Identification of a Duffing oscillator using particle Gibbs with ancestor sampling

The Duffing oscillator remains a key benchmark in nonlinear systems analysis and poses interesting challenges in nonlinear structural identification. The use of particle methods or sequential Monte Carlo (SMC) is becoming a more common approach for tackling these nonlinear dynamical systems, within structural dynamics and beyond. This paper demonstrates the use of a tailored SMC algorithm within a Markov Chain Monte Carlo (MCMC) scheme to allow inference over the latent states and parameters of the Duffing oscillator in a Bayesian manner. This approach to system identification offers a statistically more rigorous treatment of the problem than the common state-augmentation methods where the parameters of the model are included as additional latent states. It is shown how recent advances in particle MCMC methods, namely the particle Gibbs with ancestor sampling (PG-AS) algorithm is capable of performing efficient Bayesian inference, even in cases where little is known about the system parameters a priori. The advantage of this Bayesian approach is the quantification of uncertainty, not only in the system parameters but also in the states of the model (displacement and velocity) even in the presence of measurement noise

Use of SMS texts for facilitating access to online alcohol interventions: a feasibility study

A41 Use of SMS texts for facilitating access to online alcohol interventions: a feasibility study In: Addiction Science & Clinical Practice 2017, 12(Suppl 1): A4

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease