Natural Intelligence and Anthropic Reasoning

This paper aims to justify the concept of natural intelligence in the biosemiotic context. I will argue that the process of life is (i) a cognitive/semiotic process and (ii) that organisms, from bacteria to animals, are cognitive or semiotic agents. To justify these arguments, the neural-type intelligence represented by the form of reasoning known as anthropic reasoning will be compared and contrasted with types of intelligence explicated by four disciplines of biology – relational biology, evolutionary epistemology, biosemiotics and the systems view of life – not biased towards neural intelligence. The comparison will be achieved by asking questions related to the process of observation and the notion of true observers. To answer the questions I will rely on a range of established concepts including SETI (search for extraterrestrial intelligence), Fermi’s paradox, bacterial cognition, versions of the panspermia theory, as well as some newly introduced concepts including biocivilisations, cognitive/semiotic universes, and the cognitive/semiotic multiverse. The key point emerging from the answers is that the process of cognition/semiosis – the essence of natural intelligence – is a biological universal.Brunel University Londo

Somatic mosaicism and common genetic variation contribute to the risk of very-early-onset inflammatory bowel disease

Abstract: Very-early-onset inflammatory bowel disease (VEO-IBD) is a heterogeneous phenotype associated with a spectrum of rare Mendelian disorders. Here, we perform whole-exome-sequencing and genome-wide genotyping in 145 patients (median age-at-diagnosis of 3.5 years), in whom no Mendelian disorders were clinically suspected. In five patients we detect a primary immunodeficiency or enteropathy, with clinical consequences (XIAP, CYBA, SH2D1A, PCSK1). We also present a case study of a VEO-IBD patient with a mosaic de novo, pathogenic allele in CYBB. The mutation is present in ~70% of phagocytes and sufficient to result in defective bacterial handling but not life-threatening infections. Finally, we show that VEO-IBD patients have, on average, higher IBD polygenic risk scores than population controls (99 patients and 18,780 controls; P < 4 × 10−10), and replicate this finding in an independent cohort of VEO-IBD cases and controls (117 patients and 2,603 controls; P < 5 × 10−10). This discovery indicates that a polygenic component operates in VEO-IBD pathogenesis