340 research outputs found
Coupled Replicator Equations for the Dynamics of Learning in Multiagent Systems
Starting with a group of reinforcement-learning agents we derive coupled
replicator equations that describe the dynamics of collective learning in
multiagent systems. We show that, although agents model their environment in a
self-interested way without sharing knowledge, a game dynamics emerges
naturally through environment-mediated interactions. An application to
rock-scissors-paper game interactions shows that the collective learning
dynamics exhibits a diversity of competitive and cooperative behaviors. These
include quasiperiodicity, stable limit cycles, intermittency, and deterministic
chaos--behaviors that should be expected in heterogeneous multiagent systems
described by the general replicator equations we derive.Comment: 4 pages, 3 figures,
http://www.santafe.edu/projects/CompMech/papers/credlmas.html; updated
references, corrected typos, changed conten
Does the Red Queen reign in the kingdom of digital organisms?
In competition experiments between two RNA viruses of equal or almost equal
fitness, often both strains gain in fitness before one eventually excludes the
other. This observation has been linked to the Red Queen effect, which
describes a situation in which organisms have to constantly adapt just to keep
their status quo. I carried out experiments with digital organisms
(self-replicating computer programs) in order to clarify how the competing
strains' location in fitness space influences the Red-Queen effect. I found
that gains in fitness during competition were prevalent for organisms that were
taken from the base of a fitness peak, but absent or rare for organisms that
were taken from the top of a peak or from a considerable distance away from the
nearest peak. In the latter two cases, either neutral drift and loss of the
fittest mutants or the waiting time to the first beneficial mutation were more
important factors. Moreover, I found that the Red-Queen dynamic in general led
to faster exclusion than the other two mechanisms.Comment: 10 pages, 5 eps figure
CDC6:A novel canine tumour biomarker detected in circulating extracellular vesicles
Circulating nucleic acids and extracellular vesicles (EV) represent novel biomarkers to diagnose cancer. The non-invasive nature of these so-called liquid biopsies provides an attractive alternative to tissue biopsy-based cancer diagnostics. This study aimed to investigate if circulating cell cycle-related E2F target transcripts can be used to diagnose tumours in canine tumour patients with different types of tumours. Furthermore, we assessed if these mRNAs are localised within circulating EV. We isolated total RNA from the plasma of 20 canine tumour patients and 20 healthy controls. Four E2F target genes (CDC6, DHFR, H2AFZ and ATAD2) were selected based on the analysis of published data of tumour samples available in public databases. We performed reverse transcription and quantitative real-time PCR to analyse the plasma levels of selected E2F target transcripts. All four E2F target transcripts were detectable in the plasma of canine tumour patients. CDC6 mRNA levels were significantly higher in the plasma of canine tumour patients compared to healthy controls. A subset of canine tumour patient and healthy control plasma samples (n = 7) were subjected to size exclusion chromatography in order to validate association of the E2F target transcripts to circulating EV. For CDC6, EV analysis enhanced their detectability compared to total plasma analysis. In conclusion, our study reveals circulating CDC6 as a promising non-invasive biomarker to diagnose canine tumours
Co-Evolution of quasispecies: B-cell mutation rates maximize viral error catastrophes
Co-evolution of two coupled quasispecies is studied, motivated by the
competition between viral evolution and adapting immune response. In this
co-adaptive model, besides the classical error catastrophe for high virus
mutation rates, a second ``adaptation-'' catastrophe occurs, when virus
mutation rates are too small to escape immune attack. Maximizing both regimes
of viral error catastrophes is a possible strategy for an optimal immune
response, reducing the range of allowed viral mutation rates to a minimum. From
this requirement one obtains constraints on B-cell mutation rates and receptor
lengths, yielding an estimate of somatic hypermutation rates in the germinal
center in accordance with observation.Comment: 4 pages RevTeX including 2 figure
Error threshold in finite populations
A simple analytical framework to study the molecular quasispecies evolution
of finite populations is proposed, in which the population is assumed to be a
random combination of the constiyuent molecules in each generation,i.e.,
linkage disequilibrium at the population level is neglected. In particular, for
the single-sharp-peak replication landscape we investigate the dependence of
the error threshold on the population size and find that the replication
accuracy at threshold increases linearly with the reciprocal of the population
size for sufficiently large populations. Furthermore, in the deterministic
limit our formulation yields the exact steady-state of the quasispecies model,
indicating then the population composition is a random combination of the
molecules.Comment: 14 pages and 4 figure
Adaptive walks on time-dependent fitness landscapes
The idea of adaptive walks on fitness landscapes as a means of studying
evolutionary processes on large time scales is extended to fitness landscapes
that are slowly changing over time. The influence of ruggedness and of the
amount of static fitness contributions are investigated for model landscapes
derived from Kauffman's landscapes. Depending on the amount of static
fitness contributions in the landscape, the evolutionary dynamics can be
divided into a percolating and a non-percolating phase. In the percolating
phase, the walker performs a random walk over the regions of the landscape with
high fitness.Comment: 7 pages, 6 eps-figures, RevTeX, submitted to Phys. Rev.
Investigate the origins of COVID-19
On 30 December 2019, the Program for Monitoring Emerging Diseases notified the world about a pneumonia of unknown cause in Wuhan, China. Since then, scientists have made remarkable progress in understanding the causative agent, severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), its transmission, pathogenesis, and mitigation by vaccines, therapeutics, and non-pharmaceutical interventions. Yet more investigation is still needed to determine the origin of the pandemic. Theories of accidental release from a lab and zoonotic spillover both remain viable. Knowing how COVID-19 emerged is critical for informing global strategies to mitigate the risk of future outbreaks
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