Sexual selection drives the evolution of some of the most exaggerated traits in nature. Studies on sexual selection often focus on the size of these traits relative to body size, but few focus on energetic maintenance costs of the tissues that compose them, and the ways in which these costs vary with body size. The relationships between energy use and body size have consequences that may allow large individuals to invest disproportionally more in sexually selected structures, or lead to the (...) reduced per‐gram maintenance cost of enlarged structures. Although sexually selected traits can incur energetic maintenance costs, these costs are not universally high; they are dependent on the relative mass and metabolic activity of tissues associated with them. Energetic costs of maintenance may play a pervasive yet little‐explored role in shaping the relative scaling of sexually selected traits across diverse taxa. Also see the video abstract here: https://youtu.be/JyuoQIeA33Q. (shrink)

This paper proposes an abstract mathematical frame for describing some features of biological time. The key point is that usual physical (linear) representation of time is insufficient, in our view, for the understanding key phenomena of life, such as rhythms, both physical (circadian, seasonal …) and properly biological (heart beating, respiration, metabolic …). In particular, the role of biological rhythms do not seem to have any counterpart in mathematical formalization of physical clocks, which are based on frequencies along the (...) usual (possibly thermodynamical, thus oriented) time. We then suggest a functional representation of biological time by a 2-dimensional manifold as a mathematical frame for accommodating autonomous biological rhythms. The “visual” representation of rhythms so obtained, in particular heart beatings, will provide, by a few examples, hints towards possible applications of our approach to the understanding of interspecific differences or intraspecific pathologies. The 3- dimensional embedding space, needed for purely mathematical reasons, allows to introduce a suitable extra-dimension for “representation time”, with a cognitive significance. (shrink)

The current literature that attempts to bridge between geometric morphometrics (GMM) and finite element analyses (FEA) of CT-derived data from bones of living animals and fossils appears to lack a sound biotheoretical foundation. To supply the missing rigor, the present article demonstrates a new rhetoric of quantitative inference across the GMM–FEA bridge—a rhetoric bridging form to function when both have been quantified so stringently. The suggested approach is founded on diverse standard textbook examples of the relation between forms and the (...) way strains in them are produced by stresses imposed upon them. One potentially cogent approach to the explanatory purposes driving studies of this class arises from a close scrutiny of the way in which computations in both domains, shape and strain, can be couched as minimizations of a scalar quantity. For GMM, this is ordinary Procrustes shape distance; in FEA, it is the potential energy that is stored in the deformed configuration of the solid form. A hybrid statistical method is introduced requiring that all forms be subjected to the same detailed loading designs (the same “probes”) in a manner careful to accommodate the variations of those same forms before they were stressed. The proper role of GMM is argued to be the construction of regressions for strain energy density on the largest-scale relative warps in order that biological explanations may proceed in terms of the residuals from those regressions: the local residual features of strain energy density. The method, evidently a hierarchical one, might be intuitively apprehended as a geometrical approach to a formal allometric analysis of strain. The essay closes with an exhortation. (shrink)

I analyze here biological regression equations known in the literature as allometries and scaling laws. My focus is on the alleged lawlike status of these equations. In particular I argue against recent views that regard allometries and scaling laws as representing universal, non-continent, and/or strict biological laws. Although allometries and scaling laws appear to be generalizations applying to many taxa, they are neither universal nor exceptionless. In fact there appear to be exceptions to all of them. Nor are the constants (...) in allometries and scaling laws truly constant, stable, or universal in character, but vary in value across different taxa and background conditions. Moreover, these equations represent evolutionary, strongly contingent generalizations, which threatens their lawlike status. Lastly, allometries and scaling laws do not offer stable probabilities to which they hold in different backgrounds. I further suggest that many allometries and scaling laws function to elucidate explananda rather than explanantia or covering laws. (shrink)

The authors constructed an algorithm that relates leaf contour to the ratio between the two parts of the leaf using the function θ’=nθm, wherem is the allometric exponent. Using this model, it is possible to simulate the contour of symmetrical or asymmetrical leaves. The authors hypothesize that the portion of the leaf contour that agrees with the simulation is linked to a constraint imposed by the initial asymmetry of the leaf primordium. The final shape of the leaf results more from (...) a summation of cumulative processes through time than from a single process. In the analysis of foliar allometry, it is important to take into consideration the different phases of leaf development, since the nature of the allometric constants may change from one phase to the next, even though their numerical value may remain the same. (shrink)

When an agent can not recognize, immediately, the implausible part of new information received, she will usually first expand her belief state by the new information, and then she may encounter some belief conflicts, and find the implausible information based on her criteria to consolidate her belief state. This process indicates a new kind of non-prioritized multiple revision, called metabolic revision. I give some axiomatic postulates for metabolic revision and propose two functional constructions for it, namely kernel (...) class='Hi'>metabolic revision and partial meet metabolic revision, with respect to which the representation theorems are proved. I also compare metabolic revision with some related works in the literature, including semi-revision, merging with integrity constraints, evaluation, and evaluative multiple revision. (shrink)

The reprogramming of metabolism has been identified as one of the hallmarks of cancer. It is becoming more and more frequent to connect other diseases with metabolic reprogramming. This article aims to argue that metabolic reprogramming is not driven by disease but instead is the main hallmark of metabolism, based on its dynamic behavior that allows it to continuously adapt to changes in the internal and external conditions.

In larger animals a considerable part of the total body mass (e.g. body water, dissolved substances, mineral and organic deposits) does not consume significant amounts of oxygen. These materials can be considered to form a metabolically inert infrastructure which mainly serves three functions: (1) structural support to the organism, (2) storage of nutrients (building material and energy stores) and (3) transport and distribution of these materials. Considering the transport and support function of the metabolically inert structures and their interconnections it (...) is likely that the infrastructure will basically show some tree-like, branching building plan. The weight of the metabolically inert infrastructure of an organism, can be given by bW/(c+W), in which W=body weight, b and c are constants. With increasing size the weight of the metabolic inert infrastructure increases disproportionably. Experimental data concerning basic metabolic rate (M) in relation to body weight (W) better fit the equation M=a W(1-bW)/(c+W), (a=constant) than the conventional power law. (shrink)

Neural activity varies continually from moment to moment. Such temporal variability (TV) has been highlighted as a functionally specific brain property playing a fundamental role in cognition. We sought to investigate the mechanisms involved in TV changes between two basic behavioral states, namely having the eyes open (EO) or eyes closed (EC) in vivo in humans. To these ends we acquired BOLD fMRI, ASL, and [18F]-fluoro-deoxyglucose PET in a group of healthy participants (n = 15), along with BOLD fMRI and (...) [18F]-flumazenil PET in a separate group (n = 19). Focusing on an EO- vs EC-sensitive region in the occipital cortex (identified in an independent sample), we show that TV is constrained in the EO condition compared to EC. This reduction is correlated with an increase in energy consumption and with regional GABAA receptor density. This suggests that the modulation of TV by behavioral state involves an increase in overall neural activity that is related to an increased effect from GABAergic inhibition in addition to any excitatory changes. These findings contribute to our understanding of the mechanisms underlying activity variability in the human brain and its control. (shrink)

Whipple disease is a rare, infectious, disease first described from a single case by Whipple in 1907. As well as characterising the clinical and pathological features of the condition, Whipple made two suggestions regarding its aetiology. These were either than the disease was caused by an infectious agent, or that it was of metabolic origin. As the disease is now thought to be caused by infection with the bacterium Tropheryma whipplei, historical reviews of the history of the disease typically (...) mention only the first of these suggestions. In this paper, we therefore revisit Whipple’s other theory. We argue that a diverse and often successful research programme was developed around this mechanism of disease causation which gave rise to many useful findings on the condition. In the later parts of this article, we then turn to discuss the surprising neglect of this period of Whipple disease research in the current literature, and conclude by offering a brief reconstruction of this early history suitable for use in a technical context. (shrink)

Lymphangiogenesis is an important developmental process that is critical to regulation of fluid homeostasis, immune surveillance and response as well as pathogenesis of a number of diseases, among them cancer, inflammation, and heart failure. Specification, formation, and maturation of lymphatic blood vessels involves an interplay between a series of events orchestrated by various transcription factors that determine expression of key genes involved in lymphangiogenesis. These are traditionally thought to be under control of several key growth factors including vascular growth factor‐C (...) (VEGF‐C) and fibroblast growth factors (FGFs). Recent insights into VEGF and FGF signaling point to their role in control of endothelial metabolic processes such as glycolysis and fatty acid oxidation that, in turn, play a major role in regulation of lymphangiogenesis. These advances have significantly increased our understanding of lymphatic biology and opened new therapeutic vistas. Here we review our current understanding of metabolic controls in the lymphatic vasculature. (shrink)

Despite the ontogenetic allometric size effects that explain much of phyletic variation in brain components, the residuals of some structures indicates that mosaic brain evolution was an important factor in hominid evolution, and that reorganization of the hominid brain may have occurred as early as 3+ MY. Finlay et al.'s allometric technique masks residual variation around allometric trends, and the patterns of residuals relevant to species-specific departures from strict allometric trends.

In the flowering of Red-Green Thought over the past two decades, metabolic rift thinking is surely one of its most colorful varieties. The metabolic rift has captured the imagination of critical environmental scholars, becoming a shorthand for capitalism’s troubled relations in the web of life. This article pursues an entwined critique and reconstruction: of metabolic rift thinking and the possibilities for a post-Cartesian perspective on historical change, the world-ecology conversation. Far from dismissing metabolic rift thinking, my (...) intention is to affirm its dialectical core. At stake is not merely the mode of explanation within environmental sociology. The impasse of metabolic rift thinking is suggestive of wider problems across the environmental social sciences, now confronted by a double challenge. One of course is the widespread—and reasonable—sense of urgency to evolve modes of thought appropriate to an era of deepening biospheric instability. The second is the widely recognized—but inadequately internalized—understanding that humans are part of nature. (shrink)

Metabolic systems are complicated and contain very large numbers of interacting reactions and many internal regulatory mechanisms. This does not prevent the genetic composition of an organism from influencing its behavior, however, nor does it preclude the possibility that some aspects of its behavior may be amenable to simple explanations.

Background: Cognitive impairment is one of the core symptoms of schizophrenia, which is considered to be significantly correlated to prognosis. In recent years, many studies have suggested that metabolic disorders could be related to a higher risk of cognitive defects in a general setting. However, there has been limited evidence on the association between metabolism and cognitive function in patients with early-stage schizophrenia.Methods: In this study, we recruited 172 patients with early-stage schizophrenia. Relevant metabolic parameters were examined and (...) cognitive function was evaluated by using the MATRICS Consensus Cognitive Battery (MCCB) to investigate the relationship between metabolic disorder and cognitive impairment.Results: Generally, the prevalence of cognitive impairment among patients in our study was 84.7% (144/170), which was much higher than that in the general population. Compared with the general Chinese setting, the study population presented a higher proportion of metabolic disturbance. Patients who had metabolic disturbance showed no significant differences on cognitive function compared with the other patients. Correlation analysis showed that metabolic status was significantly correlated with cognitive function as assessed by the cognitive domain scores (p < 0.05), while such association was not found in further multiple regression analysis.Conclusions: Therefore, there may be no association between metabolic disorder and cognitive impairment in patients with early-stage schizophrenia.Trial Registration: Clinicaltrials.gov, NCT02880462. Registered August 26, 2016. (shrink)

The definition of metabolic syndrome has been, and still is, extremely controversial. My purpose is not to give a solution to the associated debate but to argue that the controversy is at least partially due to the different ‘causal content’ of the various definitions: their theoretical validity and practical utility can be evaluated by reconstructing or making explicit the underlying causal structure. I will therefore propose to distinguish the alternative definitions according to the kinds of causal content they carry: (...) definitions grounded on associations, definitions presupposing a causal model built upon statistical associations, and definitions grounded on underlying mechanisms. I suggest that analysing definitions according to their causal content can be helpful in evaluating alternative definitions of some diseases. I want to show how the controversy over MetS suggests a distinction among three kinds of definitions based on how explicitly they characterise the syndrome in causal terms, and on the type of causality involved. I will call ‘type 1 definitions’ those definitions that are purely associative; ‘type 2 definitions’ the definitions based on statistical associations, plus generic medical and causal knowledge; and ‘type 3 definitions’ the definitions based on mechanisms. These kinds of definitions, although different, can be related to each other. A definition with more specific causal content may be useful in the evaluation of definitions characterised by a lower degree of causal specificity. Moreover, the identification of the type of causality involved is of help to constitute a good criterion for choosing among different definitions of a pathological entity. In section I introduce the controversy about MetS, in section I propose some remarks about medical definitions and their ‘causal import’, and in section I suggest that the different attitudes towards the definition of MetS are relevant to evaluate their explicative power. (shrink)

Computational approaches in systems biology have become a powerful tool for understanding the fundamental mechanisms of cellular metabolism and regulation. However, the interplay between the regulatory and the metabolic system is still poorly understood. In particular, there is a need for formal mathematical frameworks that allow analyzing metabolism together with dynamic enzyme resources and regulatory events. Here, we introduce a metabolic-regulatory network model that allows integrating metabolism with transcriptional regulation, macromolecule production and enzyme resources. Using this model, we (...) show that the dynamic interplay between these different cellular processes can be formalized by a hybrid automaton, combining continuous dynamics and discrete control. (shrink)

How micro- and macroevolutionary evolutionary processes produce phenotypic change is without question one of the most intriguing and perplexing issues facing evolutionary biologists. We believe that roadblocks to progress lie A) in the underestimation of the role of the environment, and in particular, that of the interaction of genotypes with environmental factors, and B) in the continuing lack of incorporation of development into the evolutionary synthesis. We propose the integration of genetic, environmental and developmental perspectives on the evolution of the (...) phenotype in the form of the concept of the developmental reaction norm (DRN) The DRN represents the set of multivariate ontogenies that can be produced by a single genotype when it is exposed to environmental variation. It encompasses: 1) the processes that alter the phenotype throughout the ontogenetic trajectory, 2) the recognition that different aspects of the phenotype are (and must be) correlated and 3) the ability of a genotype to produce phenotypes in different environments. This perspective necessitates the explicit study of character expression during development, the evaluation of associations between pairs or groups of characters (e.g., multivariate allometries), and the exploration of reaction norms and phenotypic plasticity. We explicitly extend the concept of the DRN to encompass adjustments made in response to changes in the internal environment as well. Thus, ‘typical’ developmental sequences (e.g., cell fate determination) and plastic responses are simply manifestations of different scales of ‘environmental’ effects along a continuum. We present: (1) a brief conceptual review of three fundamental aspects of the generation and evolution of phenotypes: the changes in the trajectories describing growth and differentiation (ontogeny), the multivariate relationships among characters (allometry), and the effect of the environment (plasticity); (2) a discussion of how these components are merged in the concept of the developmental reaction norm; and (3) a reaction norm perspective of major determinants of phenotypes: epigenesis, selection and constraint. (shrink)

Here, we analyze how the set of nucleotides in the cell is equilibrated and how this generates simple rules that help the cell to organize itself via maintenance of a stable non‐equilibrium state. A major mechanism operating to achieve this state is thermodynamic buffering via high activities of equilibrating enzymes such as adenylate kinase. Under stable non‐equilibrium, the ratios of free and Mg‐bound adenylates, Mg2+ and membrane potentials are interdependent and can be computed. The adenylate status is balanced with the (...) levels of reduced and oxidized pyridine nucleotides through regulated uncoupling of the pyridine nucleotide pool from ATP production in mitochondria, and through oxidation of substrates non‐coupled to NAD+ reduction in peroxisomes. The set of adenylates and pyridine nucleotides constitutes a generalized cell energy status and determines rates of major metabolic fluxes. As the result, fluxes of energy and information become organized spatially and temporally, providing conditions for self‐maintenance of metabolism. (shrink)

Stewart and Korol (“De-Signing Fat,” International Journal of Applied Philosophy 23.2 [2009]) contend that obesity is benign. In support of their position they have focussed on selected papers that do not take into consideration key realities. Their attempt to minimise the impact of obesity appears to centre on how difficult it can be to lose weight by diet alone (and its risks) and problems with measurements of obesity, while failing to acknowledge the specific and well-documented impact of deleterious biochemical alterations (...) arising from central obesity. Stewart and Korol also do not point out the considerable controversy with the fat but fit (metabolically healthy obesity [MHO]) concept. Whether looping from above or below, nothing changes the biochemical realities of central obesity. Above all, Stewart and Korol never once mention the benefits of obesity prevention, rather focussing on the difficulties of losing weight. Thus, respectfully, a word of caution is put forward on the views of Stewart and Korol regarding obesity. (shrink)

Many kinds of multifunctional regulatory proteins have been identified that perform distinct biochemical functions in the nucleus, the cytoplasm, or both. Here we describe the recent discovery by Hall et al. (2004)1 of a new type of multifunctional protein: a metabolic enzyme that doubles as a transcription factor. This enzyme, Arg5,6, functions as a catalytic enzyme in ornithine biosynthesis and also binds and regulates the promoters of nuclear and mitochondrial genes. It may also regulate precursor mRNA metabolism. We discuss (...) how proteins that serve as both metabolic enzymes and transcription factors might have evolved. BioEssays 27:467–471, 2005. © 2005 Wiley Periodicals, Inc. (shrink)

I consider the case of the “simplest” living beings—bacteria—and examine how their embodied activity constitutes an organism/environment interaction, out of which emerges the possibility of learning from an environment. I suggest that this mutual co-emergence of organism and environment implies a panbiotic educational interaction that is at once the condition for, and achievement of, all living beings. Learning and being learned from are entangled in varied ways throughout the biosphere. Education is not an exclusively human project, it is part of (...) the ancient evolutionary process of elaborating and diversifying the relational possibilities inherent in metabolism that has brought forth our diverse and flourishing world.ed from context, “education” appears as a set of ways in which humans actively engage and take responsibility for the learning outcomes of relationships with each other. Insofar as we consider this distinction absolute rather than a performed construct to be assessed by its consequences, we blind ourselves to the educative dimension of other species as well as our many miseducative engagements with them. If learning processes are inherent and constitutive of ecological communities, education theorists should devote their pedagogical sensitivities and insights to the crucial challenge of developing educative sustainable human–nature relations. (shrink)

This article explores the metabolic lives of whey powder, the most popular form of protein supplement in what has become a multibillion-dollar industry during the past two decades. Faced with the slippery and elusive properties latent to this multiplicitous substance, our approach is to follow whey powder from its mid-20th century emergence as a noxious byproduct of industrial dairy production, through the human and animal bodies unevenly tasked with its processing, and out into waterways, where its nitrogen density rematerializes (...) as a pollutant. We show how whey powder emerged as a solution to the environmental damage posed by whey pollution, how such damage is an effect of the systematic overproduction endemic to agrofood industries and how whey’s toxicity persists through processes of metabolism and consumption, despite attempts to process and profit from its vital capacities. Throughout, we argue that whey exemplifies ecological embodiment, understood as the co-constitutive relations between bodily matter and ecological life, and their entanglement with processes of commodification. (shrink)

Heterogeneity in mitochondrial content has been previously suggested as a major contributor to cellular noise, with multiple studies indicating its direct involvement in biomedically important cellular phenomena. A recently published dataset explored the connection between mitochondrial functionality and cell physiology, where a non‐linearity between mitochondrial functionality and cell size was found. Using mathematical models, we suggest that a combination of metabolic scaling and a simple model of cell death may account for these observations. However, our findings also suggest the (...) existence of alternative competing hypotheses, such as a non‐linearity between cell death and cell size. While we find that the proposed non‐linear coupling between mitochondrial functionality and cell size provides a compelling alternative to previous attempts to link mitochondrial heterogeneity and cell physiology, we emphasise the need to account for alternative causal variables, including cell cycle, size, mitochondrial density and death, in future studies of mitochondrial physiology. (shrink)

Metabolic pathways underlying brain function remain largely unexplored during neurodevelopment, predominantly due to the lack of feasible techniques for use with awake infants. Broadband near-infrared spectroscopy provides the opportunity to explore the relationship between cerebral energy metabolism and blood oxygenation/haemodynamics through the measurement of changes in the oxidation state of mitochondrial respiratory chain enzyme cytochrome-c-oxidase alongside haemodynamic changes. We used a bNIRS system to measure ΔoxCCO and haemodynamics during functional activation in a group of 42 typically developing infants aged (...) between 4 and 7 months. bNIRS measurements were made over the right hemisphere over temporal, parietal and central cortical regions, in response to social and non-social visual and auditory stimuli. Both ΔoxCCO and Δ[HbO2] displayed larger activation for the social condition in comparison to the non-social condition. Integration of haemodynamic and metabolic signals revealed networks of stimulus-selective cortical regions that were not apparent from analysis of the individual bNIRS signals. These results provide the first spatially resolved measures of cerebral metabolic activity alongside haemodynamics during functional activation in infants. Measuring synchronised changes in metabolism and haemodynamics have the potential for uncovering the development of cortical specialisation in early infancy. (shrink)

This paper examines three exemplary theories of living organization with respect to their common feature of defining life in terms of metabolic closure: autopoiesis, (M, R) systems, and chemoton theory. Metabolic closure is broadly understood to denote the property of organized chemical systems that each component necessary for the maintenance of the system is produced from within the system itself, except for an input of energy. It is argued that two of the theories considered—autopoiesis and (M, R) systems—participate (...) in a hylomorphist pattern of thinking which separates the “form” of the living system from its “matter.” The analysis and critique of hylomorphism found in the work of the philosopher Gilbert Simondon is then applied to these two theories, and on the basis of this critique it is argued that the chemoton model offers a superior theory of minimal life which overcomes many of the problems associated with the other two. Throughout, the relationship between hylomorphism and the understanding of living things as machines is explored. The paper concludes by considering how hylomorphism as a background ontology for theories of life fundamentally influences the way life is defined. (shrink)

Amsterdam University Press is a leading publisher of academic books, journals and textbooks in the Humanities and Social Sciences. Our aim is to make current research available to scholars, students, innovators, and the general public. AUP stands for scholarly excellence, global presence, and engagement with the international academic community.

Evidence for the association of ‘soluble’ enzymes in vivo is extensive and compelling. These associations occur in all compartments of the cell of both prokaryotes and eukaryotes. Several factors present in vivo promote these associations among enzymes whose association in vitro is often too weak to detect. Several physiological advantages of the associated enzyme complexes can be identified, most (but not all) of which are the consequence of microcompartmentation of metabolites (substrate channeling). Substrate channeling of intermediates by either a ‘direct (...) transfer’ process or ‘proximity effects’ can occur. The latter mechanism does not require the special molecular features needed for the direct transfer mechanism and may, therefore, exist in more general situations in the cell. Criticisms of these views are discussed. We argue that these criticisms have been largely answered by experiment and theory in recent years. Studies on simple systems in vitro, nevertheless, contribute important insights concerning the more complex phenomena in vivo. (shrink)

We consider metabolic networks with reversible enzymatic reactions. The model is written as a system of ordinary differential equations, possibly with inputs and outputs. We prove the global stability of the equilibrium , using techniques of monotone systems and compartmental matrices. We show that the equilibrium does not always exist. Finally, we consider a metabolic system coupled with a genetic network, and we study the dependence of the metabolic equilibrium with respect to concentrations of enzymes. We give (...) some conclusions concerning the dynamical behavior of coupled genetic/metabolic systems. (shrink)

The importance of drug‐metabolizing enzymes in developing mammals has been recently reevaluated in view of the activities and potential inducibilities of these enzymes. The role of endogenous factors raises the question of whether there is a positive regulation of the expression of drug‐metabolizing enzymes by hormones. In humans, among the different isoenzymes of cytochrome P‐450 described in adult liver, only one is absent in 20‐week‐old fetuses. Epoxide hydrolase and glutathione S‐transferases are active while UDP‐glucuronidation develops postnatally. The consequence of this (...) asynchronous rise of activities is briefly discussed. (shrink)

The goal of synthetic biology is to create artificial organisms. To achieve this it is essential to understand what life is. Metabolism-replacement systems, or (M, R)-systems, constitute a theory of life developed by Robert Rosen, characterized in the statement that organisms are closed to efficient causation, which means that they must themselves produce all the catalysts they need. This theory overlaps in part with other current theories, including autopoiesis, the chemoton, and autocatalytic sets, all of them invoking some idea of (...) closure. A simple model of an (M, R)-system has been implemented in the computer, and behaves in ways that may shed light on the requirements for a prebiotic self-organizing system. In addition to a trivial steady state in which nothing happens, it can establish a non-trivial steady state in which all intermediates have finite concentrations, with their rates of degradation balanced by their rates of synthesis. The system can be regenerated from the set of food components plus a single intermediate, and maintain itself in that state indefinitely, despite continuous degradation. At the very low compartment volumes that may have existed in prebiotic conditions, for example in cavities in minerals, or in micelles formed by simple amphiphiles, statistical fluctuations in the numbers of molecules need to be taken into account. With the stochastic approach there is no non-trivial steady state in strict mathematical terms, because the system will always collapse to the trivial state after sufficient time. However, the average time before collapse is so long for volumes greater than $10^{-19}\;{\textsc{l}}$ (much smaller than the volume of the order of $10^{-15}\;{\textsc{l}}$ for a typical bacterial cell) that for practical purposes the self-maintaining state of non-null concentrations becomes significant, recalling the situation of bistability that is observed in deterministic analysis. In turn, there exists a minimum size below which the self-organizing system cannot maintain itself on chemically relevant time scales. The value of the critical volume depends on the particular concentrations and rate constants assumed, but the principle could apply generally. (shrink)

Among all organisms, the size of each body part or organ scales with overall body size, a phenomenon called allometry. The study of shape and form has attracted enormous interest from biologists, but the genetic, developmental and physiological mechanisms that control allometry and the proportional growth of parts have remained elusive. Recent progress in our understanding of body‐size regulation provides a new synthetic framework for thinking about the mechanisms and the evolution of allometric scaling. In particular, insulin/IGF signaling, (...) which plays major roles in longevity, diabetes and the regulation of cell, organ and body size, might also be centrally involved in regulating organismal shape. Here we review recent advances in the fields of growth regulation and endocrinology and use them to construct a developmental model of static allometry expression in insects. This model serves as the foundation for a research program that will result in a deeper understanding of the relationship between growth and form, a question that has fascinated biologists for centuries. BioEssays 29:536–548, 2007. © 2007 Wiley Periodicals, Inc. (shrink)