The power to resist: the relationship between power, stigma, and negative symptoms in schizophrenia.

Stigmatizing beliefs about mental illness can be a daily struggle for people with schizophrenia. While investigations into the impact of internalizing stigma on negative symptoms have yielded mixed results, resistance to stigmatizing beliefs has received little attention. In this study, we examined the linkage between internalized stigma, stigma resistance, negative symptoms, and social power, or perceived ability to influence others during social interactions among people with schizophrenia. Further, we sought to determine whether resistance to stigma would be bolstered by social power, with greater power in relationships with other possibly buffering against motivation/pleasure negative symptoms. Fifty-one people with schizophrenia or schizoaffective disorder completed measures of social power, internalized stigma, and stigma resistance. Negative symptoms were assessed using the Clinical Assessment Interview for Negative Symptoms (CAINS). Greater social power was associated with less internalized stigma and negative symptoms as well as more stigma resistance. Further, the relationship between social power and negative symptoms was partially mediated by stigma resistance. These findings provide evidence for the role of stigma resistance as a viable target for psychosocial interventions aimed at improving motivation and social power in people with schizophrenia

Some non perturbative calculations on spin glasses

Models of spin glasses are studied with a phase transition discontinuous in the Parisi order parameter. It is assumed that the leading order corrections to the thermodynamic limit of the high temperature free energy are due to the existence of a metastable saddle point in the replica formalism. An ansatz is made on the form of the metastable point and its contribution to the free energy is calculated. The Random Energy Model is considered along with the p-spin and the p-state Potts Models in their p < infinity expansion.Comment: 12 pages, LaTe

Dynamical fluctuations in an exactly solvable model of spin glasses

In this work we calculate the dynamical fluctuations at O(1/N) in the low temperature phase of the $p=2$ spherical spin glass model. We study the large-times asymptotic regimes and we find, in a short time-differences regime, a fluctuation dissipation relation for the four-point correlation functions. This relation can be extended to the out of equilibrium regimes introducing a function $X_{t}$ which, for large time $t$, we find scales as $t^{-1/2}$ as in the case of the two-point functions.Comment: Latex, 8 page

Complexity and line of critical points in a short-range spin-glass model

We investigate the critical behavior of a three-dimensional short-range spin glass model in the presence of an external field \eps conjugated to the Edwards-Anderson order parameter. In the mean-field approximation this model is described by the Adam-Gibbs-DiMarzio approach for the glass transition. By Monte Carlo numerical simulations we find indications for the existence of a line of critical points in the plane (\eps,T) which separates two paramagnetic phases and terminates in a critical endpoint. This line of critical points appears due to the large degeneracy of metastable states present in the system (configurational entropy) and is reminiscent of the first-order phase transition present in the mean-field limit. We propose a scenario for the spin-glass transition at \eps=0, driven by a spinodal point present above $T_c$, which induces strong metastability through Griffiths singularities effects and induces the absence of a two-step shape relaxation curve characteristic of glasses.Comment: 5 pages, 4 postscript figure, revte

Finite dimensional corrections to mean field in a short-range p-spin glassy model

In this work we discuss a short range version of the $p$-spin model. The model is provided with a parameter that allows to control the crossover with the mean field behaviour. We detect a discrepancy between the perturbative approach and numerical simulation. We attribute it to non-perturbative effects due to the finite probability that each particular realization of the disorder allows for the formation of regions where the system is less frustrated and locally freezes at a higher temperature.Comment: 18 pages, 5 figures, submitted to Phys Rev

Glass transition in the quenched and annealed version of the frustrated lattice gas model

In this paper we study the 3d frustrated lattice gas model in the annealed version, where the disorder is allowed to evolve in time with a suitable kinetic constraint. Although the model does not exhibit any thermodynamic transition it shows a diverging peak at some characteristic time in the dynamical non-linear susceptibility, similar to the results on the p-spin model in mean field and Lennard-Jones mixture recently found by Donati et al. [cond-mat/9905433]. Comparing these results to those obtained in the model with quenched interactions, we conclude that the critical behavior of the dynamical susceptibility is reminiscent of the thermodynamic transition present in the quenched model, and signaled by the divergence of the static non-linear susceptibility, suggesting therefore a similar mechanism also in supercooled glass-forming liquids.Comment: 8 pages, 14 figure

Self Consistent Screening Approximation For Critical Dynamics

We generalise Bray's self-consistent screening approximation to describe the critical dynamics of the $\phi^4$ theory. In order to obtain the dynamical exponent $z$, we have to make an ansatz for the form of the scaling functions, which fortunately can be much constrained by general arguments. Numerical values of $z$ for $d=3$, and $n=1,...,10$ are obtained using two different ans\"atze, and differ by a very small amount. In particular, the value of $z \simeq 2.115$ obtained for the 3-d Ising model agrees well with recent Monte-Carlo simulations.Comment: 21 pages, LaTeX file + 4 (EPS) figure

Enterohemorrhagic E. coli Requires N-WASP for Efficient Type III Translocation but Not for EspFU-Mediated Actin Pedestal Formation

Upon infection of mammalian cells, enterohemorrhagic E. coli (EHEC) O157:H7 utilizes a type III secretion system to translocate the effectors Tir and EspFU (aka TccP) that trigger the formation of F-actin-rich ‘pedestals’ beneath bound bacteria. EspFU is localized to the plasma membrane by Tir and binds the nucleation-promoting factor N-WASP, which in turn activates the Arp2/3 actin assembly complex. Although N-WASP has been shown to be required for EHEC pedestal formation, the precise steps in the process that it influences have not been determined. We found that N-WASP and actin assembly promote EHEC-mediated translocation of Tir and EspFU into mammalian host cells. When we utilized the related pathogen enteropathogenic E. coli to enhance type III translocation of EHEC Tir and EspFU, we found surprisingly that actin pedestals were generated on N-WASP-deficient cells. Similar to pedestal formation on wild type cells, Tir and EspFU were the only bacterial effectors required for pedestal formation, and the EspFU sequences required to interact with N-WASP were found to also be essential to stimulate this alternate actin assembly pathway. In the absence of N-WASP, the Arp2/3 complex was both recruited to sites of bacterial attachment and required for actin assembly. Our results indicate that actin assembly facilitates type III translocation, and reveal that EspFU, presumably by recruiting an alternate host factor that can signal to the Arp2/3 complex, exhibits remarkable versatility in its strategies for stimulating actin polymerization

Clustering of Nck by a 12-residue Tir phosphopeptide is sufficient to trigger localized actin assembly

Enteropathogenic Escherichia coli (EPEC) translocates effector proteins into mammalian cells to promote reorganization of the cytoskeleton into filamentous actin pedestals. One effector, Tir, is a transmembrane receptor for the bacterial surface adhesin intimin, and intimin binding by the extracellular domain of Tir is required for actin assembly. The cytoplasmic NH2 terminus of Tir interacts with focal adhesion proteins, and its tyrosine-phosphorylated COOH terminus binds Nck, a host adaptor protein critical for pedestal formation. To define the minimal requirements for EPEC-mediated actin assembly, Tir derivatives were expressed in mammalian cells in the absence of all other EPEC components. Replacement of the NH2 terminus of Tir with a viral membrane-targeting sequence promoted efficient surface expression of a COOH-terminal Tir fragment. Artificial clustering of this fusion protein revealed that the COOH terminus of Tir, by itself, is sufficient to initiate a complete signaling cascade leading to pedestal formation. Consistent with this finding, clustering of Nck by a 12-residue Tir phosphopeptide triggered actin tail formation in Xenopus egg extracts