Keynote Speakers

Prof. Brian Skyrms 

Distinguished professor of Logic and Philosophy of Science, Economics, and Philosophy
at U.C. Irvine, and Professor of Philosophy at Stanford University.

Title: From Democritus to Signaling Networks


Prof. Brian Skyrms is a fellow of the American Academy of Arts and Sciences and of the National Academy of Sciences of the USA. His books include:

Evolution of the Social Contract,
The Stag Hunt and the Evolution of Social Structure,
Signals: Evolution Learning and Information, and most recently
Ten Great Ideas About Chance co-authored with Persi Diaconis.


Prof. Sheri M. Markose.

Professor of Economics at the University of Essex, UK

Title: The Digital Origins of Intelligence: How we became smart and protean


Sheri Markose has a PhD from the London School of Economics and has been a professor of Economics at the University of Essex, UK, since 2006. As founder director (2002-2009) of the Centre For Computational Finance and Economic Agents (CCFEA), Sheri pioneered a multi-disciplinary curricula covering agent based computational economics (ACE) and complexity sciences. She is well known for data driven network based ACE models developed for projects on managing systemic risk when she was a researcher for the IMF, Academic Advisor to G20 OTC Derivatives Reforms, and a Senior Consultant for the Reserve Bank of India (2011-2015). Her long standing interest in Gödel logic was prompted by the Austrian economist, F.A Hayek, in the context of his work on complex phenomena, and by Ken Binmore who pointed out in 1987 that extant game theory was flawed in failing to deal with the Gödel archetype of the Liar who negates what can be computed. Culminating in her 2017 paper in Journal of Dynamics and Games (AIMS), Sheri laid the groundwork for a Genomic Nash Equilibrium as one where the Gödel sentence, often regarded to be a funky and esoteric construction, is shown to be ubiquitous in code based genomic systems as it permits a code to self-report that it is under attack. In the absence of this, ‘thinking outside the box’, strategic innovation and an arms race in novelty production are not possible. Subsequently, Sheri was invited to be an Associate Editor of Frontiers of AI and Robotics: Computational Intelligence.

Paper Title and Abstract

The Digital Origins of Intelligence: How we became smart and protean

In the spirit of the ‘dynamic’ genome of Barbara McClintock, I use a new notion of a Genomic Nash Equilibrium (GNE), to show how the Gödel-Turing-Post conditions of computational universality, acquired at critical points of genomic evolution, make us smart and protean. The key aspect of a GNE is that the genomic system encodes the famous self-referential Gödel sentence as one where a code self-reports it is under attack or negated by, what is effectively, a hacker/virus (aka ‘Liar’). If the latter cannot be eliminated, such code based digital systems embark on an arms race of novelty production with syntactic objects or phenotypes not previously there. It is widely known that viral software of genomic transposons provides scope for reuse and replication as in routine digital operations of ‘scissor-paste’ and ‘copy-paste’. However, few recognize that the workings of the adaptive immune system (AIS) in tissues like the thymus medulla, as also the mirror neuron system for complex social cognition, are text book cases of information processing in a formal recursive Gödel meta-mathematics. This is typically organized in a tuple of a code centred self and the ‘other’ in an offline domain of recordings and simulations that have a bijective relationship with online machine executions of the same codes. The thymus medulla remarkably makes ‘copies’, in an offline environment, of ~85% of the genome that involves codes of programs that halt, viz. are ‘theorems’ in the system of ribosomal machine executions of 3-D prints of the morphology and regulation of the organism. Application of negation on these halting codes generates a digitally listable set of codes of self-antigens analogous to refutable propositions formalized in the Emil Post theory of creative and productive sets. GNE implies exciting new hypotheses on AIS and social cognition, and on the high incidence of repeat sequences in the human genome due to the model of regulatory networks as a distributed ledger.


Michael Lotze, MD

Professor of Surgery, Immunology, and Bio-engineering, University of Pittsburgh School of Medicine

Title: Know Yourself: Evaluating the Full Adaptome in TIL, PBMC, and Lymph Nodes in Solid Tumor Patients


“If you know the enemy and know yourself, you need not fear the result of a hundred battles. If you know yourself but not the enemy, for every victory gained you will also suffer a defeat. If you know neither the enemy nor yourself, you will succumb in every battle.” ― Sun Tzu, The Art of War

The adaptive immune system is the ‘best doctor’ in wartime for both diagnosing and treating diseases, integrating five elemental, highly networked lymphoid cells that both support and counter-regulate each other: NK cells, NKT cells, αβ T-cells, γδ T-cells, and B cells expressing an IgH and κ or λ light chains. It carries out these tasks with unmatched precision, with the help of rearranged T and B cell receptors, our most diverse set of expressed and rearranged genes, fundamentally distinguishing one individual from another. Even identical twins only share ~6% of their repertoire. This autologous receptor diversity, ranging from 1015 to 1025 for each chain of the rearranged receptors, contains only two chains expressed in each cell. By combining dimer avoidance multiplex PCR and next generation sequencing (NGS), we have developed, in partnership with iRepertoire, Inc., high-throughput methods to study adaptive immunity. The adaptome is the sum-total of expressed T and B cell receptor genes in a sample, composed of seven chains, including the αβ and γδ chains for T cells, and IgH heavy chains and κ or λ light chains for B cells. The immune repertoire, is the sum-total of the individual clonotypes within one chain, including individual CDR3 sequences. In order to reflect the breadth and depth of the adaptome, the following criteria assessing any method needs to be ascertained AFTER validation:

1) Does it demonstrate inclusive and quantitative methods that are reproducible between sites (Huntsville/iRepertoire and Hillman/UPMC Adaptome Center);

2) Can analysis comprising bulk sequencing provide robust identification of high frequency clones (and enable subsequent assessment of underlying ‘important’ biology);

3) Do measures of clonal diversity enable understanding of the underlying structure and providence of the repertoire, integrating with neoepitope and common antigen/metabolite expression; and

4) Is there evidence of convergent evolution that could allow homologous or identical CDR3’s to be associated with individual disease entities, creating hope for novel diagnostics and/or disease burden assessments?

Integrating studies of the peripheral blood, lymph nodes, and tumor allows for dynamic interrogation of the immune alterations occurring with age, treatment, and response to emergent and established immunotherapies. Confirming that this analysis can also be conducted on archival tissues increases its value.