On a generic class of two-node queueing systems

This paper analyzes a generic class of two-node queueing systems. A first queue is fed by an on–off Markov fluid source; the input of a second queue is a function of the state of the Markov fluid source as well, but now also of the first queue being empty or not. This model covers the classical two-node tandem queue and the two-class priority queue as special cases. Relying predominantly on probabilistic argumentation, the steady-state buffer content of both queues is determined (in terms of its Laplace transform). Interpreting the buffer content of the second queue in terms of busy periods of the first queue, the (exact) tail asymptotics of the distribution of the second queue are found. Two regimes can be distinguished: a first in which the state of the first queue (that is, being empty or not) hardly plays a role, and a second in which it explicitly does. This dichotomy can be understood by using large-deviations heuristics

Blood DNA methylation sites predict death risk in a longitudinal study of 12,300 individuals

This is the final version. Available on open access from Impact Journals via the DOI in this recordDNA methylation has fundamental roles in gene programming and aging that may help predict mortality. However, no large-scale study has investigated whether site-specific DNA methylation predicts all-cause mortality. We used the Illumina-HumanMethylation450-BeadChip to identify blood DNA methylation sites associated with all-cause mortality for 12, 300 participants in 12 Cohorts of the Heart and Aging Research in Genetic Epidemiology (CHARGE) Consortium. Over an average 10-year follow-up, there were 2,561 deaths across the cohorts. Nine sites mapping to three intergenic and six gene-specific regions were associated with mortality (P < 9.3x10-7) independently of age and other mortality predictors. Six sites (cg14866069, cg23666362, cg20045320, cg07839457, cg07677157, cg09615688)-mapping respectively to BMPR1B, MIR1973, IFITM3, NLRC5, and two intergenic regions-were associated with reduced mortality risk. The remaining three sites (cg17086398, cg12619262, cg18424841)-mapping respectively to SERINC2, CHST12, and an intergenic region-were associated with increased mortality risk. DNA methylation at each site predicted 5%-15% of all deaths. We also assessed the causal association of those sites to age-related chronic diseases by using Mendelian randomization, identifying weak causal relationship between cg18424841 and cg09615688 with coronary heart disease. Of the nine sites, three (cg20045320, cg07839457, cg07677157) were associated with lower incidence of heart disease risk and two (cg20045320, cg07839457) with smoking and inflammation in prior CHARGE analyses. Methylation of cg20045320, cg07839457, and cg17086398 was associated with decreased expression of nearby genes (IFITM3, IRF, NLRC5, MT1, MT2, MARCKSL1) linked to immune responses and cardiometabolic diseases. These sites may serve as useful clinical tools for mortality risk assessment and preventative care