Possible loss and recovery of Gibbsianness during the stochastic evolution of Gibbs measures

We consider Ising-spin systems starting from an initial Gibbs measure $\nu$ and evolving under a spin-flip dynamics towards a reversible Gibbs measure $\mu\not=\nu$. Both $\nu$ and $\mu$ are assumed to have a finite-range interaction. We study the Gibbsian character of the measure $\nu S(t)$ at time $t$ and show the following: (1) For all $\nu$ and $\mu$, $\nu S(t)$ is Gibbs for small $t$. (2) If both $\nu$ and $\mu$ have a high or infinite temperature, then $\nu S(t)$ is Gibbs for all $t>0$. (3) If $\nu$ has a low non-zero temperature and a zero magnetic field and $\mu$ has a high or infinite temperature, then $\nu S(t)$ is Gibbs for small $t$ and non-Gibbs for large $t$. (4) If $\nu$ has a low non-zero temperature and a non-zero magnetic field and $\mu$ has a high or infinite temperature, then $\nu S(t)$ is Gibbs for small $t$, non-Gibbs for intermediate $t$, and Gibbs for large $t$. The regime where $\mu$ has a low or zero temperature and $t$ is not small remains open. This regime presumably allows for many different scenarios

Wingspread Declaration on Renewing the Civic Mission of the American Research University

Civic engagement is essential to a democratic society, but far too many Americans have withdrawn from participation in public affairs. Higher education can contribute to civic engagement, but most research universities do not perceive themselves as part of the problem or of its solution. Whereas universities were once centrally concerned with education for democracy and knowledge for society, today\u27s institutions have often drifted away from their civic mission

Instability statistics and mixing rates

We claim that looking at probability distributions of \emph{finite time} largest Lyapunov exponents, and more precisely studying their large deviation properties, yields an extremely powerful technique to get quantitative estimates of polynomial decay rates of time correlations and Poincar\'e recurrences in the -quite delicate- case of dynamical systems with weak chaotic properties.Comment: 5 pages, 5 figure

Risk of non-affective psychotic disorder and post-traumatic stress disorder by refugee status in Sweden

BACKGROUND: Refugees have different experiences of obtaining a refugee status, however it remains unclear if this affects their risk of psychiatric disorders. The aim of this study was to investigate whether risk for non-affective psychotic disorder (NAPD) and post-traumatic stress disorder (PTSD) differs between quota refugees (resettled from refugee camps) and non-quota refugees (former asylum seekers). METHOD: A register-based cohort with a sample size of 52 561 refugees in Sweden starting 1 January 1997 ending 31 December 2011. EXPOSURE: refugee status (quota or non-quota refugees). Cox regression models estimated adjusted HRs with 95% CIs for NAPD (International Classification of Diseases, Tenth Revision (ICD-10), F20-29) and PTSD (ICD-10, F43.1) by refugee status. RESULTS: There were more non-quota refugees (77.0%) than quota refugees (23.0%). In total we identified 401 cases of NAPD, 1.0% among quota refugees and 0.7% among non-quota refugees, and 1070 cases of PTSD, 1.9% among quota refugees and 2.1% among non-quota refugees. Male quota refugees were at increased risk for NAPD compared with male non-quota refugees (HRmale=1.41, 95% CI 1.09 to 1.82 and HRfemale=0.65, 95% CI 0.42 to 1.00). All quota refugees were at a reduced risk of PTSD compared with non-quota refugees (HR=0.74, 95% CI 0.64 to 0.87). CONCLUSIONS: This study suggests that risk of NAPD and PTSD varies for quota and non-quota refugees, highlighting the possibility that different experiences of the migration process differentiate the risk of psychiatric disorders among refugees

Identification of the growth arrest and DNA damage protein GADD34 in the normal human heart and demonstration of alterations in expression following myocardial ischaemia

Growth arrest and DNA damage protein 34 (GADD34) is a multifunctional protein upregulated in response to cellular stress and is believed to mediate DNA repair and restore protein synthesis. In the present study we have examined GADD34 immunoreactivity in human myocardial tissue at defined survival times following cardiac arrest and determined alterations in expression following ischaemia. In the normal human heart, GADD34 immunoreactivity was generally intense and present within most cells. GADD34 immunoreactivity was downregulated in tissue displaying ischaemic damage and remained intense in adjacent non-infarcted tissue. Unlike brain, GADD34 was not found to be upregulated in the peri-infarct zone. Cells displaying apoptotic changes were located in regions displaying reduced GADD34 immunoreactivity. In the brain, it is thought that GADD34 supports re-initiation of protein synthesis following ischaemia. Similarly, GADD34 may perform important functions in cardiac tissue in response to ischaemia

Limiting Behaviour of the Mean Residual Life

In survival or reliability studies, the mean residual life or life expectancy is an important characteristic of the model. Here, we study the limiting behaviour of the mean residual life, and derive an asymptotic expansion which can be used to obtain a good approximation for large values of the time variable. The asymptotic expansion is valid for a quite general class of failure rate distributions--perhaps the largest class that can be expected given that the terms depend only on the failure rate and its derivatives.Comment: 19 page

A bulky glycocalyx fosters metastasis formation by promoting G1 cell cycle progression.

Metastasis depends upon cancer cell growth and survival within the metastatic niche. Tumors which remodel their glycocalyces, by overexpressing bulky glycoproteins like mucins, exhibit a higher predisposition to metastasize, but the role of mucins in oncogenesis remains poorly understood. Here we report that a bulky glycocalyx promotes the expansion of disseminated tumor cells in vivo by fostering integrin adhesion assembly to permit G1 cell cycle progression. We engineered tumor cells to display glycocalyces of various thicknesses by coating them with synthetic mucin-mimetic glycopolymers. Cells adorned with longer glycopolymers showed increased metastatic potential, enhanced cell cycle progression, and greater levels of integrin-FAK mechanosignaling and Akt signaling in a syngeneic mouse model of metastasis. These effects were mirrored by expression of the ectodomain of cancer-associated mucin MUC1. These findings functionally link mucinous proteins with tumor aggression, and offer a new view of the cancer glycocalyx as a major driver of disease progression