Search arXiv⌕ Search
Home/Archive/arXiv

arXiv · q-bio/0412044

Exact law of live nature

Mark Ya. Azbel'
View original source ↗Read source document ↗Export metadata ↓

Abstract

Exact law of mortality dynamics in changing populations and environment is derived. The law is universal for all species, from single cell yeast to humans. It includes no characteristics of animal- environment interactions (metabolism etc) which are a must for life. Such law is unique for live systems with their homeostatic self-adjustment to environment. Its universal dynamics for all animals, with their drastically different biology, evolutionary history, and complexity, is also unique for live systems-cf different thermodynamics of e.g. liquids and glasses. The law which is valid for all live, and only live, systems is a life specific law of nature. Mortality is an instrument of natural selection and biological diversity. Its law which is preserved in evolution of all species is a conservation law of mortality, selection, evolution, biology. The law implies new kind of mortality and adaptation which dominate in evolutionary unprecedented protected populations and, in contrast to species specific natural selection, proceed via universal stepwise rungs. The law demonstrates that intrinsic mortality and at least certain aspects of aging are disposable evolutionary byproducts, and directed genetic and/or biological changes may yield healthy and vital Methuselah lifespan. This is consistent with experiments. Universality implies that single cell yeast may provide a master key to the cellular mechanism of universal mortality, aging, selection, evolution, and its regulation in all animals. One may look for its manifestations in animal cells also, e.g., in their replicative senescence.

Explore related subjects

q-bio.PEcond-mat.stat-mechq-bio.QM

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Mark Ya. Azbel'. 2004-12-26. Exact law of live nature. https://doi.org/10.1016/j.physa.2005.01.044

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related papers

arXiv2026

Predator self limitation controls pattern formation in a predator prey system with additional food: a Turing Hopf analysis

Supplying a released predator with additional, non reproducing food is a standard lever in augmentative biological control, with a known drawback with nothing limiting the predators own numbers, the extra food lets its population grow without bound. Competition among the predators supplies the missing brake. Howthis self limitation reshapes the spatial arrangement of the two species has not been asked. We address it with a reaction diffusion model of a logistically growing prey and a predator feeding through a Holling type II response that also draws on additional food , the predators competing among themselves at strength. In the well mixed setting we locate the Hopf bifurcation of the coexistence state exactly and show the cycle born there is stable, so weak competition gives boom bust oscillations, not runaway growth. Allowing movement, we obtain the diffusion driven Turing threshold at which the uniform state breaks into stationary patches of high and low density, and find the uniform oscillation stable as it appears. With prey mobility and competition strength as control parameters, the pattern forming and oscillatory instabilities meet at a single point, where we compute the dynamics. Simulations confirm the sequence weak competition gives a wholefield oscillation, stronger competition with faster prey spread gives fixed patterns, and near the crossover the two combine into patterns that pulse in time. Predator self competition therefore sets the spatial structure of the community, which is what matters when additional food is used to steer a control agent in the field.

q-bio.PE↗
arXiv2026

Mathematical Modelling of Within-Host HIV Dynamics with Cytotoxic Immune Response and Antiretroviral Therapy

We develop and analyse a mechanistic ODE model of within-host HIV dynamics that includes uninfected CD4$^+$ T cells, latently and productively infected cells, free virions, and cytotoxic immune effectors. Antiretroviral therapy is described by two time-dependent efficacy functions that separately reduce new infections and virion production. We show that solutions remain non-negative and bounded, identify the infection-free and endemic equilibria, and derive the basic reproduction number together with the local stability condition for the infection-free state. We also obtain treatment-dependent suppression thresholds and an analytical estimate of when this threshold is crossed as treatment efficacy declines. Numerical simulations consider untreated infection, ART initiation, periodic variation in efficacy, and progressive loss of treatment effect. Without therapy, the model approaches a state of persistent infection. ART reduces viral load and promotes recovery of the CD4$^+$ T-cell population, while the latent reservoir persists under the parameter set considered. Periodic changes in treatment efficacy produce sustained forced oscillations. These results connect the analytical threshold conditions with the treatment-dependent dynamics of the model and provide a basis for future calibration, sensitivity analysis, uncertainty quantification, and extensions informed by clinical data.

q-bio.PE↗
arXiv2026

Consistent determination of stability regimes in natural ecological communities from abundance time series

The stability of an ecological community is conventionally defined through species interactions, which quantify how species affect one another. Interaction strengths are notoriously difficult to measure in species-rich assemblages. Long-term monitoring of species-rich communities, however, provides species abundance time series, increasingly available across habitats and taxa but not yet connected to the stability properties of the communities they describe. Here we develop a statistical framework that infers stability regimes in large ecological communities directly from abundance time series. We study stochastic Generalized Lotka--Volterra dynamics with random interactions and environmental fluctuations using dynamical mean-field theory, reducing the multispecies system to an effective stochastic process for a representative species. The theory predicts three stability regimes (stable coexistence, intermittent dynamics close to extinction, and unbounded growth) separated by analytical boundaries, and shows that environmental stochasticity systematically destabilizes coexistence by promoting intermittent low-abundance dynamics. The resulting steady-state species abundance distribution is a Gamma law that ties the dynamical phases to the variability-based stability metrics used in empirical studies. Recasting the effective dynamics as a multivariate regression model, we infer interaction statistics, environmental variability and the characteristic timescale of the dynamics from community data, without reconstructing the interaction network. Applied to natural communities spanning a broad range of habitats and taxa, the method resolves contrasting stability regimes and yields quantitative estimates of species extinction risk.

q-bio.PE↗