using the effective interface model, we derive the finite size scaling function for the surface order parameter and show that the theory accounts well for the finite size behavior of the DO3 ordering but not for that of B2 ordering. The situation is even more complicated in the neighborhood of the (100) surface, due to the presence of an ordering field which couples to the B2 order.Comment: To appear in Physical Review

National Climate Change Adaptation Research Plan Terrestrial Biodiversity: update 2017

In 2011, a National Climate Change Adaptation Research Plan (NARP) was developed for the terrestrial ecosystems and biodiversity theme of climate change adaptation (Terrestrial NARP 2011). The Terrestrial NARP aims to identify priority research questions for climate change adaptation issues relevant to Australia's cities, towns and regions, including coastal communities and regions. This NARP was updated in 2013 (Terrestrial NARP 2013). The purpose of this document is to review the Terrestrial NARP 2013 and this was done through a series of workshops with key stakeholders in 2015-16. The most important component of the NARPs is to identify and prioritise adaptation research questions that are important, often urgent, and will provide knowledge needed by adaptation stakeholders across Australia. Based on the stakholder review, a total of 20 priority research questions (Table 1) are presented in this report within four research themes

Dynamics of Wetting Fronts in Porous Media

We propose a new phenomenological approach for describing the dynamics of wetting front propagation in porous media. Unlike traditional models, the proposed approach is based on dynamic nature of the relation between capillary pressure and medium saturation. We choose a modified phase-field model of solidification as a particular case of such dynamic relation. We show that in the traveling wave regime the results obtained from our approach reproduce those derived from the standard model of flow in porous media. In more general case, the proposed approach reveals the dependence of front dynamics upon the flow regime.Comment: 4 pages, 2 figures, revte

A Point Mutation in the Hair Cell Nicotinic Cholinergic Receptor Prolongs Cochlear Inhibition and Enhances Noise Protection

The transduction of sound in the auditory periphery, the cochlea, is inhibited by efferent cholinergic neurons projecting from the brainstem and synapsing directly on mechanosensory hair cells. One fundamental question in auditory neuroscience is what role(s) this feedback plays in our ability to hear. In the present study, we have engineered a genetically modified mouse model in which the magnitude and duration of efferent cholinergic effects are increased, and we assess the consequences of this manipulation on cochlear function. We generated the Chrna9L9′T line of knockin mice with a threonine for leucine change (L9′T) at position 9′ of the second transmembrane domain of the α9 nicotinic cholinergic subunit, rendering $\alpha$9-containing receptors that were hypersensitive to acetylcholine and had slower desensitization kinetics. The Chrna9L9′T allele produced a 3-fold prolongation of efferent synaptic currents in vitro. In vivo, Chrna9L9′T mice had baseline elevation of cochlear thresholds and efferent-mediated inhibition of cochlear responses was dramatically enhanced and lengthened: both effects were reversed by strychnine blockade of the $\alpha$9$\alpha$10 hair cell nicotinic receptor. Importantly, relative to their wild-type littermates, Chrna9$^{L9′T/L9′T}$ mice showed less permanent hearing loss following exposure to intense noise. Thus, a point mutation designed to alter $\alpha$9$\alpha$10 receptor gating has provided an animal model in which not only is efferent inhibition more powerful, but also one in which sound-induced hearing loss can be restrained, indicating the ability of efferent feedback to ameliorate sound trauma

The divergent DSL ligand Dll3 does not activate Notch signaling but cell autonomously attenuates signaling induced by other DSL ligands

Mutations in the DSL (Delta, Serrate, Lag2) Notch (N) ligand Delta-like (Dll) 3 cause skeletal abnormalities in spondylocostal dysostosis, which is consistent with a critical role for N signaling during somitogenesis. Understanding how Dll3 functions is complicated by reports that DSL ligands both activate and inhibit N signaling. In contrast to other DSL ligands, we show that Dll3 does not activate N signaling in multiple assays. Consistent with these findings, Dll3 does not bind to cells expressing any of the four N receptors, and N1 does not bind Dll3-expressing cells. However, in a cell-autonomous manner, Dll3 suppressed N signaling, as was found for other DSL ligands. Therefore, Dll3 functions not as an activator as previously reported but rather as a dedicated inhibitor of N signaling. As an N antagonist, Dll3 promoted Xenopus laevis neurogenesis and inhibited glial differentiation of mouse neural progenitors. Finally, together with the modulator lunatic fringe, Dll3 altered N signaling levels that were induced by other DSL ligands

Effects of confinement and surface enhancement on superconductivity

Within the Ginzburg-Landau approach a theoretical study is performed of the effects of confinement on the transition to superconductivity for type-I and type-II materials with surface enhancement. The superconducting order parameter is characterized by a negative surface extrapolation length $b$. This leads to an increase of the critical field $H_{c3}$ and to a surface critical temperature in zero field, $T_{cs}$, which exceeds the bulk $T_c$. When the sample is {\em mesoscopic} of linear size $L$ the surface induces superconductivity in the interior for $T T_{cs}$. In analogy with adsorbed fluids, superconductivity in thin films of type-I materials is akin to {\em capillary condensation} and competes with the interface delocalization or "wetting" transition. The finite-size scaling properties of capillary condensation in superconductors are scrutinized in the limit that the ratio of magnetic penetration depth to superconducting coherence length, $\kappa \equiv \lambda/\xi$, goes to zero, using analytic calculations. While standard finite-size scaling holds for the transition in non-zero magnetic field $H$, an anomalous critical-point shift is found for H=0. The increase of $T_c$ for H=0 is calculated for mesoscopic films, cylindrical wires, and spherical grains of type-I and type-II materials. Surface curvature is shown to induce a significant increase of $T_c$, characterized by a shift $T_c(R)-T_c(\infty)$ inversely proportional to the radius $R$.Comment: 37 pages, 5 figures, accepted for PR