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Intelligence is a human construct to represent the ability to achieve goals. Given this wide berth, intelligence has been defined countless times, studied in a variety of ways and represented using numerous measures. Understanding intelligence ultimately requires theory and quantification, both of which have proved elusive. I develop a framework -- the Theory of Intelligences (TIS) -- that applies across all systems from physics, to biology, humans and AI. TIS likens intelligence to a calculus, differentiating, correlating and integrating information. Intelligence operates at many levels and scales and TIS distils these into a parsimonious macroscopic framework centered on solving, planning and their optimization to accomplish goals. Notably, intelligence can be expressed in informational units or in units relative to goal difficulty, the latter defined as complexity relative to system (individual or benchmarked) ability. I present general equations for intelligence and its components, and a simple expression for the evolution of intelligence traits. The measures developed here could serve to gauge different facets of intelligence for any step-wise transformation of information. I argue that proxies such as environment, technology, society and collectives are essential to a general theory of intelligence and to possible evolutionary transitions in intelligence, particularly in humans. I conclude with testable predictions of TIS and offer several speculations., Comment: 37 pages, 1 Table, 6 figures

I employ a simple mathematical model of an epidemic process to evaluate how four basic quantities: the reproduction number (R), the numbers of sensitive (S) and infectious individuals(I), and total community size (N) affect strategies to control COVID-19. Numerical simulations show that strict suppression measures at the beginning of an epidemic can create low infectious numbers, which thereafter can be managed by mitigation measures over longer periods to flatten the epidemic curve. The stronger the suppression measure, the faster it achieves the low numbers of infections that are conducive to subsequent management. We discuss the predictions of this analysis and how it fits into longer-term sequences of measures, including using the herd immunity concept to leverage acquired immunity., Comment: 14 pages, 2 tables, 4 figures

Tomasetti and Vogelstein (2015a) find that the incidence of a set of cancer types is correlated with the total number of normal stem cell divisions. Here, we separate the effects of standing stem cell number (i.e., organ or tissue size) and per stem cell lifetime replication rate. We show that each has a statistically significant and independent effect on explaining variation in cancer incidence over the 31 cases considered by Tomasetti and Vogelstein. When considering the total number of stem cell divisions and when removing cases associated with disease or carcinogens, we find that cancer incidence attains a plateau of approximately 0.6% incidence for the cases considered by these authors. We further demonstrate that grouping by anatomical site explains most of the remaining variation in risk between cancer types. This new analysis suggests that cancer risk depends not only on the number of stem cell divisions but varies enormously ($\sim$10,000 times) depending on the stem cell's environment. Future research should investigate how tissue characteristics (anatomical site, type, size, stem cell divisions) explain cancer incidence over a wider range of cancers, to what extent different tissues express specific protective mechanisms, and whether any differential protection can be attributed to natural selection., Comment: 17 pages

Cancer poses danger because of its unregulated growth, development of resistant subclones, and metastatic spread to vital organs. Although the major transitions in cancer development are increasingly well understood, we lack quantitative theory for how chemoprevention is predicted to affect survival. We employ master equations and probability generating functions, the latter well known in statistical physics, to derive the dynamics of tumor growth as a mean-field approximation. We also study numerically the associated stochastic birth-death process. Our findings predict exponential tumor growth when a cancer is in its early stages of development and hyper-exponential growth thereafter. Numerical simulations are in general agreement with our analytical approach. We evaluate how constant, low impact treatments affect both neoplastic growth and the frequency of chemoresistant clones. We show that therapeutic outcomes are highly predictable for treatments starting either sufficiently early or late in terms of initial tumor size and the initial number of chemoresistant cells, whereas stochastic dynamics dominate therapies starting at intermediate neoplasm sizes, with high outcome sensitivity both in terms of tumor control and the emergence of resistant subclones. The outcome of chemoprevention can be understood in terms of both minimal physiological impacts resulting in long-term control and either preventing or slowing the emergence of resistant subclones. We argue that our model and results can also be applied to the management of early, clinically detected cancers after tumor excision.

Resistance to chemotherapies, particularly to anticancer treatments, is an increasing medical concern. Among the many mechanisms at work in cancers, one of the most important is the selection of tumor cells expressing resistance genes or phenotypes. Motivated by the theory of mutation-selection in adaptive evolution, we propose a model based on a continuous variable that represents the expression level of a resistance gene (or genes, yielding a phenotype) influencing in healthy and tumor cells birth/death rates, effects of chemotherapies (both cytotoxic and cytostatic) and mutations. We extend previous work by demonstrating how qualitatively different actions of chemotherapeutic and cytostatic treatments may induce different levels of resistance. The mathematical interest of our study is in the formalism of constrained Hamilton-Jacobi equations in the framework of viscosity solutions. We derive the long-term temporal dynamics of the fittest traits in the regime of small mutations. In the context of adaptive cancer management, we also analyse whether an optimal drug level is better than the maximal tolerated dose.