Quenching and Propagation of Combustion Without Ignition Temperature Cutoff

We study a reaction-diffusion equation in the cylinder $\Omega = \mathbb{R}\times\mathbb{T}^m$, with combustion-type reaction term without ignition temperature cutoff, and in the presence of a periodic flow. We show that if the reaction function decays as a power of $T$ larger than three as $T\to 0$ and the initial datum is small, then the flame is extinguished -- the solution quenches. If, on the other hand, the power of decay is smaller than three or initial datum is large, then quenching does not happen, and the burning region spreads linearly in time. This extends results of Aronson-Weinberger for the no-flow case. We also consider shear flows with large amplitude and show that if the reaction power-law decay is larger than three and the flow has only small plateaux (connected domains where it is constant), then any compactly supported initial datum is quenched when the flow amplitude is large enough (which is not true if the power is smaller than three or in the presence of a large plateau). This extends results of Constantin-Kiselev-Ryzhik for combustion with ignition temperature cutoff. Our work carries over to the case $\Omega = \mathbb{R}^n\times\mathbb{T}^m$, when the critical power is $1 + 2/n$, as well as to certain non-periodic flows

Describing the set of words generated by interval exchange transformation

Let $W$ be an infinite word over finite alphabet $A$. We get combinatorial criteria of existence of interval exchange transformations that generate the word W.Comment: 17 pages, this paper was submitted at scientific council of MSU, date: September 21, 200

Posttraumatic Stress Disorder Prevalence and Risk of Recurrence in Acute Coronary Syndrome Patients: A Meta-analytic Review

BACKGROUND:Acute coronary syndromes (ACS; myocardial infarction or unstable angina) can induce posttraumatic stress disorder (PTSD), and ACS-induced PTSD may increase patients' risk for subsequent cardiac events and mortality. OBJECTIVE:To determine the prevalence of PTSD induced by ACS and to quantify the association between ACS-induced PTSD and adverse clinical outcomes using systematic review and meta-analysis. DATA SOURCES:Articles were identified by searching Ovid MEDLINE, PsycINFO, and Scopus, and through manual search of reference lists. METHODOLOGY/PRINCIPAL FINDINGS:Observational cohort studies that assessed PTSD with specific reference to an ACS event at least 1 month prior. We extracted estimates of the prevalence of ACS-induced PTSD and associations with clinical outcomes, as well as study characteristics. We identified 56 potentially relevant articles, 24 of which met our criteria (N = 2383). Meta-analysis yielded an aggregated prevalence estimate of 12% (95% confidence interval [CI], 9%-16%) for clinically significant symptoms of ACS-induced PTSD in a random effects model. Individual study prevalence estimates varied widely (0%-32%), with significant heterogeneity in estimates explained by the use of a screening instrument (prevalence estimate was 16% [95% CI, 13%-20%] in 16 studies) vs a clinical diagnostic interview (prevalence estimate was 4% [95% CI, 3%-5%] in 8 studies). The aggregated point estimate for the magnitude of the relationship between ACS-induced PTSD and clinical outcomes (ie, mortality and/or ACS recurrence) across the 3 studies that met our criteria (N = 609) suggested a doubling of risk (risk ratio, 2.00; 95% CI, 1.69-2.37) in ACS patients with clinically significant PTSD symptoms relative to patients without PTSD symptoms. CONCLUSIONS/SIGNIFICANCE:This meta-analysis suggests that clinically significant PTSD symptoms induced by ACS are moderately prevalent and are associated with increased risk for recurrent cardiac events and mortality. Further tests of the association of ACS-induced PTSD and clinical outcomes are needed

Stress, ageing and their influence on functional, cellular and molecular aspects of the immune system

The immune response is essential for keeping an organism healthy and for defending it from different types of pathogens. It is a complex system that consists of a large number of components performing different functions. The adequate and controlled interaction between these components is necessary for a robust and strong immune response. There are, however, many factors that interfere with the way the immune response functions. Stress and ageing now consistently appear in the literature as factors that act upon the immune system in the way that is often damaging. This review focuses on the role of stress and ageing in altering the robustness of the immune response first separately, and then simultaneously, discussing the effects that emerge from their interplay. The special focus is on the psychological stress and the impact that it has at different levels, from the whole system to the individual molecules, resulting in consequences for physical health