Biosystems最新文献

Robert Rosen proposed in the late 1950s the metabolism-repair or the (M, R)-system as a general model of living organization, or any "autonomous life form." Since then, the model has persisted as a recurring subject of interest in certain areas of theoretical biology; however, beyond those specific circles, its influence on biological thought has remained minor. One likely reason for this is the difficulty of interpreting the conceptual insights of the model in concrete terms, which Rosen himself identified as the basically unresolved "realization problem." In more recent literature, attempts to do so have focused relatively strictly on the cellular or even biochemical context, and suggested changes to the model's basic nomenclature: most notably, the technical term 'replication' appearing in the model has been interpreted as something quite unrelated to replication in the usual biological meaning of the term. The aims of the present paper are to argue, firstly, that this is likely to be a deviation from Rosen's original intentions, and secondly, that quite apart from those intentions, there is a practical way of applying the (M, R)-system for organizing standard empirical knowledge about any living organism, multicellulars included, and furthermore in such a way that formal 'replication' directly relates to biological replication. Without supposing this new practical scheme to be perfect or beyond further refinement, it is shown to exemplify an analytical point of view that is not covered by more familiar biological theories.

Neurodegenerative diseases have recently garnered significant attention. To better understand the pathogenesis of these diseases and find effective treatments, scientists are increasingly using model organisms in their research. Nematodes, a model organism for studying neurodegenerative diseases, offer crucial insights into the relationship between genes, motor neurons, and locomotion behavior. By identifying the positions of nematodes using a head and tail localization model and automatically counting head swings and omega turns, the analysis of behavioral differences among various nematode strains demonstrates the connection between locomotion behavior and motor neurons. The results from automated counting serve as key indicators of motor neuron integrity, emphasizing the importance of nervous regulation in nematode locomotion behavior and providing new avenues for studying sensory systems and behavioral mechanisms. This has potential implications for the treatment of neurodegenerative diseases.

Understanding how thermodynamic principles drive the emergence of organized chemical systems from abiotic geochemistry represents a central challenge in prebiotic evolution. We develop a quantitative framework for systems removed from equilibrium, establishing formulations for organizational complexity (C) and persistence (P). Complexity, the volumetric rate of free energy dissipation maintaining non-equilibrium organization, scales with substrate gradients and kinetic accessibility. Persistence is the system's capacity to export internally generated entropy across membrane boundaries, determined by geometric constraints and transport impedances. Bejan's Constructal Law provides the optimization principle by which protocell geometry morphs to achieve this balance, providing a deterministic basis for protocell dimensions and molecular architecture. For mineral-catalyzed chemistry at hydrothermal vents (〈Ea〉≈ 50 kJ/mol, T ≈ 338 K), the framework predicts optimal radius r ≈0.56μm for volume-distributed chemistry (n = 3), matching observed dimensions of experimental protocells and minimal cells. Conversely, surface-limited chemistry (n = 2) predicts mechanically unstable configurations, establishing the internalization of metabolism as a thermodynamic necessity. Geological subsidence at polar regions provides deterministic forcing driving protocell populations toward increasing complexity over multi-million-year timescales. The transition from monomers to polymers is a necessary strategy to mitigate osmotic stress during subsidence, effectively responding to a baric forcing of complexity. The framework generates falsifiable predictions where ln(r) ∝ 1/T, with a slope determined by activation energy and dimensionality. The framework transforms a prebiotic system from a statistical improbability into a predictable physical outcome, establishing the foundations for life as a thermodynamic necessity operating under early Earth constraints.

How meaningful, heritable structure first emerged in prebiotic chemical systems remains a central open question in origins-of-life research. Classical frameworks such as the quasispecies and RNA-world models assume that accurate template-based replication is required for stable information and functional specificity to evolve. This work introduces a minimal agent-based protocell model in which short RNA-like oligomers bind metabolites along local 5-nt motifs, generating spatial organization without catalysis or replication. Protocells inherit molecular contents solely through noisy physical partitioning, allowing assessment of whether semantic structure-quantified as mutual information between motif identity and metabolite class-can arise under purely compositional heredity. Across an inheritance-fidelity sweep (0.1-1.0), a sharp semantic threshold was identified: below moderate fidelity, motif-metabolite correlations cannot accumulate, whereas above the threshold (∼0.7), semantic information increases rapidly and stabilizes as a heritable population property. Fitness gains lag behind semantic structure and become substantial only at high fidelity, indicating that meaning emerges before adaptive function. These results establish a pre-genetic information system in which environmental semantics arises without replication, providing a conceptual bridge between compositional inheritance models and sequence-based evolutionary theories.

Triosephosphate isomerase (TIM) is one of the most efficient enzymes known, yet its catalytic precision is not fully explained by classical biochemistry. Here we propose that TIM operates as a quantum logic gate, in which the proton transfer between dihydroxyacetone phosphate and glyceraldehyde-3-phosphate arises from quantum tunneling within a reversible two-state system. We extend this catalysis model by introducing a non-unitary decay channel that quantitatively describes the loss of quantum coherence (decoherence) at the level of the enediol intermediate. In this framework, the formation of methylglyoxal (MG) is reinterpreted as a measure of quantum inefficiency, representing the biochemical signature of decoherence. We formalize this using unitary operators and Kraus maps, linking the probability of MG formation to the failure of tunneling events. This allows us to hypothesize MG formation as the result of a "quantum pathogenic noxa", a dissipative quantum event with measurable toxic consequences. Finally, we illustrate one possible biomedical implication by applying the model to sodium-glucose cotransporter 2 inhibitors, which may reduce decoherence probability by altering catalytic cycling. This work introduces a quantitative approach to quantum pathogenicity and suggests that metabolic disorders may, in part, emerge from disrupted quantum coherence at the enzymatic level.

A consistent physical approach underlying the origin of a genetic code (GC) based on the energy development in an open thermodynamic system (OTS) is considered. The main idea is to present the complex impact of physical environment to open system in the unified form of infinite number of random energy-based factors. Structurally, the suggested approach is divided into two parts. The initial, evolution-irrelevant, part deals with an appearance in OTS's energy space of the triple-based energy structure due to the performance of the bifurcation points, given the quaternary flow of nucleotides contributing to the forming of 64 total/20 unique codons. The second, evolutionary related part introduces the high-level three-step molecular machine to transform the incoming unique codon into one of 20 specific amino acids. Since formally the second part transformation is an equation of a dynamic energy balance, the suggested approach is aligned with the direction of evolutionary changes in OTS. Then, in general, the steps of GC evolution are (1) the forming of binary logic in considered energy space; (2) segregation of evolutionary energy space (EES); (3) splitting of EES into a few (2, 3, or 6 energy phases; (4) interaction of 4-kinds flow of free nucleotides with the multi-phase EES; (5) the forming of original GC; (6) concurrence of the formed realizations of GC and arising of the master 4³ version. The properties of the simulated GC are checked against the concrete observables. The used physical factors of an environment are the conserved quantities: energy, momentum, angular momentum, electric charge, and others.

This paper examines a biochemical paradox in microbial pathogenicity: the most lethal human pathogens (viruses, protozoa, prions) systematically lack D-amino acid usage, coherent fractal morphology, and Hz-level biological oscillations; these characteristics prevail in beneficial and treatable bacterial pathogens. Systematic analysis of 47 major human pathogens and quantitative fractal dimension analysis of 40 cryo-electron microscopy structures unveil refined hierarchical patterns within universally low structural complexity. Bacterial pathogens employ D-amino acids in peptidoglycan synthesis and exhibit a broad structural repertoire spanning from 1.2610 to 1.9625 (mean 2D fractal dimension = 1.5502 ± 0.2543), overlapping the upper protozoal band (mean = 1.5865 ± 0.1322). Protozoa therefore show the highest central complexity, while bacteria display the widest variance and retain access to higher-order organization. Increasingly lethal pathogens systematically lack these features and occupy progressively reduced complexity bands (Fungi: 1.5074 ± 0.1600; Virus: 1.4388 ± 0.2575; Prion: 1.4060 ± 0.1727). Among all structures analyzed, the HIV-1 capsid displayed the lowest complexity (D₂D = 1.1095), consistent with its historically high lethality and over 40 million cumulative deaths since the 1980s. We propose that this evolutionary minimalism represents a convergent pathogenic strategy in which successful pathogens attain reduced complexity, with the most lethal variants pushing simplification to extreme levels characterized by biochemical invisibility and structural incoherence. D-amino acid absence enables evasion of host innate immune recognition through D-amino acid oxidase, while lack of intrinsic circadian rhythms prevents metabolic synchronization and immune detection. This framework provides measurable criteria for pathogen threat assessment and suggests new therapeutic approaches rooted in complexity-based medicine.