Universal neural field computation

Turing machines and G\"odel numbers are important pillars of the theory of computation. Thus, any computational architecture needs to show how it could relate to Turing machines and how stable implementations of Turing computation are possible. In this chapter, we implement universal Turing computation in a neural field environment. To this end, we employ the canonical symbologram representation of a Turing machine obtained from a G\"odel encoding of its symbolic repertoire and generalized shifts. The resulting nonlinear dynamical automaton (NDA) is a piecewise affine-linear map acting on the unit square that is partitioned into rectangular domains. Instead of looking at point dynamics in phase space, we then consider functional dynamics of probability distributions functions (p.d.f.s) over phase space. This is generally described by a Frobenius-Perron integral transformation that can be regarded as a neural field equation over the unit square as feature space of a dynamic field theory (DFT). Solving the Frobenius-Perron equation yields that uniform p.d.f.s with rectangular support are mapped onto uniform p.d.f.s with rectangular support, again. We call the resulting representation \emph{dynamic field automaton}.Comment: 21 pages; 6 figures. arXiv admin note: text overlap with arXiv:1204.546

Novel Loci for Adiponectin Levels and Their Influence on Type 2 Diabetes and Metabolic Traits : A Multi-Ethnic Meta-Analysis of 45,891 Individuals

J. Kaprio, S. Ripatti ja M.-L. Lokki työryhmien jäseniä.Peer reviewe

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