The aim of this work is to study complex ecological models exhibiting simple dynamics. We consider large scale systems which can be decomposed into weakly coupled subsystems. Perturbation Theory is used in order to get a reduced set of differential equations governing slow time varying global variables. As examples, we study the influence of the individual behaviour of animals in competition and predator-prey models. The animals are assumed to do many activities all day long such as searching for food of (...) different types. The degree of competition as well as the predation pressure are dependent upon these activities. Preys are more vulnerable when doing some activities during which they are very exposed to predators attacks rather than for others during which they are hidden. We study the effect of a change in the average individual behaviour of the animals on interspecific relationships. Computer simulations of the whole sets of equations are compared to simulations of the reduced sets of equations. (shrink)

We study the influence of the individual behaviour of animals on predator-prey models. Populations of preys and predators are divided into sub-populations corresponding to different activity classes. The animals are assumed to do many activities all day long such as searching for food of different types. The preys are more vulnerable when doing some activities during which they are very exposed to predators attacks rather than for others during which they are hidden. We study activity sequences of the animals and (...) also the effect of a change in the average individual behaviour of the animals on Lotka-Volterra prey-predator interactions. Numerical simulations are realized for the whole sets of equations (governing the subpopulations) and are compared to the simulations of the reduced sets of equation (governing the populations). We look for the validity of the method with respect to a scaling factor which measures the differences between the two time scales associated to the fast-varying variables and to the slow-time varying global variables. It is shown that when the two time scales differ of about two orders of magnitude, the approximation is satisfying. (shrink)

In multicellular organisms, cells are frequently programmed to die. This makes good sense: cells that fail to, or are no longer playing important roles are eliminated. From the cell’s perspective, this also makes sense, since somatic cells in multicellular organisms require the cooperation of clonal relatives. In unicellular organisms, however, programmed cell death poses a difficult and unresolved evolutionary problem. The empirical evidence for PCD in diverse microbial taxa has spurred debates about what precisely PCD means in the case of (...) unicellular organisms. In this article, we survey the concepts of PCD in the literature and the selective pressures associated with its evolution. We show that definitions of PCD have been almost entirely mechanistic and fail to separate questions concerning what PCD fundamentally is from questions about the kinds of mechanisms that realize PCD. We conclude that an evolutionary definition is best able to distinguish PCD from closely related phenomena. Specifically, we define “true” PCD as an adaptation for death triggered by abiotic or biotic environmental stresses. True PCD is thus not only an evolutionary product but must also have been a target of selection. Apparent PCD resulting from pleiotropy, genetic drift, or trade-offs is not true PCD. We call this “ersatz PCD.”. (shrink)

Organismal death is foundational to the evolution of life, and many biological concepts such as natural selection and life history strategy are so fashioned only because individuals are mortal. Organisms, irrespective of their organization, are composed of basic functional units—cells—and it is our understanding of cell death that lies at the heart of most general explanatory frameworks for organismal mortality. Cell death can be exogenous, arising from transmissible diseases, predation, or other misfortunes, but there are also endogenous forms of death (...) that are sometimes the result of adaptive evolution. These endogenous forms of death—often labeled programmed cell death, PCD—originated in the earliest cells and are maintained across the tree of life. Here, we consider two problematic issues related to PCD (and cell mortality generally). First, we trace the original discoveries of cell death from the nineteenth century and place current conceptions of PCD in their historical context. Revisions of our understanding of PCD demand a reassessment of its origin. Our second aim is thus to structure the proposed origin explanations of PCD into coherent arguments. In our analysis we argue for the evolutionary concept of PCD and the viral defense-immunity hypothesis for the origin of PCD. We suggest that this framework offers a plausible account of PCD early in the history of life, and also provides an epistemic basis for the future development of a general evolutionary account of mortality. (shrink)

The present study investigated whether individual differences between psychologists in thinking styles are associated with accuracy in diagnostic classification. We asked novice and experienced clinicians to classify two clinical cases of clients with two co-occurring psychological disorders. No significant difference in diagnostic accuracy was found between the two groups, but when combining the data from novices and experienced psychologists accuracy was found to be negatively associated with certain decision making strategies and with a higher self-assessed ability and preference for a (...) rational thinking style. Our results underscore the idea that it might be fruitful to look for explanations of differences in the accuracy of diagnostic judgments in individual differences between psychologists (such as in thinking styles or decision making strategies used), rather than in experience level. (shrink)

Limitations of antiarrhythmic drugs on cardiac sudden death prevention appeared since the early 80's. The "Cardiac Arrhythmia Suppression Trial"(CAST) showed more recently that mortality was significantly higher inpatients treated with some particular antiarrhythmic drugs than in non-treated patients. In this field, our group recently demonstrated that a bolus of a Class 1B antiarrhythmic drug was able to trigger a ventricular fibrillation due to transient blocks induction. The aim of the present work was to systematically study, by use of the van (...) Capelle and Durrer (VCD) model which allows to simulate ventricular activation wave propagation, the link between arrhythmogenic effects and the ability of transient blocks to possibly degenerate in severe arrhythmias. A fragment of the ventricular wall is represented by an array of 16384elements electrically coupled. Effects of induction of one or several transient blocks, as the effects of their size and duration on possible induction of reentries have been studied. Results obtained show that various combinations between these different parameters may trigger reentries, ventricular tachycardia and/or more complex patterns assimilable to ventricular fibrillation. These results clearly evidence the fact that possible induction of transient blocks may directly be related to risk factor associated to arrhythmogenic effects of antiarrhythmic drugs. (shrink)

The present work is aimed at investigating the effects of myocardial infarction and ischemia on induction of ventricular fibrillation. Electrophysiologic effects of global and local ischemia (variation of the dispersion of refractory periods as well as conduction velocity) on initiation of reentry mechanisms was studied by means of computer simulations based on a cellular automata model of propagation of activation wave through a ventricular surface element. A local area of ischemia where effects of the dispersion of refractory periods are investigated (...) is then simulated. This is made using a Gaussian distribution characterized by its mean and standard deviation. These simulations show that ischemia is capable of initiating reentry phenomena which propagate through the whole ventricle; they are responsible for ventricular fibrillation which causes sudden cardiac death, even when ischemia only involves limited parts of the myocardium. Statistical study of the probability of reentries as a function of both of the size of ischemic zones and the rate of dispersion of refractory periods shows that the latter parameter is of primary importance in triggering cardiac reentries. (shrink)

Programmed cell death (PCD) in unicellular organisms is in some instances an altruistic trait. When the beneficiaries are clones or close kin, kin selection theory may be used to explain the evolution of the trait, and when the trait evolves in groups of distantly related individuals, group or multilevel selection theory is invoked. In mixed microbial communities, the benefits are also available to unrelated taxa. But the evolutionary ecology of PCD in communities is poorly understood. Few hypotheses have been offered (...) concerning the community role of PCD despite its far-reaching effects. The hypothesis we consider here is that PCD is a black queen. The Black Queen Hypothesis (BQH) outlines how public goods arising from a leaky function are exploited by other taxa in the community. Black Queen (BQ) traits are essential for community survival, but only some members bear the cost of possessing them, while others lose the trait In addition, BQ traits have been defined in terms of adaptive gene loss, and it is unknown whether this has occurred for PCD. Our conclusion is that PCD fulfils the two most important criteria of a BQ (leakiness and costliness), but that more empirical data are needed for assessing the remaining two criteria. In addition, we hold that for viewing PCD as a BQ, the original BQH needs to include social traits. Thus, despite some empirical and conceptual shortcomings, the BQH provides a helpful avenue for investigating PCD in microbial communities. (shrink)

We study the case of two sibling species ofHippolais(Aves). Very little differences can be observed in the morphology of both species. The breeding area of these species are complementary. Roughly, one species breeds North and East of Europe (Hippolais icterina) while the other breeds South and West of Europe (Hippolais polyglotta). There exitst a narrow zone of sympatry passing through Burgundy. Since several years, it has been observed that this area of sympatry was moving in the North-East direction at a (...) European scale. This means that progressivelyH. icterina is declining and is replaced byH. polyglotta. Some assumptions can be made in order to explain this evolution, for instance competition or predation. Series of observations concerning the diets of nestlings of both species have been realized. These observations show some differences in the diet compositions. The breeding success of the two species has been studied. Numerical simulations of a competition model taking into account the observed differences between the food types eaten by the two species are presented. These simulations do not explain the regression ofH. icterina. Then, we present numerical simulations of a predation model with one predator attacking the nestlings of both species. These simulations show that with time one of the two preys must extinct. Predation rather than competition seems to be the right explanation. (shrink)

Diauxie is at the origin of research that led Jacques Monod, François Jacob, and André Lwoff to win the Nobel Prize in Physiology or Medicine in 1965 for their description of the first genetic regulatory model. Diauxie is a term coined by Jacques Monod in 1941 in his doctoral dissertation that refers to microbial growth in two phases. In this article, we first examine Monod’s thesis to demonstrate how and why Monod interpreted diauxie as a phenomenon of enzyme inhibition or (...) suppression of adaptive enzymes. We also briefly investigate prior enzyme suppression studies, before Monod’s work, which indicate that he is the first person to observe diauxic growth. Second, we analyse Monod’s post-thesis publications throughout his scientific career, revealing that diauxic inhibition was a significant part of Monod’s scientific activities and greatly fascinated Monod until the end of his life. Paradoxically, Monod’s work and interest on diauxic inhibition are still neglected in historical recounts, focused mostly on Monod’s enzymatic adaptation studies. Indeed, we uncovered a statement by Monod’s colleague, Lwoff, who transformed a quotation from Monod by replacing the word phenomenon with enzymatic adaptation, which we believe has influenced historians. Finally, we offer hypotheses to explain why Lwoff altered Monod’s statement. (shrink)

The small ubiquitin‐like modifier SUMO regulates many aspects of cellular physiology to maintain cell homeostasis, both under normal conditions and during cell stress. Components of the transcriptional apparatus and chromatin are among the most prominent SUMO substrates. The prevailing view is that SUMO serves to repress transcription. However, as we will discuss in this review, this model needs to be refined, because recent studies have revealed that SUMO can also have profound positive effects on transcription.

Why would a philosopher choose to convey his ideas in the form of Manga? This discussion between Masahiro Morioka, author of Manga Introduction to Philosophy, and the translator of its French edition, Pierre Bonneels, shows how philosopher and artist Morioka became acquainted, through images, with fundamental abstract notions. After a short historical analysis of the aesthetic advantages of Manga, consideration is given to this unique way of provoking thought. On this basis, theoretical aspects of “time” and the “I” proposed (...) by Ōmori Shōzō are compared with Morioka’s Manga presentation. Although the questions raised are universal, the authors note that the use of Japanese metaphors enables these two thinkers to draw on a concrete understanding of notions like temporality and identity. (shrink)

Are conspiracy theory beliefs pathological? That depends on what is meant by "pathological." This paper begins by unpacking that ill-defined and value-laden term before making the case that widespread conspiracy theory belief should not be conceptualized through the “othering’ perspective of individual psychopathology. In doing so, it adopts a phenomenological perspective to argue that conspiracy theory beliefs can be reliably distinguished from paranoid delusions based on falsity, belief conviction, idiosyncrasy, and self-referentiality. A socio-epistemic model is then presented that characterizes the (...) broader phenomenon of conspiracy theory belief as a product of a sick society plagued by epistemic mistrust and vulnerability to misinformation that is ubiquitous in today’s post-truth world. Finally, it is proposed that for individuals, the harmfulness of conspiracy theory belief is less related to belief content as it is to belief conviction and degree of self-relevant consequentiality. Staging conspiracy theory belief in terms of ideological commitment offers a conceptual framework to estimate behavioral risks and test hypotheses about the effectiveness of interventions along a continuum of belief conviction and associated socio-epistemic dynamics. Interventions should target not only individuals, but the dysfunctional social conditions that give rise to the pervasive and enduring phenomenon of conspiracy theory belief. (shrink)

The author describes and sociocognitive skills that he argues as being necessary for tool use. We propose that those skills could be based on simpler detection systems humans could share with other animal tool users. More specifically, we discuss the impact of object affordances on the understanding and the social learning of tool use.

The proceedings of the first major international conference on the philosophy of Spinoza to be held in the United States are published here.

The emerging field of neuroeducation, concerned with the interaction between mind, brain and education, has proved revolutionary in educational research, introducing concepts, methods, and technologies into many advanced institutions around the world. The Educated Brain presents a broad overview of the major topics in this new discipline: Part I examines the historical and epistemological issues related to the mind/brain problem and the scope of neuroeducation; Part II provides a view of basic brain research in education and use of imaging techniques, (...) and the study of brain and cognitive development; and Part III is dedicated to the neural foundations of language and reading in different cultures, and the acquisition of basic mathematical concepts. With contributions from leading researchers in the field, this book features the most recent and advanced research in cognitive neurosciences. (shrink)

For every uncountable regular cardinalκ and any cardinalλ≧κ,P κ λ denotes the set $\left\{ {x \subseteqq \lambda :\left| x \right|< \kappa } \right\}$ . Furthermore, < denotes the binary operation defined inP κ λ byx (...) + denotes the setP κ λ−I, andI * the filter dual toI.An idealI overP κ λ is said to benormal iff every functionf:P κ λ→λ with the property that {x∈P κ λ:f(x)∈x}∈I + is constant on a set inI +.I is said to bestrongly normal iff every functionf:P κ λ→P κ λ with the property that {x∈P κ λ:x∩xκ≠Ø∧f(x)shrink)

The mammalian pineal gland contains two types of N‐acetyltransferases which act on aromatic amines. One type preferentially acetylates arylamines such as phenetidine and aniline, whereas the other preferentially acetylates arylalkylamines such as tryptamine and phenylethylamine. The two enzymes can be distinguished by (1) molecular size, (2) regulation, and (3) inactivation characteristics. Arylalkylamine N‐acetyltransferase is involved in the regulation of melatonin synthesis in the pineal gland. A specific function of pineal arylamine N‐acetyltransferase has not been established; it may function as a (...) nonspecific detoxification mechanism. (shrink)