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مصدر الموتانتات المتكيفة: قياس كمي؟

Origin of adaptive mutants: a quantum measurement?

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 نشر من قبل Vasily Ogryzko V
 تاريخ النشر 2007
  مجال البحث علم الأحياء
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 تأليف Vasily Ogryzko




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This is a supplement to the paper arXiv:q-bio/0701050, containing the text of correspondence sent to Nature in 1990.



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168 - Vasily Ogryzko 2009
I compare two quantum-theoretical approaches to the phenomenon of adaptive mutations, termed here Q-cell and Q-genome. I use fluctuation trapping model as a general framework. I introduce notions of R-error and D-error and argue that the fluctuation trapping model has to employ a correlation between the R- and D- errors. Further, I compare how the two approaches can justify the R-D-error correlation, focusing on the advantages of the Q-cell approach. The positive role of environmentally induced decoherence (EID) on both steps of the adaptation process is emphasized. A starving bacterial cell is proposed to be in an einselected state. The intracellular dynamics in this state has a unitary character and I propose to interpret it as exponential growth in imaginary time, analogously to the commonly considered diffusion interpretation of the Schroedinger equation. Addition of a substrate leads to Wick rotation and a switch from imaginary time reproduction to a real time reproduction regime. Due to the variations at the genomic level (such as base tautomery), the starving cell has to be represented as a superposition of different components, all reproducing in imaginary time. Adidtion of a selective substrate, allowing only one of these components to amplify, will cause Wick rotation and amplification of this component, thus justifying the occurence of the R-D-error correlation. Further ramifications of the proposed ideas for evolutionary theory are discussed.
Increasing number in global COVID-19 cases demands for mathematical model to analyze the interaction between the virus dynamics and the response of innate and adaptive immunity. Here, based on the assumption of a weak and delayed response of the inna te and adaptive immunity in SARS-CoV-2 infection, we constructed a mathematical model to describe the dynamic processes of immune system. Integrating theoretical results with clinical COVID-19 patients data, we classified the COVID-19 development processes into three typical modes of immune responses, correlated with the clinical classification of mild & moderate, severe and critical patients. We found that the immune efficacy (the ability of host to clear virus and kill infected cells) and the lymphocyte supply (the abundance and pool of naive T and B cell) play important roles in the dynamic process and determine the clinical outcome, especially for the severe and critical patients. Furthermore, we put forward possible treatment strategies for the three typical modes of immune response. We hope our results can help to understand the dynamical mechanism of the immune response against SARS-CoV-2 infection, and to be useful for the treatment strategies and vaccine design.
213 - Emmanuel Tannenbaum 2007
This paper develops a simplified set of models describing asexual and sexual replication in unicel- lular diploid organisms. The models assume organisms whose genomes consist of two chromosomes, where each chromosome is assumed to be functional if it is equal to some master sequence $ sigma_0 $, and non-functional otherwise. The first-order growth rate constant, or fitness, of an organism, is determined by whether it has zero, one, or two functional chromosomes in its genome. For a population replicating asexually, a given cell replicates both of its chromosomes, and splits its genetic material evenly between the two cells. For a population replicating sexually, a given cell first divides into two haploids, which enter a haploid pool, fuse into diploids, and then divide via the normal mitotic process. Haploid fusion is modeled as a second-order rate process. When the cost for sex is small, as measured by the ratio of the characteristic haploid fusion time to the characteristic growth time, we find that sexual replication with random haploid fusion leads to a greater mean fitness for the population than a purely asexual strategy. However, independently of the cost for sex, we find that sexual replication with a selective mating strategy leads to a higher mean fitness than the random mating strategy. This result is based on the assumption that a selective mating strategy does not have any additional time or energy costs over the random mating strategy, an assumption that is discussed in the paper. The results of this paper are consistent with previous studies suggesting that sex is favored at intermediate mutation rates, for slowly replicating organisms, and at high population densities.
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A didactic introduction, dated by 1999, to the ideas of the papers arXiv:q-bio/0701050 and arXiv:0704.0034
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