Tetz’s theory and law of longevity

Here, we present new theory and law of longevity intended to evaluate fundamental factors that control lifespan. This theory is based on the fact that genes affecting host organism longevity are represented by subpopulations: genes of host eukaryotic cells, commensal microbiota, and non-living genetic elements. Based on Tetz’s theory of longevity, we propose that lifespan and aging are defined by the accumulation of alterations over all genes of macroorganism and microbiome and the non-living genetic elements associated with them. Tetz’s law of longevity states that longevity is limited by the accumulation of alterations to the limiting value that is not compatible with life. Based on theory and law, we also propose a novel model to calculate several parameters, including the rate of aging and the remaining lifespan of individuals. We suggest that this theory and model have explanatory and predictive potential to eukaryotic organisms, allowing the influence of diseases, medication, and medical procedures to be re-examined in relation to longevity. Such estimates also provide a framework to evaluate new fundamental aspects that control aging and lifespan.     

Haeckel’s scientific monism as theory of history

Summary Recent research at the Haeckel Haus at the University of Jena goes far to confirm Haeckel’s role as an ideological progenitor of fascist ideology. This is true not only for Germany, but also for the birth of fascist thought in Italy and France. Haeckel’s Monism is the main inspiration for the origin of French and Italian fascism as well as other vital manifestations of modernist culture. In general, the history of science reveals more fully than any other theoretical approach, the roots of fascism as well as avant-garde modernism.     

Do we need a ‘theory’ of development?

Edited by Alessandro Minelli and Thomas Pradeu, Towards a Theory of Development gathers essays by biologists and philosophers, which display a diversity of theoretical perspectives. The discussions not only cover the state of art, but broaden our vision of what development includes and provide pointers for future research. Interestingly, all contributors agree that explanations should not just be gene-centered, and virtually none use design and other engineering metaphors to articulate principles of cellular and organismal organization. I comment in particular on the issue of how to construe the notion of a ‘theory’ and whether developmental biology has or should aspire to have theories, which four of the contributions discuss in detail while taking opposing positions. Beyond construing a theory in terms of its empirical content (established knowledge about biological phenomena), my aim is to shift the focus toward the role that theories have for guiding future scientific theorizing and practice. Such a conception of ‘theory’ is particularly important in the context of development, because arriving at a theoretical framework that provides guidance for the discipline of developmental biology as a whole is more plausible than a unified representation of development across all taxa.     

A quantum probability explanation for violations of ‘rational’ decision theory

Two experimental tasks in psychology, the two-stage gambling game and the Prisoner''s Dilemma game, show that people violate the sure thing principle of decision theory. These paradoxical findings have resisted explanation by classical decision theory for over a decade. A quantum probability model, based on a Hilbert space representation and Schrödinger''s equation, provides a simple and elegant explanation for this behaviour. The quantum model is compared with an equivalent Markov model and it is shown that the latter is unable to account for violations of the sure thing principle. Accordingly, it is argued that quantum probability provides a better framework for modelling human decision-making.     

Ape imagination? A sentimentalist critique of Frans de Waal’s gradualist theory of human morality

This essay draws on Adam Smith’s moral sentimentalism to critique primatologist Frans de Waal’s gradualist theory of human morality. De Waal has spent his career arguing for continuity between primate behavior and human morality, proposing that empathy is a primary moral building block evident in primate behavior. Smith’s moral sentimentalism—with its emphasis on the role of sympathy in moral virtue—provides the philosophical framework for de Waal’s understanding of morality. Smith’s notion of sympathy and the imagination involved in sympathy is qualitatively different from animal sympathy. I argue that Smithian sympathy includes the ability to represent propositional attitudes and take into account multiple perspectives which are then synthesized into a singular impartial perspective. Furthermore, Smithian moral judgment requires the capacity for emotion regulation and moral self-cultivation, or the ability to shape and control one’s reactive attitudes. Taken together, these capacities far outstrip the capacities of animals, disrupting de Waal’s gradualism.     

One hundred years of continental drift: the early Italian reaction to Wegener’s ‘visionary’ theory

One hundred years ago in 1915 ‘Die Entstehung der Kontinente und Ozeane’ by Alfred Wegener was published, destined to become one of the most controversial geological opus in the first half of the twentieth century. Wegener is the first to combine the most diverse geological (sensu lato) evidences in a single great synthesis. Nonetheless, apart from few upholders, the initial reaction to the drift hypothesis was fierce opposition, and the strongest criticism came from geophysics, the same discipline that, paradoxically, starting from the 1950s led to the Plate Tectonics revolution and, ultimately, to a complete re-evaluation of Wegener’s hypothesis. In the present paper we discuss the initial reaction of Italian scientists to the original continental drift theory, with particular focus on the period between the two world wars. Italian geologists like Fossa-Mancini and Gortani were almost favourable to the new theory, while authors such as Vardabasso and Sacco were neutral or even hostile to the new hypothesis, so iconoclastic for the widely accepted fixist vision of the time. In any case, all these scientists agreed that the new theory had great potential for reopening an enthusiastic debate on issues that were given as established paradigms – the genuine way for progress in science.     

On Carl Gegenbaur’s theory on head metamerism and the selection of taxa for comparisons

Summary After the rejection of the idealistic “vertebral theory of the skull,” the basic idea of the theory had been taken up again by the German morphologist Carl Gegenbaur. He proposed a metameric ordering system of the vertebrate head based on a comparative investigation of selachians. This “segmentation theory of the vertebrate head” had a stimulating effect on comparative anatomy. Traces of the basic ideas are still inherent in the biological sciences. Despite the fact that Carl Gegenbaur proposed a rather phylogenetic approach, his systematic investigations remained on a typological level. It is argued herein, that the reason for that was his inability to perform his comparisons independent of a rather intuitive a priori hypothesis about phylogenetic relationships, thus leaving no possibilities for testing homologies. This is exemplified by Carl Gegenbaur’s choice of species for comparative work as well as his use of these species in comparative work. Choosing species for comparisons is discussed.     

Acanthamoeba and mimivirus interactions: the role of amoebal encystment and the expansion of the ‘Cheshire Cat’ theory

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Can the theory of evolution be falsified?

In this paper we discuss the epistemological positions of evolution theories. A sharp distinction is made between the theory that species evolved from common ancestors along specified lines of descent (here called the theory of common descent), and the theories intended as causal explanations of evolution (e.g. Lamarck's and Darwin's theory). The theory of common descent permits a large number of predictions of new results that would be improbable without evolution. For instance, (a) phylogenetic trees have been validated now; (b) the observed order in fossils of new species discovered since Darwin's time could be predicted from the theory of common descent; (c) owing to the theory of common descent, the degrees of similarity and difference in newly discovered properties of more or less related species could be predicted. Such observations can be regarded as attempts to falsify the theory of common descent. We conclude that the theory of common descent is an easily-falsifiable & often-tested & still-not-falsified theory, which is the strongest predicate a theory in an empirical science can obtain. Theories intended as causal explanations of evolution can be falsified essentially, and Lamarck's theory has been falsified actually. Several elements of Darwin's theory have been modified or falsified: new versions of a theory of evolution by natural selection are now the leading scientific theories on evolution. We have argued that the theory of common descent and Darwinism are ordinary, falsifiable scientific theories.     

It’s the song,not the singer: an exploration of holobiosis and evolutionary theory

That holobionts (microbial communities and their animal or plant hosts) are units of selection squares poorly with the observation that microbes are often recruited (horizontally acquired) from the environment, not passed down vertically from parent to offspring, as required for collective reproduction. The taxonomic makeup of a holobiont’s microbial community may vary over its lifetime and differ from that of conspecifics. In contrast, biochemical functions of the microbiota and contributions to host biology are more conserved, with taxonomically variable but functionally similar microbes recurring across generations and hosts. To save what is of interest in holobiont thinking, we propose casting metabolic and developmental interaction patterns, rather than the taxa responsible for them, as units of selection. Such units need not directly reproduce or form parent-offspring lineages: their prior existence has created the conditions under which taxa with the genes necessary to carry out their steps have evolved in large numbers. These taxa or genes will reconstruct the original interaction patterns when favorable conditions occur. Interaction patterns will vary (for instance by the alteration or addition of intermediates) in ways that affect the likelihood of and circumstances under which such reconstruction occurs. Thus, they vary in fitness, and evolution by natural selection will occur at this level. It is on the persistence, reconstruction, and spread of such interaction patterns that students of holobiosis should concentrate, we suggest. This model also addresses other multi-species collectively beneficial interactions, such as biofilms or biogeochemical cycles maintaining all life.     

What remains of the Cholodny-Went theory? Introduction

The Cholodny-Went theory, which states that plant tropisms in roots and shoots are due to the unequal distribution of the growth regulator auxin in reponse to light or gravity, presented a simple and direct explanation of these phenomena. This was significant in the 1930s when simple explanations were lacking, and much research into this theory has been performed since that time. From the 1980s forward, there has been much questioning and controversy surrounding the theory. In this introduction to 15 brief articles, the author describes how leading scientists in the field were asked to air their opinions of the theory and formulate questions for each other. The resulting articles are presented in an attempt to stimulate discussion and give insights into the state of the Cholodny-Went theory in the 1990s.     

The heat dissipation limit theory and evolution of life histories in endotherms--time to dispose of the disposable soma theory?

A major factor influencing life-history strategies of endotherms is body size. Larger endotherms live longer, develop more slowly, breed later and less frequently, and have fewer offspring per attempt at breeding. The classical evolutionary explanation for this pattern is that smaller animals experience greater extrinsic mortality, which favors early reproduction at high intensity. This leads to a short lifespan and early senescence by three suggested mechanisms. First, detrimental late-acting mutations cannot be removed because of the low force of selection upon older animals (mutation accumulation). Second, genes that promote early reproduction will be favored in small animals, even if they have later detrimental effects (antagonistic pleiotropy). Third, small animals may be forced to reduce their investment in longevity assurance mechanisms (LAMs) in favor of investment in reproduction (the disposable soma theory, DST). The DST hinges on three premises: that LAMs exist, that such LAMs are energetically expensive and that the supply of energy is limited. By contrast, the heat dissipation limit (HDL) theory provides a different conceptual perspective on the evolution of life histories in relation to body size. We suggest that rather than being limited, energy supplies in the environment are often unlimited, particularly when animals are breeding, and that animals are instead constrained by their maximum capacity to dissipate body heat, generated as a by-product of their metabolism. Because heat loss is fundamentally a surface-based phenomenon, the low surface-to-volume ratio of larger animals generates significant problems for dissipating the body heat associated with reproductive effort, which then limits their current reproductive investment. We suggest that this is the primary reason why fecundity declines as animal size increases. Because large animals are constrained by their capacity for heat dissipation, they have low reproductive rates. Consequently, only those large animals living in habitats with low extrinsic mortality could survive leading to the familiar patterns of life-history trade-offs and their links to extrinsic mortality rates. The HDL theory provides a novel mechanism underpinning the evolution of life history and ageing in endotherms, and makes a number of testable predictions that directly contrast with the predictions arising from the DST.     

Spatial and temporal relation rule acquisition of eutrophication in Da’ning River based on rough set theory

Since the mechanisms of eutrophication are complicated and many other factors affect these mechanisms, methods such as quantitative statistics and numerical simulation, have their limitations in analyzing the spatiotemporal relations of eutrophication. The rough set theory (RST) was used to describe the spatiotemporal relations of eutrophication in Da’ning River without any of other prior knowledge. Rules of relations in time and space affecting eutrophication in the Da’ning River backwater area were extracted by taking representation of relations in time and space among eutrophication at a long river section of Da’ning River backwater area, by taking nine sets of encrypted monitoring data in 2003 as example, and by making season, area and eutrophication level as the decision attributes, respectively, to represent specific features of the eutrophication phenomenon in the Da’ning River backwater area from the points of view of time, space, and level by analysis of spatiotemporal relationship rules. This study result shows that the temporal and spatial differences between eutrophication phenomena in the long river section of the Da’ning River backwater area are significant. Eutrophication for each section is less serious in autumn, more in spring and most in summer. Eutrophication degree gradually decreases from estuary to upstream, which is in conformity with reality. The RST of eutrophication in Da’ning River may inform environmental decision-makers and assist them in making more cost-effective decisions.     

Garbage catastrophe theory of aging: imperfect removal of oxidative damage?

Increasing evidence suggests an important role of oxidant-induced damage in the progress of senescent changes, providing support for the free radical theory of aging proposed by Harman in 1956. However, considering that biological organisms continuously renew their structures, it is not clear why oxidative damage should accumulate with age. No strong evidence has been provided in favor of the concept of aging as an accumulation of synthetic errors (e.g. Orgel's 'error-catastrophe' theory and the somatic mutation theory). Rather, we believe that the process of aging may derive from imperfect clearance of oxidatively damaged, relatively indigestible material, the accumulation of which further hinders cellular catabolic and anabolic functions. From this perspective, it might be predicted that: (i) suppression of oxidative damage would enhance longevity; (ii) accumulation of incompletely digested material (e.g. lipofuscin pigment) would interfere with cellular functions and increase probability of death; (iii) rejuvenation during reproduction is mainly provided by dilution of undigested material associated with intensive growth of the developing organism; and (iv) age-related damage starts to accumulate substantially when development is complete, and mainly affects postmitotic, cells and extracellular matrix, not proliferating cells. There is abundant support for all these predictions.     

Contributions to the mathematical theory of epidemics—I

(1) A mathematical investigation has been made of the progress of an epidemic in a homogeneous population. It has been assumed that complete immunity is conferred by a single attack, and that an individual is not infective at the moment at which he receives infection. With these reservations the problem has been investigated in its most general aspects, and the following conclusions have been arrived at. (2) In general a threshold density of population is found to exist, which depends upon the infectivity, recovery and death rates peculiar to the epidemic. No epidemic can occur if the population density is below this threshold value. (3) Small increases of the infectivity rate may lead to large epidemics; also, if the population density slightly exceeds its threshold value the effect of an epidemic will be to reduce the density as far below the threshold value as initially it was above it. (4) An epidemic, in general, comes to an end, before the susceptible population has been exhausted. (5) Similar results are indicated for the case in which transmission is through an intermediate host.     

Mechanism of meiotic recombination in eukaryotes—A theory

It is proposed that in meiotic chromosomes single strand breaks of DNA originate either in the delayed regions of replicons or as a result of the excision activity of DNA polymerase during zygotene DNA synthesis. Rejoining of the break points belonging to non-sister chromatids takes place by switching over of the polymerase from one strand of DNA to another non-sister strand of the same polarity and gives rise to recombination intermediates (half-chromatid chiasmata). Strand migration in a recombination intermediate or copying of the same parental strand twice during zygotene as a consequence of a delay in copying the homologous strand would lead to gene conversion. Nicking of the cross strands (parental strands) in any recombination intermediate and subsequent repair leads to recombination for flanking markers. A possible way in which three-strand double crossovers occur and the process of recombination are discussed.     

Is the oxidative stress theory of aging dead?

Currently, the oxidative stress (or free radical) theory of aging is the most popular explanation of how aging occurs at the molecular level. While data from studies in invertebrates (e.g., C. elegans and Drosophila) and rodents show a correlation between increased lifespan and resistance to oxidative stress (and in some cases reduced oxidative damage to macromolecules), direct evidence showing that alterations in oxidative damage/stress play a role in aging are limited to a few studies with transgenic Drosophila that overexpress antioxidant enzymes. Over the past eight years, our laboratory has conducted an exhaustive study on the effect of under- or overexpressing a large number and wide variety of genes coding for antioxidant enzymes. In this review, we present the survival data from these studies together. Because only one (the deletion of the Sod1 gene) of the 18 genetic manipulations we studied had an effect on lifespan, our data calls into serious question the hypothesis that alterations in oxidative damage/stress play a role in the longevity of mice.