The paper aims to explore what it means for something to be a social cycle, for a theory to be a social cycle theory, and to offer a suggestion for a simple, yet, we believe, fundamentally grounded schema for categorizing them. We show that a broad range of cycle theories can be described within the concept of disruption and adjustments. Further, many important cycle theories are true endogenous social cycle theories in which the theory provides a reason why the cycle (...) should recur. We find that many social cycle theories fit with a two-population disruption and adjustment model similar to the well-known predator-prey model. This implies that a general modeling framework could be established for creating agent-based models of many social cycle theories. (shrink)

Alternative splicing allows for the production of many gene products from a single coding sequence. I introduce the concept of alternative splicing via some examples. I then discuss some current hypotheses about the explanatory role of alternative splicing, including the claim that splicing is a significant contributor to the difference in complexity between the human genome and proteosome. Hypotheses such as these bring into question our working concepts of the gene. I examine several gene concepts (...) introduced to cope with processes such as alternative splicing. Next I introduce some hypotheses about the evolution of mechanisms alternative splicing in higher organisms. I conclude that attention to alternative splicing reveals that we adopt an attitude that developmental theorizing must inform evolutionary theorizing and vice versa. (shrink)

Book Review: What Genes Can’t Do By Lenny Moss .

Cooperation is rife in the microbial world, yet our best current theories of the evolution of cooperation were developed with multicellular animals in mind. Hamilton’s theory of inclusive fitness is an important case in point: applying the theory in a microbial setting is far from straightforward, as social evolution in microbes has a number of distinctive features that the theory was never intended to capture. In this article, I focus on the conceptual challenges posed by the project of extending Hamilton’s (...) theory to accommodate the effects of gene mobility. I begin by outlining the basics of the theory of inclusive fitness, emphasizing the role that the concept of relatedness is intended to play. I then provide a brief history of this concept, showing how, over the past fifty years, it has departed from the intuitive notion of genealogical kinship to encompass a range of generalized measures of genetic similarity. I proceed to argue that gene mobility forces a further revision of the concept. The reason in short is that, when the genes implicated in producing social behaviour are mobile, we cannot talk of an organism’s genotype simpliciter; we can talk only of an organism’s genotype at a particular stage in its life cycle. We must therefore ask: with respect to which stage(s) in the life cycle should relatedness be evaluated? For instance: is it genetic similarity at the time of social interaction that matters to the evolution of social behaviour, or is it genetic similarity at the time of reproduction? I argue that, strictly speaking, it is neither of these: what really matters to the evolution of social behaviour is diachronic genetic similarity between the producers of fitness benefits at the time they produce them and the recipients of those benefits at the end of their life-cycle. I close by discussing the implications of this result. The main payoff is that it makes room for a possible new mechanism for the evolution of altruism in microbes that does not require correlated interaction among bearers of the genes for altruism. The importance of this mechanism in nature remains an open empirical question. (shrink)

In this paper, we provide an overview of our ongoing project in the Genetics and Human Agency Initiative sponsored by the John Templeton Foundation. Our project focuses on the ways that lay beliefs about the heritability of virtue influence reasoning about the nature of virtue, parenting behaviors, and the development of virtue in children. First, we provide philosophical perspectives on the nature of virtue and suggest that viewing virtue as a malleable skill may have important advantages. Next, we review theory (...) and research that highlights the ways that lay heritability beliefs potentially undermine conceptualizations of virtue as a malleable skill. Finally, we discuss how lay heritability beliefs might ultimately affect parent–child interactions and child virtue development. The paper thus provides a brief description our project’s theoretical foundation and a general look at the empirical questions it will tackle. (shrink)

Personalized genomics companies (PG; also called ‘direct-to-consumer genetics’) are businesses marketing genetic testing to consumers over the Internet. While much has been written about these new businesses, little attention has been given to their roles in science communication. This paper provides an analysis of the gene concept presented to customers and the relation between the information given and the science behind PG. Two quite different gene concepts are present in company rhetoric, but only one features in the (...) science. To explain this, we must appreciate the delicate tension between PG, academic science, public expectation, and market forces. (shrink)

A far-reaching and influential view in evolutionary biology claims that species are cohesive units held together by gene flow. Biologists have recognized empirical problems facing this view; after sharpening the expression of the view, we present novel conceptual problems for it. At the heart of these problems is a distinction between two importantly different concepts of cohesion, what we call integrative and response cohesion. Acknowledging the distinction problematizes both the explanandum of species cohesion and the explanans of (...) class='Hi'>gene flow that are central to the view we discuss. We conclude by tracing four broader implications for the study and conceptualization of species. (shrink)

We attempt to improve the understanding of the notion of agene being `for a phenotypic trait or traits. Considering theimplicit functional ascription of one thing being `for another,we submit a more restrictive version of `gene for talk.Accordingly, genes are only to be thought of as being forphenotypic traits when good evidence is available that thepresence or prevalence of the gene in a population is the resultof natural selection on that particular trait, and that theassociation between that trait and (...) the gene in question isdemonstrably causal. It is therefore necessary to gatherstatistical, biochemical, historical, as well as ecologicalinformation before properly claiming that a gene is for aphenotypic trait. Instead of hampering practical use of the `genefor talk, our approach aims at stimulating much needed researchinto the functional ecology and comparative evolutionary biologyof gene action. (shrink)

The gene's-eye view of evolution is an influential but contentious perspective on biology. It emerged in the aftermath of the Modern Synthesis and both proponents and detractors have stressed the link between the two. In particular, both the Modern Synthesis and the gene's-eye view have been criticized for overemphasizing the role genes at the expense of organisms in evolutionary explanations. In this chapter, I discuss the connection between the Modern Synthesis and the gene’s-eye view and evaluate the (...) status of genes and organisms in contemporary biology. I show that while the gene’s-eye view traces its origin back to the Modern Synthesis, it can most accurately be said to represent a specific – adaptationist and gene-centric – version of it. To assess the role of genes and organisms, I examine the intimate relationship between the gene’s-eye view and another post-Synthesis development, the concept of inclusive fitness. I argue that the popularity and influence of inclusive fitness theory demonstrate that the individual organism remains safe at the heart of modern evolutionary biology. (shrink)

Many arguments have been made against gene editing. This paper addresses the commonly invoked argument that gene editing violates human dignity and is ultimately a subversion of human nature. There are several drawbacks to this argument. Above all, the concept of what human dignity means is unclear. It is not possible to condemn a practice that violates human dignity if we do not know exactly what is being violated. The argument’s entire reasoning is thus undermined. Analyses of the (...) arguments involved in this discussion have often led to the conclusion that gene editing contravenes the principle of genetic identity (genetic immutability) thereby subverting a requisite of human dignity and ultimately threatening human nature. This paper refutes these arguments and shows that any opposition to gene editing cannot rely on the human dignity argument. (shrink)

I want to exhibit the deeper metaphysical reasons why some common ways of describing the causal role of genes in development and evolution are problematic. Specifically, I show why using the concept of information in an intentional sense in genetics is inappropriate, even given a naturalistic account of intentionality. Furthermore, I argue that descriptions that use notions such as programming, directing or orchestrating are problematic not for empirical reasons, but because they are not strictly causal. They are intentional. By contrast, (...) other notions that are part of the received view in genetics and evolutionary theory are defensible if understood correctly, in particular the idea that genes are the main replicators in evolution. The paper concludes that dropping all intentional or intentionally laden concepts does not force us to accept the so-called causal parity thesis, at least not in its stronger form. (shrink)

The unit of selection is the concept of that ‘something’ to which biologists refer when they speak of an adaptation as being ‘for the good of’ something. Darwin identified the organism as the unit of selection because for him the ‘struggle for existence’ was an issue among individuals. Later on it was suggested that, in order to understand the evolution of social behavior, it is necessary to argue that groups, and not individuals, are the units of selection. The last addition (...) to this debate was the formulation by Dawkins, in 1976, that the genes themselves are the units of selection while the organisms are merely the temporary receptacles and vehicles for such genes. Thus, the preposterous dissolution of the organism into genes and the proteins coded by such genes has been introduced in the evolutionary discourse by neglecting that the explanations for biological phenomena can be either synchronic or diachronic, depending on the phenomenon to be explained. Therefore explanations in molecular biology are synchronic while evolutionary biology needs diachronic explanations. Nevertheless, for ultra-Darwinians such as Dawkins, efficient replication is all that biology is about. Here I develop an argument in order to show that there is nothing in molecular and cell biology that might support such a contention and that the idea of the gene as the unit of selection is incompatible with the evident evolution of biological complexity. (shrink)

One of the defining features of the classical gene was its position. In molecular genetics, positions are defined instead as nucleotide numbers and there is no clear correspondence with its classical counterpart. However, the classical gene position did not simply disappear with the development of the molecular approach, but survived in the lab associated to different genetic practices. The survival of classical gene position would illustrate Waters’ view about the practical persistence of the genetic approach beyond reductionism (...) and anti-reductionist claims. We show instead that at the level of laboratory practices there are also reductive processes, operating through the rise and fall of different techniques. Molecular markers made the concept of classical gene position practically dispensable, leading us to rethink whether it had any causal role or was just a mere heuristic. (shrink)

Mosquito-borne diseases represent a significant global disease burden, and recent outbreaks of such diseases have led to calls to reduce mosquito populations. Furthermore, advances in ‘gene-drive’ technology have raised the prospect of eradicating certain species of mosquito via genetic modification. This technology has attracted a great deal of media attention, and the idea of using gene-drive technology to eradicate mosquitoes has been met with criticism in the public domain. In this paper, I shall dispel two moral objections that (...) have been raised in the public domain against the use of gene-drive technologies to eradicate mosquitoes. The first objection invokes the concept of the ‘sanctity of life’ in order to claim that we should not drive an animal to extinction. In response, I follow Peter Singer in raising doubts about general appeals to the sanctity of life, and argue that neither individual mosquitoes nor mosquitoes species considered holistically are appropriately described as bearing a significant degree of moral status. The second objection claims that seeking to eradicate mosquitoes amounts to displaying unacceptable degrees of hubris. Although I argue that this objection also fails, I conclude by claiming that it raises the important point that we need to acquire more empirical data about, inter alia, the likely effects of mosquito eradication on the ecosystem, and the likelihood of gene-drive technology successfully eradicating the intended mosquito species, in order to adequately inform our moral analysis of gene-drive technologies in this context. (shrink)

Never was dogmatic reductionism helpful in conceiving the phenomenon of life. The post-genomic era has made it clear that genes alone cannot explain the functioning of whole organisms. Already each cell represents a unique, non-recurring individual. Recent progress in developmental biology has conveyed new perspectives both on the makings of individual organisms (ontogeny), as on evolutionary change (Evo-Devo). The genome (the entirety of all genes) of an animal remains constant from fertilization onwards in each cell. The realization of genes requires (...) molecular environments, in particular pertinent to the cytoplasm of the unfertilized egg. Individuality of an organism therefore is not only determined by its genome, but is shaped through developmental processes (it needs time!). Organisms can only exist through mutual interplays with their respective (molecular and cellular) environments at all levels of organization. Thus, life can be conceived of as endless networks of communication, e.g. as a mutual continuum, connecting all individuals, all species and all generations within their given environments. Evolutionarily, nature does not select fitting genes, but rather viable traits. The presented concepts render it unlikely that it was genes that founded our living world, but rather that distinct environments shaped “genes” (of whatever chemical nature) which proved to be “life-suitable”. (shrink)

This chapter addresses a general question: What is responsible risking? It explores the notion of "responsible risking" as a thick moral concept, and it argues that the notion can be given moral content that could be action-guiding and add an important tool to our moral toolbox. To impose risks responsibly, on this view, is to take on responsibility in a good way. A core part of responsible risking, this chapter argues, is some version of a Forethought Condition. Such a condition (...) requires us to not make decisions or plans such that we could not deliver on our responsibility obligations. This chapter argues that three moral obligations can be derived from descriptive notions of responsibility. They are (1) the control condition, (2) the responsibility to fix condition, and (3) the responsibility to explain condition. The idea is that in order to impose risks responsibly we ought not act in ways that undermine our ability to remain in control over the risks, undermine our ability to sort out negative outcomes by reparations or compensation, or undermine our prospects of providing an explanation for our actions that also makes sense in hindsight and to those affected. This idea is then tried out on the case of germline gene editing. It is argued that such a moral notion of responsibility is also action-guiding when we do not know for certain what is the morally right or obligatory action all-things-considered due to epistemic gaps. (shrink)

I argue that four of the fundamental claims of those calling themselves `genic pluralists'Philip Kitcher, Kim Sterelny, and Ken Watersare defective. First, they claim that once genic selectionism is recognized, the units of selection problems will be dissolved. Second, Sterelny and Kitcher claim that there are no targets of selection. Third, Sterelny, Kitcher, and Waters claim that they have a concept of genic causation that allows them to give independent genic causal accounts of all selection processes. I argue that each (...) one of these claims is either false or misleading. Moreover, the challenge that arises from the availability of genic causal accounts, namely, the inability to choose on rational grounds among genic and higher-level accounts, is unsupported. (shrink)

This paper examines the claims that moral objections to the patenting of human genes are misplaced and rest on confusions about what a patent is, or what is patented by a human gene patent. It shows that theese objections rest on too simple a conception of property rights, and the connections betwteen familiar moral objections to private property and moral objections to the patenting of human genes. Above all, the paper claims, objections to HGPs often reflect worries about the (...) lack of democratic oversight, accountability and participation involved in grants of intellectual property. The paper claims that we should take these worries seriously, whether or not we think HGPs immoral. (shrink)

According to neo-Aristotelian ethical naturalism, moral goodness is an instance of natural goodness, a kind of normativity supposedly already present in nature in the biological realm of non-human living things. Proponents of this view appeal to Michael Thompson’s conception of a life-form--the form of a living organism--to give an account of natural goodness. However, although neo-Aristotelians call themselves naturalists, they hardly ever consult the science of biology to defend their commitments regarding biological organisms. This has led many critics to argue (...) that the neo-Aristotelian account of natural normativity is out of touch with the findings of modern evolutionary biology. One line of response to this objection, presented by John Hacker-Wright and Micah Lott, claims that the neo-Aristotelian concept of a living organism has to be presupposed in evolutionary biology as long as organisms are the subjects of evolutionary explanation. In this paper, I examine this response by tracing the concept of organism in modern evolutionary biology. I first argue that the Modern Synthesis theory of evolution, which understands evolution as change in gene frequencies within a population, does not presuppose the relevant concept of organism. I then explore an alternative view of evolution that has emerged in the past twenty years from advances in evolutionary developmental biology. I argue that this so called ‘evo-devo’ approach makes room for an explanatory concept of organism that can be reconciled with the neo-Aristotelian view. Moreover, I argue that although the explanatory role of the concept of organism in evolutionary biology is still contentious, the well-established role of this concept in developmental biology can be used to defend the biological commitments of neo-Aristotelian naturalism. (shrink)

In a now classic paper published in 1991, Alberch introduced the concept of genotype–phenotype (G!P) mapping to provide a framework for a more sophisticated discussion of the integration between genetics and developmental biology that was then available. The advent of evo-devo first and of the genomic era later would seem to have superseded talk of transitions in phenotypic space and the like, central to Alberch’s approach. On the contrary, this paper shows that recent empirical and theoretical advances have only sharpened (...) the need for a different conceptual treat- ment of how phenotypes are produced. Old-fashioned metaphors like genetic blueprint and genetic programme are not only woefully inadequate but positively misleading about the nature of G!P, and are being replaced by an algorithmic approach emerging from the study of a variety of actual G!P maps. These include RNA folding, protein function and the study of evolvable soft- ware. Some generalities are emerging from these disparate fields of analysis, and I suggest that the concept of ‘developmental encoding’ (as opposed to the classical one of genetic encoding) provides a promising computational–theoretical underpinning to coherently integrate ideas on evolvability, modularity and robustness and foster a fruitful framing of the G!P mapping problem. (shrink)

How the universe came to be what it is now is a key philosophical question. The hypothesis that it came from nothing or śūnya (as proposed by Stephen Hawking, among others) proves to be dissembling, since the quantum vacuum can hardly be considered a void (śūnya). In modern science, it is generally assumed that matter existed before the universe came to be. Modern science hypothesizes that the manifestation of life on earth is nothing but a mere increment in the complexity (...) of matter – and hence is an outcome of evolution of matter (chemical evolution) following the Big Bang. After the manifestation of life, modern science believed that chemical evolution transformed itself into biological evolution, which then had caused the entire biodiversity on our planet. In the framework of materialism, the major attention is to find general organizational laws stimulated by physical sciences, ignoring the uniqueness of life. The main goal of materialism is to reduce consciousness to natural processes, which in turn can be translated into the language of math, physics, and chemistry. Following this approach, scientists have made several attempts to deny the living organism of its veracity as an immortal soul, in favor of genes, molecules, atoms, and so on. However, advancement in various fields of biology has repeatedly given rise to questions against such a denial and has supplied more and more evidence against the completely misleading ideological imposition that living entities are particular states of matter. In the recent past, however, the realization has arisen that cognitive nature of life at all levels has begun presenting significant challenges to the views of materialism in biology and has created a more receptive environment for the soul hypothesis (Shanta BN. Commun Integr Biol 8(5):e1085138, 2015). Therefore, instead of adjudicating different aprioristic claims, the development of an authentic theory of origin of life and universe needs both proper scientific knowledge and the appropriate tools of philosophical analysis of life. This talk will highlight the uniqueness of biological systems that offers a considerable challenge to the mainstream materialism and proposes the Vedāntic philosophical view as a viable alternative for development of a theory worthy of origin of life and universe. (shrink)

Increasingly, in data-intensive areas of the life sciences, experimental results are being described in algorithmically useful ways with the help of ontologies. Such ontologies are authored and maintained by scientists to support the retrieval, integration and analysis of their data. The proposition to be defended here is that ontologies of this type – the Gene Ontology (GO) being the most conspicuous example – are a part of science. Initial evidence for the truth of this proposition (which some will find (...) self-evident) is the increasing recognition of the importance of empirically-based methods of evaluation to the ontology development work being undertaken in support of scientific research. The ontologies created by scientists must, of course, be associated with implementations satisfying the requirements of software engineering. But these ontologies are not themselves engineering artifacts, and to conceive them as such brings grievous consequences. Rather, we shall argue, ontologies such as the GO are comparable to scientific theories, to scientific databases, or to scientific journal publications. Such a view implies a radically new conception of what is involved in the authoring, maintenance and application of ontologies in scientific contexts, and therewith also a radically new approach to the evaluation of ontologies and to the training of ontologists. (shrink)

This paper examines causal theories of reference with respect to how plausible an account they give of non-physical natural kind terms such as ‘gene’ as well as of the truth of the associated theoretical claims. I first show that reference fixism for ‘gene’ fails. By this, I mean the claim that the reference of ‘gene’ was stable over longer historical periods, for example, since the classical period of transmission genetics. Second, I show that the theory of partial (...) reference does not do justice to some widely held realist intuitions about classical genetics. This result is at loggerheads with the explicit goals usually associated with partial theories of reference, which is to defend a realist semantics for scientific terms. Thirdly, I show that, contrary to received wisdom and perhaps contrary to physics and chemistry, neither reference fixism nor partial reference are necessary in order to hold on to scientific realism about biology. I pinpoint the reasons for this in the nature of biological kinds, which do not even remotely resemble natural kinds (i.e., Lockean real essences) as traditionally conceived. (shrink)

Terms loaded with informational connotations are often employed to refer to genes and their dynamics. Indeed, genes are usually perceived by biologists as basically ‘the carriers of hereditary information.’ Nevertheless, a number of researchers consider such talk as inadequate and ‘just metaphorical,’ thus expressing a skepticism about the use of the term ‘information’ and its derivatives in biology as a natural science. First, because the meaning of that term in biology is not as precise as it is, for instance, in (...) the mathematical theory of communication. Second, because it seems to refer to a purported semantic property of genes without theoretically clarifying if any genuinely intrinsic semantics is involved. Biosemiotics, a field that attempts to analyze biological systems as semiotic systems, makes it possible to advance in the understanding of the concept of information in biology. From the perspective of Peircean biosemiotics, we develop here an account of genes as signs, including a detailed analysis of two fundamental processes in the genetic information system (transcription and protein synthesis) that have not been made so far in this field of research. Furthermore, we propose here an account of information based on Peircean semiotics and apply it to our analysis of transcription and protein synthesis. (shrink)

The recent literature on causality has seen the introduction of several distinctions within causality, which are thought to be important for understanding the widespread scientific practice of focusing causal explanations on a subset of the factors that are causally relevant for a phenomenon. Concepts used to draw such distinctions include, among others, stability, specificity, proportionality, or actual-difference making. In this contribution, I propose a new distinction that picks out an explanatorily salient class of causes in biological systems. Some select (...) causes in complex biological systems, I argue, have the property of enabling coherent causal control of these systems. Examples of such control variables include hormones and other signaling molecules, e.g., TOR (target of rapamycin), morphogens or the products of homeotic selector genes in embryonic pattern formation. I propose an analysis of this notion based on concepts borrowed from causal graph theory. (shrink)

We begin at the beginning, with an outline of Aristotle’s views on ontology and with a discussion of the influence of these views on Linnaeus. We move from there to consider the data standardization initiatives launched in the 19th century, and then turn to investigate how the idea of computational ontologies developed in the AI and knowledge representation communities in the closing decades of the 20th century. We show how aspects of this idea, particularly those relating to the use of (...) the term 'concept' in ontology development, influenced SNOMED CT and other medical terminologies. Against this background we then show how the Foundational Model of Anatomy, the Gene Ontology, Basic Formal Ontology and other OBO Foundry ontologies came into existence and discuss their role in the development of contemporary biomedical informatics. (shrink)

Genes are often described by biologists using metaphors derived from computa- tional science: they are thought of as carriers of information, as being the equivalent of ‘‘blueprints’’ for the construction of organisms. Likewise, cells are often characterized as ‘‘factories’’ and organisms themselves become analogous to machines. Accordingly, when the human genome project was initially announced, the promise was that we would soon know how a human being is made, just as we know how to make airplanes and buildings. Impor- tantly, (...) modern proponents of Intelligent Design, the latest version of creationism, have exploited biologists’ use of the language of information and blueprints to make their spurious case, based on pseudoscientific concepts such as ‘‘irreducible complexity’’ and on flawed analogies between living cells and mechanical factories. However, the living organ- ism = machine analogy was criticized already by David Hume in his Dialogues Concerning Natural Religion. In line with Hume’s criticism, over the past several years a more nuanced and accurate understanding of what genes are and how they operate has emerged, ironically in part from the work of computational scientists who take biology, and in particular developmental biology, more seriously than some biologists seem to do. In this article we connect Hume’s original criticism of the living organism = machine analogy with the modern ID movement, and illustrate how the use of misleading and outdated metaphors in science can play into the hands of pseudoscientists. Thus, we argue that dropping the blueprint and similar metaphors will improve both the science of biology and its understanding by the general public. (shrink)

Species concepts aim to define the species category. Many of these rely on defining species in terms of natural lineages and groupings. A dominant gene-centred metaconception has shaped notions of what constitutes both a natural lineage and a natural grouping. I suggest that relying on this metaconception provides an incomplete understanding of what constitute natural lineages and groupings. If we take seriously the role of epigenetic, behavioural, cultural, and ecological inheritance systems, rather than exclusively genetic inheritance, a broader (...) notion of what constitutes a natural grouping or lineage may be required. I conclude by outlining an alternative metaconception that is a de-centred metaschema for species. (shrink)

In this chapter, we describe three areas within the broad field of ecogenomics or postgenomics: epigenetics, proteomics, and microbiomics. We argue that these fields challenge traditional bioethics in different ways. Since epigenetic, proteomic, and microbiomic data may contain phenotypical information, they may intensify discussions about consent, privacy, and return of results. But these fields also firmly position organisms, including human beings, as deeply entangled with their environments, as constituted by context, history, and experiences as much as genes. This yields new (...) insights into concepts of health and development. We discuss precision medicine as an example of a systemic approach to health. We argue that acknowledging the entanglement of organism and environment also means recognizing the importance of interdisciplinarity for bioethics and thinking together biomedical ethics and environmental ethics. (shrink)

Increasingly, in data-intensive areas of the life sciences, experimental results are being described in algorithmically useful ways with the help of ontologies. Such ontologies are authored and maintained by scientists to support the retrieval, integration and analysis of their data. The proposition to be defended here is that ontologies of this type – the Gene Ontology (GO) being the most conspicuous example – are a part of science. Initial evidence for the truth of this proposition (which some will find (...) self-evident) is the increasing recognition of the importance of empirically-based methods of evaluation to the ontology development work being undertaken in support of scientific research. Ontologies created by scientists must, of course, be associated with implementations satisfying the requirements of software engineering. But the ontologies are not themselves engineering artifacts, and to conceive them as such brings grievous consequences. Rather, ontologies such as the GO are in different respects comparable to scientific theories, to scientific databases, and to scientific journal publications. Such a view implies a new conception of what is involved in the authoring, maintenance and application of ontologies in scientific contexts, and therewith also a new approach to the evaluation of ontologies and to the training of ontologists. (shrink)

Xenophon’s conception of the dialectical method shares many similarities with Antisthenes’ point of view regarding the relation between language and reality. The key element supporting this reading is the parallel between Xenophon’s method of dialegein kata genē and Antisthenes’ method of episkepsis tōn onomatōn. In this paper, I claim that a correct understanding of both methods yields a clear structural proximity between the two Socratics on the issue of dialectics. Although they present some significant differences, which I will also explore, (...) I will argue that both variants express a single Socratic motive with regard to dialectics. That is that dialectics, in its basic structure, consists of organizing reality through discourse in order to make it comprehensible. In particular, this is done through establishing unified instances capable of comprehending a multiplicity. This nuclear position could also be extended to include middle Plato’s concept of dialectics. This concurrence takes up different forms in Plato, Xenophon and Antisthenes. Nevertheless, they share the same structure, which indicates quite plausibly a major characteristic of Socratic philosophies, as opposed to previous attempts by the Presocratics and the Sophists. (shrink)

Two popular, yet highly controversial concepts of non-human agency from two different fields of knowledge are compared in this essay: the theory of the Selfish Gene, introduced into neo-Darwinian evolutionary biology by Richard Dawkins, and Actor-Network Theory, as brought forward in Science & Technology Studies by Bruno Latour. It is argued that the two theories, despite all apparent differences, share key motifs and motivations when they try to forward knowledge in their respective fields by adopting a vocabulary that (...) aims at metaphorical redescriptions of the origins of intentionality – in both senses: as purposefulness of action and as meaning. (shrink)

The concepts of the origin of the genetic code and the definitions of life changed dramatically after the RNA world hypothesis. Main narratives in molecular biology and genetics such as the “central dogma,” “one gene one protein” and “non-coding DNA is junk” were falsified meanwhile. RNA moved from the transition intermediate molecule into centre stage. Additionally the abundance of empirical data concerning nonrandom genetic change operators such as the variety of mobile genetic elements, persistent viruses and defectives do (...) not fit with the dominant narrative of error replication events (mutations) as being the main driving forces creating genetic novelty and diversity. The reductionistic and mechanistic views on physico-chemical properties of the genetic code are no longer convincing as appropriate descriptions of the abundance of non-random genetic content operators which are active in natural genetic engineering and natural genome editing. (shrink)

Chapter 1 (To know in order to survive) & Chapter 2 (A critique of evolved reason) explain human knowledge and its limits from an evolutionary point of view. Chapter 3 (Captured in our Cockpits) explains the evolution of consciousness, using value driven decision theory. Chapter 4-6 (Chapter 4 Sociobiology, Chapter 5 Culture: the Human Arena), Chapter 6, Genes, Memes, and the Environment) show that to understand culture you have at least to deal with 4 levels: genes, brains, the environment, culture. (...) Chapter 7-8 (Why some apes became humans) give a model of human evolution in which Alexander's concept of 'ecological dominace' plays a crucial role. (shrink)

Recognition of the plasticity of development — from gene expression to neuroplasticity — is increasingly undermining the traditional distinction between structure and function, or anatomy and behavior. At the same time, dynamic systems theory — a set of tools and concepts drawn from the physical sciences — has emerged as a way of describing what Maurice Merleau-Ponty calls the “dynamic anatomy” of the living organism. This article surveys and synthesizes dynamic systems models of development from biology, neuroscience, and (...) psychology in order to propose an integrated account of growth, learning, and behavior. Key to this account is the concept of self-differentiation or symmetry-breaking. I argue that development can be understood as a cascade of symmetry-breaking events brought about by the ongoing interactions of multiple, nested, nonlinear dynamic systems whose self-organizing behaviors gradually alter their own anatomical conditions. I begin by introducing the concept of symmetry-breaking as a way of understanding anatomical development. I then extend this approach to motor development by arguing that the organism’s behavior grows along with its body, like a new organ. Finally, I argue that the organism’s behavior and its world grow together dialectically, each driving the other to become more complex and asymmetrical through its own increasing asymmetry. Thus development turns out to be a form of cognition or sense-making, and cognition a form of development. (shrink)

DIFERENCIAÇÃO SEXUAL -/- Emanuel Isaque Cordeiro da Silva Instituto Agronômico de Pernambuco Embrapa Semiárido -/- • _____OBJETIVO -/- Os estudantes de Veterinária e de Zootecnia estão ligados à disciplina Reprodução Animal, um pelos mecanismos fisiológicos para evitar e tratar as possíveis patologias do trato reprodutivo dos animais domésticos, e outro para o entendimento dos processos fisiológicos visando o manejo reprodutivo e a procriação para a formação de um plantel geneticamente melhorado. Sendo assim, a finalidade do presente trabalho é apresentar os (...) mecanismos que regulam as diferenças sobre o desenvolvimento embrionário relativos à diferenciação e determinação sexual de machos e fêmeas, que também incluem o desenvolvimento dos órgãos envolvidos na reprodução e a origem das diferenças entre ambos os sexos. -/- •____INTRODUÇÃO -/- Os organismos que se reproduzem sexualmente são descendentes de organismos ao qual não existia a diferenciação sexual. Em algum momento da evolução surgiu a reprodução sexual como um mecanismo para incrementar a diversidade genética e facilitar a troca de informações genéticas mediante o material genético da fêmea com o do macho. Devido sua origem comum, na maioria das espécies, tanto os machos como as fêmeas possuem todos os genes necessários para desenvolverem-se em qualquer dos sexos. O que efetivamente faz diferença entre os sexos é a forma e a ordem ao qual se expressam os genes durante o processo de desenvolvimento. A diferenciação sexual é regulada principalmente por mecanismos epigenéticos, mais do que as diferenças genéticas de grande magnitude entre os sexos. Todo o controle epigenético de qualquer processo de desenvolvimento depende basicamente de uma série de expressões gênicas, através da qual a expressão de certa combinação de genes resulta na presença de determinadas proteínas, conhecidas como os fatores de transcrição, que induzem ou reprimem a expressão de outro(os) gene(es), a partir dos quais se produzem novas proteínas, que em certos casos também atuam como fatores de transcrição para outros genes, e assim sucessivamente. Logo, a expressão ou falta de expressão de um gene ao início da série pode resultar em um ladrão totalmente diferente da expressão de outros genes subsequentes, o que pode ocasionar profundas mudanças no processo de desenvolvimento e até a mutações indesejáveis. O padrão predeterminado de expressões gênica relativo a diferenciação sexual na maioria das espécies tanto domésticas quanto selvagens, leva ao desenvolvimento de um dos sexos (o padrão predeterminado dos mamíferos é o sexo feminino). Em consequência, a diferenciação faz com que um indivíduo do sexo oposto exija a expressão de um gene de determinação sexual que desvie a subsequente série de expressões gênica em direção ao dito sexo. Nos mamíferos, a expressão do gene SRY, localizado no cromossomo Y (e portanto ausente nas fêmeas), redige o padrão de diferenciação sexual de sua via pré-estabelecida feminina em direção ao padrão masculino. A existência de uma única diferença genética (presença do gene SRY nos machos e ausentes nas fêmeas), vai se amplificando e termina resultando no desenvolvimento de indivíduos diferentes entre si. Esse é um mecanismo de diferenciação sexual cromossômica. O primeiro passo de uma série de diferenciação sexual, em sentido estrito, não depende nem requer necessariamente a presença de um gene diferente em algum dos sexos. O gene “disparador” da diferenciação sexual pode estar presente em todos os embriões, porém pode expressar-se somente em algum deles, devido a fatores ambientais que formam parte da sua regulação epigenética, isto é, uma determinação sexual ambiental. Em algumas espécies de tartarugas ou de lagartos a expressão ou falta de expressão do gene “disparador”, por exemplo, depende da temperatura existente durante a incubação dos ovos, pelo qual alguns embriões desenvolvem-se como machos e outros como fêmeas, apesar de não existir diferença genética entre eles, simplesmente como consequência da temperatura: a determinação sexual depende da temperatura a que cada um deles foi submetido durante a incubação. Em certas espécies as temperaturas mais elevadas facilitam o desenvolvimento de fêmeas e outras de machos, enquanto que em outras espécies as temperaturas amenas (intermediárias) resultam em machos, e as inferiores como as superiores induzem o desenvolvimento de fêmeas. A existência dessa diversidade indica que a temperatura por si mesma não é a que induz ou a que provoca o desenvolvimento do macho e da fêmea, senão a que atua somente como um regulador inicial da diferenciação sexual. Em outras espécies o fator ambiental que regula a determinação sexual pode ser distinto. A densidade populacional, por exemplo, pode atuar como um regulador. Podemos concluir que a determinação sexual dependente da temperatura ou de outros fatores ambientais estabelece-se antes da determinação sexual cromossômica, a qual evoluiu depois como um método que oferece maior certeza e resultado, já que a proporção de machos e fêmeas não é afetada por mudanças ambientais ou de hábitat. -/- •___FORMAÇÃO INICIAL DA GÔNADA -/- Basicamente em todos os embriões, inicialmente se formam as chamadas gônadas indiferenciadas (com o potencial de desenvolver-se em ovários ou testículos) a partir da invasão das cristas genitais pelas células germinais primordiais, que migram desde seu local de origem no epiblasto, perto do lugar onde o saco vitelino se une com o intestino primitivo e que chegam até às cristas genitais que são engrossamentos de tecido situados na região mesonéfrica do embrião. A migração das células germinais primordiais ocorre muito cedo sobre o processo de desenvolvimento do embrião (dia 26 nos bovinos). Ao chegas as cristas genitais, as células germinativas proliferam-se e se organizam com as células somáticas já existentes nas cristas para ir formando a gônada (figura 1). Para regular essa remodelação e conformação adequada da gônada vários genes se expressam, como o OCT-4 (que aparentemente mantém a totipotencialidade da gônada), assim como o SF-1 (Fator esteroidogênico 1) e o WT-1 (gene associado ao tumor de Wilms). Esses dois últimos genes estimulam a proliferação celular e estabelecimento dos cordões sexuais. Nessa etapa inicial do desenvolvimento todos esses genes se expressam sem distinção de sexo, pelo que a gônada em formação mantém a capacidade de se diferenciar em testículo ou em ovário. -/- Figura 1: migração das células germinais primordiais em direção a crista gonodal. Diferenciação das gônadas femininas e masculinas. Fonte: ZARCO, 2018. -/- •___SEXO CROMOSSÔMICO -/- Têm-se observado que nos mamíferos a determinação sexual depende diretamente dos cromossomos. As fêmeas possuem dois cromossomos sexuais X (um contribuído do óvulo e o outro por um espermatozoide “X”). Os machos, por sua vez, possuem um cromossomo sexual X(proveniente do óvulo) e um cromossomo sexual Y, que provém de um espermatozoide “Y” (figura 2). A metade dos espermatozoides produzidos por um macho são X e a metade Y, isso porque durante a espermatogênese a divisão meiótica provoca que a partir de cada espermatócito primário, célula diploide que por pertencer a um indivíduo macho tem um cromossomo X e um Y, se originem das espermátides haploides a cada um das que eles tocam cromossomos X, e outras espermátides haploides as que eles tocam os cromossomos Y. Dessa forma, de acordo com o tipo do espermatozoide que fertilize o ovócito, se originará um indivíduo com cariótipo feminino “XX” ou um cariótipo masculino “XY” (figura 2). Esse processo é conhecido como sexo cromossômico, ao qual se determina o momento da fertilização. Figura 2: nos mamíferos todos os óvulos produzidos pelas fêmeas possuem um cromossomo sexual X. A metade dos espermatozoides produzidos pelos machos possuem um cromossomo X e a outra metade possui um cromossomo Y. Dependendo do cromossomo presente no espermatozoide que fertilize o óvulo pode-se gerar um indivíduo XX (fêmea) ou um XY (macho). Fonte: ZARCO, 2018. -/- O cromossomo “Y” é uma “invenção” relativamente recente na história da evolução das espécies e do estudo da genética. Surgiu a partir de uma mutação de um cromossomo “X”, que resultou na perda de um de seus braços, que é por onde se originou a morfologia do cromossomo Y. A maioria dos genes presentes no cromossomo Y também existem no cromossomo X; assim mesmo somente alguns genes do cromossomo Y foram evoluídos até ser diferentes dos genes do cromossomo X. Embora os machos possuam um cromossomo que não está presente nas fêmeas, esse mesmo cromossomo não aporta toda a informação genética original. Todos os genes existentes nas fêmeas estão também presentes nos dos machos, já que eles também possuem um cromossomo X. Uma particularidade do cromossomo Y, ao existir somente uma cópia nos machos, é que ele sofre um entrecruzamento com um cromossomo análogo durante o processo de meiose, pelo que o cromossomo Y de um macho é idêntico ao de seu progenitor e ao de seus descendentes, exceto no caso em que ocorra uma mutação espontânea. Em contraste, os cromossomos X das fêmeas (um proveniente do pai e outro da mãe) se entrecruzam durante a meiose, por onde cada óvulo produzido pela fêmea terá uma combinação de alelos distinta em seu cromossomo X. Ao estudar as diferenças presentes na sequência de DNA do cromossomo Y, é possível identificar a distância filogenética entre os indivíduos (quanto mais diferenças existirem entre os cromossomos significa que seu ancestral comum está mais longe). Algo análogo ocorre com o DNA das mitocôndrias, que sempre são aportados pela mãe e nunca sofrem recombinação genética. Gene SRY -/- Um dos poucos genes do cromossomo Y que não possuem correspondência com o cromossomo X é o gene SRY (Sex-determining Region of the Y chromossome – região do cromossomo Y determinante do sexo). Esse gene se expressa somente na gônada em formação nos embriões machos, em particular em células precursoras das células de Sertoli; ele codifica uma proteína da família SOX (SRY-like Box) que é uma família formada por proteínas que possuem um domínio de união ao DNA e que atuam como fatores de transcrição. Ao produzir-se a proteína SRY nas células precursoras das células de Sertoli estimula-se a expressão (transcrição) de outro gene análogo, denominado SOX-9 que, por sua vez, atua como um fator de transcrição que ativa a expressão de outros genes, como o FGF-9 (Fibroblast Growth Factor-9), ou seja ele é o estimulante de ativação dos demais. Os produtos dos genes SOX-9 e FGF-9 iniciam uma cascata de expressões que provocam a diferenciação das células de suporte da gônada indiferenciada (crista genital) em células de Sertoli. Em seguida, essas células dirigem a diferenciação das células intersticiais da crista genital em células de Leydig, o que finalmente resulta na formação de um testículo. Outro dos efeitos da proteína codificada por SOX-9 é um estímulo maior da expressão de seu próprio gene, pelo qual é produzido um ciclo de retroalimentação positiva que favorece a continuidade do processo de formação testicular. Como nos embriões da fêmea não existe o gene SRY, a gônada indiferenciada não é estimulada para expressar os genes SOX-9 nem o FGF-9 nas células de suporte (que nesse caso serão precursoras de células da granulosa). A gônada, em mudança, expressa em forma constitutiva, isto é, sem a necessidade de estimulação, outra cascata de genes que incluem o WNT4 (Wingless-integration Factor 4) e o RAPO1 (Respondina-1), que por sua vez iniciam uma cascata de expressão gênica, a qual provoca a diferenciação das células somáticas da gônada indiferenciada para formação das células da granulosa e células da teca, esse feito conduz, por sua vez, a formação de um ovário. No embrião macho a proteína SOX-9 inibe a expressão dos genes WNT4 e RSPO-1, pelo que a presença do gene SRY, e portanto de SOX-9, inibem a formação de um ovário ao mesmo tempo que estimulam a formação do testículo (figura 3). Em suma, se o embrião possui genótipo XY (um embrião macho), o gene SRY começa a expressar-se sobre as células precursoras da gônada imediatamente depois da formação da mesma, quando os cordões sexuais primários estão se desenvolvendo na medula. A expressão do gene, assim como a presença subsequente das proteínas SOX-9 e FGF-9 estimula a distinção das células de Sertoli e que se organizem os tubos seminíferos a partir dos cordões sexuais primários. Em contrapartida, em um embrião com genótipo XX (fêmea) não existe o gene SRY, pelo qual é impossível que se elevem os níveis das proteínas SOX-9 e FGF-9 e as células precursoras não se diferenciam em células de Sertoli, e portanto os cordões sexuais primários sofrem regressão. Depois de alguns dias, começam a organizar-se os cordões sexuais secundários e as células precursoras iniciam a expressão do gene WNT4, o que leva as mesmas a diferenciar-se em células da granulosa, que serão a base para a conformação dos folículos ovarianos. Se em um embrião XY, macho, a expressão do gene SRY demora, é formada um ovo-testículo devido a que algumas das células somáticas das cristas gonodais começam a expressar o gene WNT4, e a diferenciar-se em células da granulosa, enquanto que em outras a proteína SRY chega a tempo para dirigir a diferenciação para formação das células de Sertoli. No ovário em formação é expressado um gene denominado DAX-1 (Dosage-sensitive Sex Reversal). Esse gene, localizado no cromossomo X, codifica uma proteína que é um membro da família dos receptores nucleares ao que lhe falta o domínio de união ao DNA, pelo que parece atuar no bloqueio de diversos fatores de transcrição, entre os que se encontra o SRY. Como a proteína DAX-1 impede a ação da proteína SRY, um excesso de expressão do gene DAX-1 pode provocar a feminilização gonodal de indivíduos XY, macho, embora tenham SRY. Em condições normais, a expressão adequada do gene DAX-1 não é capaz de evitar a masculinização gonodal de embriões com o gene SRY, daqui o nome de reversão sexual dependente da dose. Figura 3: série de expressão gênica para a determinação gonodal. SRY (Região do cromossomo Y determinante do sexo), SOX-9 (SRY-like Box-9), FGF-9 (Fator de crescimento de fibroblastos-9), WNT4 (Wingless-integration Factor-4), RSPO-1 (Respondina-1). Uma vez que o SRY induz a expressão de SOX-9 na gônada masculina, inicia-se um processo de feedback positivo mediante o qual os níveis de expressão de SOX-9 e FGF-9 vão aumentando, ao mesmo tempo que inibem a expressão de WNT-4 e RSPO-1. Na gônada feminina não se expressam SRY, SOX-9 e nem FGF-9, o que permite que se expressem os genes WNT-4 e RSPO-1, que iniciam uma cascata de sinalização que dirige a formação de um ovário. Fonte: ZARCO, 2018. -/- • ___DIFERENCIAÇÃO SEXUAL DOS GENITAIS -/- Uma vez que se formam os testículos, todo o desenvolvimento subsequente dos órgãos e as características “masculinas” em lugar das femininas é em consequência dos hormônios produzidos pelos testículos em formação, incluindo os andrógenos e o hormônio inibidor dos ductos de Müller. Mediante a ausência de testículos todo o desenvolvimento dos órgãos genitais internos e externos segue um padrão feminino, sem levar em conta se estão presentes os ovários; o que significa a ausência de hormônios gonodais determina que o embrião se desenvolva como fêmea, uma vez que não requerem hormônios ovarianos para desencadear o padrão feminino. Por sua vez, as gônadas masculinas (os testículos), produzem substâncias que desviam o desenvolvimento em direção ao padrão masculino. Sob etapas relativamente rápidas da diferenciação todos os embriões possuem dois pares de dutos sexuais, os dutos de Wolff ou mesonéfricos e os dutos de Müller ou paramesonéfricos (figura 4). A testosterona secretada pelos testículos do feto macho em desenvolvimento atua sobre os dutos de Wolff, o que induz a formação posterior dos dutos deferentes, do epidídimo e das glândulas seminais (figura 4). Figura 4: formação dos órgãos genitais internos a partir dos dutos de Wolff no macho e dos dutos de Müller na fêmea. Fonte: ZARCO, 2018. -/- Os testículos produzem ao mesmo tempo, uma glicoproteína chamada Hormônio Inibidor dos Dutos de Müller (Müllerian Inhibiting Hormone, MIH, também chamado de Anti-Müllerian Hormone, AMH); como o seu nome indica, inibe o desenvolvimento dos dutos de Müller ou paramesonéfricos, provocando sua regressão, que impede a formação dos órgãos genitais característicos da fêmea como os ovidutos, o útero, a cérvix e a porção cranial da vagina (figura 4). O MIH é uma glicoproteína da família dos fatores de crescimento transformativo β (TGFβ). O gene MIH possui locais de união para os produtos dos genes SOX-9 e SF-1, pelo que a presença simultânea de ambos fatores de transcrição é necessária para a secreção do MIH e leva a cabo sua função de iniciação dos dutos de Müller sobre o embrião macho (vale lembrar que nessa etapa tanto a gônada de embriões machos como de embriões fêmeas expressam o gene SF-1, mas somente o macho expressa o SOX-9, para que unicamente esse último produza MIH). O certo é que na gônada do embrião fêmea não se produzem quantidades importantes da proteína SOX-9, além de que se produz a proteína DAX-1, mesma que antagoniza tanto a SOX-9 como a SF-1, todo o qual impede a produção de MIH e resulta no desenvolvimento dos dutos de Müller até a formação dos ovidutos, útero, cérvix e a porção cranial da vagina (figura 4). Assim, na fêmea, ao não haver testículos não circulam concentrações elevadas de andrógenos, o que impedirá o desenvolvimento dos dutos de Wolff, enquanto que os dutos de Müller se desenvolvem já que não haverá a presença do MIH para impedi-lo. O desenvolvimento dos genitais internos e externos femininos não requerem a presença de nenhum hormônio ovariano o que levará a cabo de maneira predeterminada (ou pré-estabelecida) na ausência de testículos. Outra estrutura interna que também se desenvolve de forma distinta nos machos e nas fêmeas é o seio urogenital, que no embrião macho é estimulado pela testosterona para formação da próstata, das glândulas bulbouretrais e da uretra peniana, enquanto que na fêmea forma a porção caudal da vagina. A respeito dos órgãos genitais externos (figura 5), nos embriões de ambos os sexos existem estruturas precursoras chamadas de tubérculo genital e pregas vestibulares. Na fêmea o tubérculo genital da origem ao clitóris e as pregas vestibulares dão origem aos lábios vulvares sem a necessidade da atuação de hormônios ovarianos, já que o padrão “por via pré-estabelecida” é feminino. Em contrapartida, no macho, tanto o tubérculo genital quanto as pregas vestibulares respondem ao hormônio 5α-dehidro-testosterona (DHT), ao qual se formam as células da pele da zona genital a partir da testosterona que é secretada pelos testículos. Para isso existem nas células a enzima 5α-reductasa, que transforma a testosterona em DHT. Uma vez formada, a DHT atua sobre as pregas vestibulares do embrião macho para que se fusionem e formem o escroto (em lugar dos lábios vulvares), e sobre o tubérculo genital para formar o pênis (em lugar do clitóris). Figura 5: estruturas que se desenvolvem nos embriões de cada sexo a partir do seio urogenital, o tubérculo genital e as pregas vestibulares. A cor do né de cada estrutura final corresponde com a cor do nome da estrutura a partir da qual se originou. Fonte: ZARCO, 2018. -/- • ___DIFERENCIAÇÃO SEXUAL DO SISTEMA NERVOSO -/- Existem inúmeras diferenças funcionais entre o sistema nervoso da fêmeas e o do machos, em humanos podem incluir diferenças tão complexas como a maior capacidade de verbal da mulher ou a maior capacidade de orientação espacial do homem. Nessa parte será abordada aquelas diferenças que influenciam diretamente sobre a função reprodutiva, como as diferenças na regulação da secreção de gonadotropinas ou as diferenças na capacidade de comportamento sexual masculino ou feminino. É necessário lembrar que, apesar de que essas diferenças se originem durante um período crítico da vida fetal ou neonatal (dependendo da espécie), geralmente se fazem presentes até que o animal chegue a vida adulta e demonstre obter ou não a capacidade para se comportar como macho ou como fêmea uma vez que é exposto aos hormônios sexuais que são secretada depois da puberdade. Igualmente aos processos acima citados, podemos afirmar que nos mamíferos o padrão pré-estabelecido de comportamento sexual e de secreção de gonadotropinas é o feminino. Se durante os primeiros dias de vida neonatal uma rata fêmea não é exposta a nenhum hormônio gonodal, ao chegar a vida adulta ela terá a capacidade de se comportar como fêmea na presença de estrógenos, assim como de secretar um pico pré-ovulatório de GnRH/LH em resposta aos mesmos (figura 6). Essa rata, portanto, não poderá se comportar como macho embora que em sua vida adulta seja exposta a testosterona. O sistema nervoso do rato macho recém-nascido que é exposto aos andrógenos produzidos pelos testículos, em detrimento, faz com que adquiram o potencial para se comportar como machos em sua vida adulta e que perdem o potencial para ter conduta de fêmeas na presença e/ou administração de estrógenos (processo conhecido como desfeminização do SNC). Se por meios de experimentos injetamos testosterona em uma rata fêmea recém-nascida, essa rata não poderá se comportar como fêmea em sua vida adulta, e passará a se comportar como macho. A castração neonatal de um rato (visando evitar a exposição de seu SNC a andrógenos testiculares), assim mesmo, resultará em sua vida adulta um padrão feminino (SNC feminizado e não masculinizado). O hipotálamo das ratas adultas possui uma área em que o número, características e densidade dos corpos neurais difere em machos e fêmeas, essa área é denominada como “núcleo sexualmente dimórfico do hipotálamo”, e tem demonstrado que quando as ratas são tratadas com testosterona na vida neonatal, a morfologia de seu núcleo sexualmente dimórfico será masculinizado em sua vida adulta, enquanto que a castração neonatal de ratos resulta em um núcleo sexualmente dimórfico feminizado em sua vida adulta. Isso significa que a exposição ou não a testosterona na vida neonatal é o que determina que tipo de núcleo sexualmente dimórfico se desenvolverá, o que por sua vez está relacionado com o tipo de conduta que o animal poderá expressar em sua vida adulta. Não deixa de ser um paradoxo que ao injetar uma dose elevada de estrógenos nos primeiros dias de vida de uma rata, os núcleos sexualmente dimórficos da mesma se desenvolverão como macho e em sua vida adulta seu potencial de conduta estará masculinizado e desfeminizado. O hormônio “feminino” conhecido como estradiol, masculiniza o hipotálamo e a conduta do animal. Logo, se a rata neonatal for exposta a injeção de andrógeno não-aromatizado (que não pode ser transformado em estrógenos pelas células) ela não se masculiniza. A masculinização e desfeminização dos ratos ou das ratas tratados com testosterona, na realidade, não são provocados pela própria testosterona, senão pelos estrógenos que se formam dentro dos neurônios quando absorvem a testosterona do sangue e a aromatizam para transformá-la em estrógenos (figura 6). Figura 6: desfeminização e masculinização do sistema nervoso central por meio da testosterona, que quando não absorvida pela α-fetoproteína pode entrar nos neurônios, onde se aromatizam para serem transformados em estrógenos, hormônio que é responsável pela desfeminização. Fonte: ZARCO, 2018. Por que as ratas, que possuem ovários funcionalmente produtores de estrógenos, não se masculinizam? A resposta está em uma proteína denominada α-fetoproteína que circula em altas concentrações nos fetos e nos recém-nascidos. Essa proteína possui a capacidade de unir-se aos estrógenos, ao qual impede seu entrada nas células. Os ratos, em desenvolvimento, produzem testosterona, no entanto não possui afinidade pela α-fetoproteína, o que permite com que ela circule livremente. Ao chegar ao SNC, a testosterona (que não foi absorvida) pode entrar nos neurônios e dentro deles se aromatizam e transformam-se em estrógenos, que finalmente masculinizam o SNC. A diferenciação sexual do hipotálamo depende, em síntese, da presença ou ausência dos testículos, o que permite que se produza ou não o hormônio testosterona que pode não ser absorvida por parte da α-fetoproteína, transformar-se em estrógenos e masculinizar o SNC. -/- •___CONCLUSÃO -/- Nos mamíferos todo o processo que se requerem para o desenvolvimento de um macho depende da existência de somente um gene do cromossomo Y, o gene SRY; a ausência desse gene resulta no desenvolvimento de uma fêmea. A presença ou ausência do gene SRY determina, então, a cadeia de eventos morfogênicos que ocorrerá em sua expressão ou não, para desenvolver todos os órgãos e características de um macho ou de uma fêmea. Por essa razão, os indivíduos com uma monossomia XOA (síndrome de Turner) são fêmeas (por não possuir o cromossomo Y nem o gene SRY), enquanto que os indivíduos triploides XXY (síndrome de Kleinefelter) são machos embora possuam dois cromossomos X. Em algumas espécies, no entanto, têm-se identificado machos que são cromossomicamente XX; nesses casos é determinado invariavelmente que por ser um erro durante a meiose a região do cromossomo Y em que reside o gene SRY tem sido transloucada ao cromossomo X. Da mesma forma, em alguns casos tem sido encontrado fêmeas com cariótipo XY; que nelas se identifica uma mutação inabilitante do gene SRY. Isso demonstra experimentalmente que por meio da engenharia genética é possível produzir machos com cariótipo XY mas com o gene SRY eliminado (knockout). Como é de se esperar, esses machos desenvolvem ovários e todos seus órgãos genitais, tanto internos quanto externos, e se desenvolvem como fêmeas. Os machos cromossomicamente XX transgênicos aos que se insertam uma cópia do gene SRY, desenvolvem testículos e um fenótipo masculino, embora sejam estéreis por causa da ausência de alguns genes do cromossomo Y que são necessários para a realização de uma espermatogênese normal. As falhas nos mecanismos de diferenciação sexual podem, diretamente, ocasionar anormalidades como as observadas nas bezerras Freemartin, que são bezerras originadas de uma gestação gemelar em que seu gêmeo era macho. O que sucede é que na espécie bovina, quando há uma gestação gemelar, é produzido um certo grau de anastomose entre as placentas dos fetos, o que permite a troca de sangue e de células entre ambos. Os produtos recebem, então, algumas células de seu gêmeos, que encontram seu lugar no órgão correspondente e se integram a ele. No caso particular das gônadas, quando o ovário primitivo de um embrião fêmea é colonizado por algumas células gonodais de seu gêmeo macho, essas células expressam o gene SRY, o que fará com que essa região da gônada se diferencie como testículo. Como resultado, se desenvolve um ovo-testículo (com maior ou menor proporção de tecido testicular dependendo do grau de colonização da gônada em formação por células provenientes do gêmeo macho). Ademais, ao haver certa quantidade de tecido testicular produtor de MIH, circularão sobre o feto fêmea níveis desse hormônio que, embora baixos, afetarão o desenvolvimento normal dos dutos de Müller, fazendo com que as bezerras Freemartin possuam genitálias internas ausentes ou pouco desenvolvidas. Os andrógenos produzidos pelas zonas de tecido testicular, por fim, são suficientes para causar um certo grau de masculinização, que se manifesta como um clitóris mais grande que o normal ou um desenvolvimento corporal masculinizado. -/- REFERÊNCIAS BIBLIOGRÁFICAS -/- ARNOLD, Arthur P.; CHEN, Xuqi; ITOH, Yuichiro. What a difference an X or Y makes: sex chromosomes, gene dose, and epigenetics in sexual differentiation. In: Sex and gender differences in pharmacology. Springer, Berlin, Heidelberg, 2013. p. 67-88. CUNNINGHAM, James. Tratado de fisiologia veterinária. Elsevier Health Sciences, 2011. DERIVAUX, Jules; BARNABÉ, Renato Campanarut. Reprodução dos animais domésticos. Zaragoza: Acribia, 1980. DA SILVA, Emanuel Isaque Cordeiro. Desenvolvimento Embrionário e Diferenciação Sexual nos Animais Domésticos. Disponível em:. Acesso em: Julho de 2020. HAFEZ, Elsayed Saad Eldin; HAFEZ, Bahaa. Reprodução animal. São Paulo: Manole, 2004. HIDALGO, C. Galina et al. Reproducción de animales domésticos. México: Limusa, 2008. MACLAUGHLIN, David T.; DONAHOE, Patricia K. Sex determination and differentiation. New England Journal of Medicine, v. 350, n. 4, p. 367-378, 2004. MCCARTHY, Margaret M.; ARNOLD, Arthur P. Reframing sexual differentiation of the brain. Nature neuroscience, v. 14, n. 6, p. 677, 2011. PLANT, Tony M.; ZELEZNIK, Anthony J. (Ed.). Knobil and Neill's physiology of reproduction. Academic Press, 2014. REY, Rodolfo. Diferenciación sexual embrio-fetal: De las moléculas a la anatomía. Revista chilena de anatomía, v. 19, n. 1, p. 75-82, 2001. SENGER, P. L. Embryogenesis of the pituitary gland and male or female reproductive system. In. Pathways to Pregnancy and Parturition. Current Conception Inc, v. 1, p. 8-76, 1997. ZARCO, L. Diferenciación sexual. In. PORTA, L. R.; MEDRANO, J. H. H. Fisiología reproductiva de los animales domésticos. Cidade do México: FMVZ-UNAM, 2018. -/- REALIZAÇÃO -/- . (shrink)

Seit Beginn der frühen Neuzeit ist das naturwissenschaftliche Verfahren maßgeblich durch ein neues Konzept geprägt: das Konzept des experimentellen, gestalterischen Eingriffs in die Natur. Es geht nun nicht mehr darum, eine Geschichte der "freien und ungebundenen Natur" (Bacon) zu erzählen, die in ihrem eigenen Lauf belassen und als vollkommene Bildung betrachtet wird. Es geht vielmehr darum, der "gebundenen und bezwungenen Natur" (Bacon) vermittels der experimentellen Tätigkeit des Menschen die Geheimnisse zu entreißen. Diese technisch-praktische Konzeption grenzt sich explizit von den klassischen (...) kontemplativen Wissenschaftsvorstellungen der Antike ab. Wie es Kant paradigmatisch in Bezug auf Bacon formuliert hat, ist diese "Revolution der Denkart" maßgeblich durch ein gewandeltes Verständnis des Verhältnisses des Menschen zur Natur geprägt. Der Mensch als Experimentator hat für Kant nicht mehr die "Qualität eines Schülers", der sich passiv von der Natur belehren läßt und an ihrem "Leitbande" (Kant) gegängelt wird. Seine neu gewonnene Autorität verleiht ihm vielmehr den Status eines Richters, der nun die Natur nötigen kann, auf gestellte Fragen zu antworten. Die Laborforschung der modernen Naturwissenschaft ist von den Formen der alten Naturwissenschaft so weit entfernt, daß sie den Vorwurf auf sich zog, sie untersuche Artekakte, aber nicht Natur. Die grundlegenden Theorien über Natur können in der Regel nur unter den künstlichen Bedingungen des Labors aufgestellt werden. Daraus darf aber nicht geschlossen werden, die anhand von Laborphänomenen aufgestellten und getesteten Theorien handelten nicht von der Natur außerhalb der Labore. Aber ihrer exakten und detaillierten Anwendung auf Prozesse außerhalb der Labore stehen eine Fülle von Schwierigkeiten entgegen. Insofern markiert das Labor sehr wohl eine Grenze exakter Naturforschung, die für den Umgang der wissenschaftlich-technischen Zivilisation mit der Natur wichtige Konsequenzen hat. Inhalt: Kristian Köchy / Gregor Schiemann: Natur im Labor Lothar Schäfer: Die Erscheinung der Natur unter Laborbedingungen Holm Tetens: Das Labor als Grenze der exakten Naturforschung Christoph Rehmann-Sutter: Genes in Labs - Concepts of Development and the Standard Environment Kristian Köchy: Lebewesen im Labor. Das Experiment in der Biologie Jutta Weber: Mannigfaltige Techno-Naturen. Von epistemischen Modellsystemen und situierten Maschinen Thomas Sören Hoffmann: Gezeigte versus sich zeigende Natur. Eine Skizze im Blick auf das Verhältnis von Labor und Natur Klaus Michael Meyer-Abich: Laborforschung im Erkenntnishandeln der Experimentiergesellschaft. Eine holistisch-pragmatische Perspektive für die Wissenschaftstheorie. (shrink)

The co-evolutionary concept of Three-modal stable evolutionary strategy of Homo sapiens is developed. The concept based on the principle of evolutionary complementarity of anthropogenesis: value of evolutionary risk and evolutionary path of human evolution are defined by descriptive (evolutionary efficiency) and creative-teleological (evolutionary correctly) parameters simultaneously, that cannot be instrumental reduced to others ones. Resulting volume of both parameters define the trends of biological, social, cultural and techno-rationalistic human evolution by two gear mechanism ˗ gene-cultural co-evolution and techno- humanitarian (...) balance. The resultant each of them can estimated by the ratio of socio-psychological predispositions of humanization/dehumanization in mentality. Explanatory model and methodology of evaluation of creatively teleological evolutionary risk component of NBIC technological complex is proposed. Integral part of the model is evolutionary semantics (time-varying semantic code, the compliance of the biological, socio-cultural and techno-rationalist adaptive modules of human stable evolutionary strategy). (shrink)

For some the gene-centered reductionism that permeates contemporary neo-Darwinism is an obstacle for finding a common explanatory framework for both biological and cultural evolution. Thus social scientists are tempted to find new concepts that might bridge the divide between biology and sociology. Yet since Aristotle we know that the level of explanation must be commensurate with the particular question to be answered. In modern natural science there are many instances where a reductionist approach has failed to provide the (...) right answer to the corresponding question. Thus social scientists risk becoming non-relevant when mimicking some features of the natural sciences (such as hard or soft reductionism) just for the sake of it, instead of finding autonomous explanations commensurate with the level of phenomena studied by social science. (shrink)

Since Aristotle the central question in biology was the origin of organic form; a question put in the backyard by neo-Darwinism that considers organic form as a side effect of the interactions between genes and their products. On the other hand, the fashionable notion of self-organization also fails to provide a true causal explanation for organic form. For Aristotle form is both a cause and the principle of intelligibility and this coupled to the classical concepts of potentiality and actuality (...) provides a rational framework,currently embodied in the contemporary concept of ‘attractor’, for understanding the origin of organic form. (shrink)

Debate about legal and policy reform has been haunted by a pernicious confusion about human nature, the idea that it is a set of rigid dispositions, today generally conceived as genetic, that is manifested the same way in all circumstances. Opponents of egalitarian alternatives argue that we cannot depart far from the status quo because human nature stands in the way. Advocates of such reforms too often deny the existence of human nature because, sharing this conception, they think it would (...) prevent changes they deem desirable. Both views rest on deep errors about what it is to have a nature and how genetics works. Human nature, like the nature of anything else, is a set of potentials to behave certain ways in given environments, not a nonsocial genetic something that inevitably produces the same result in any environment. To say that existing inequalities, are due to our genes, inalterable because heritable, ignores that genetic propensities may be differently manifested in different environments. Heritability has meaning only relative to an environment and a population and implies nothing about inevitability. A better sort of inegalitarian argument is that a proposed reform, given our nature, would be too costly even if possible. However, this sort of argument is too rarely supported by evidence and generally ignores the costs of existing inequalities. But egalitarians err in supposing that, if behavior is unconstrained by biology, the status quo is easily alterable. The environment may be extremely hard to change. Legal and policy debate should adopt a correct understanding of human nature as a set of propensities and ask of any proposed reform agreed to be otherwise desirable what and how alterable are its causes, genetic, environmental, or more accurately both. (shrink)

The Modern Synthesis (MS) is the current paradigm in evolutionary biology. It was actually built by expanding on the conceptual foundations laid out by its predecessors, Darwinism and neo-Darwinism. For sometime now there has been talk of a new Extended Evolutionary Synthesis (EES), and this article begins to outline why we may need such an extension, and how it may come about. As philosopher Karl Popper has noticed, the current evolutionary theory is a theory of genes, and we still lack (...) a theory of forms. The field began, in fact, as a theory of forms in Darwin’s days, and the major goal that an EES will aim for is a unification of our theories of genes and of forms. This may be achieved through an organic grafting of novel concepts onto the foundational structure of the MS, particularly evolvability, phenotypic plasticity, epigenetic inheritance, complexity theory, and the theory of evolution in highly dimensional adaptive landscapes. (shrink)

Il s’agit d’un excellent examen des interactions génétiques / environnement sur le comportement et, en dépit d’être un peu daté, est une lecture facile et utile. Ils commencent par des études jumelles qui montrent l’impact écrasant de la génétique sur le comportement. Ils notent les études de plus en plus connues de Judith Harris qui étendent et résument les faits que l’environnement familial partagé n’a presque aucun effet sur le comportement et que les enfants adoptés grandissent pour être aussi différents (...) de leurs demi-frères et soeurs que les personnes choisies au hasard. Un point fondamental qu’ils (et presque tous ceux qui discutent de la génétique comportementale) ne parviennent pas à noter est que les centaines (des milliers selon votre point de vue) des universels comportementaux humains, y compris toutes les bases de nos personnalités, sont 100% déterminés par nos gènes, sans aucune variation dans les normales. Tout le monde voit un arbre comme un arbre et non une pierre, cherche et mange de la nourriture, se met en colère et jaloux, etc. Donc, ce dont ils parlent surtout ici, c’est de la quantité d’environnement (culture) qui peut influer sur la mesure dans laquelle les divers traits sont montrés, plutôt que leur apparence. Enfin, ils discutent de l’eugénisme de la manière politiquement correcte habituelle, à défaut de noter que nous et tous les organismes sommes les produits de l’eugénisme de la nature et que les tentatives de vaincre la sélection naturelle avec la médecine, l’agriculture, et la civilisation dans son ensemble, sont désastreuses pour toute société qui persiste à le faire. Jusqu’à 50% de toutes les conceptions, soit environ 100 millions par an, se terminent par un avortement spontané précoce, presque tous sans que la mère soit au courant. Cet abattage naturel de gènes défectueux stimule l’évolution, nous maintient relativement génétiquement sains et rend la société possible. Dysgenics est suffisant pour détruire la civilisation, mais la surpopulation sera do ild’abord. Ceux qui souhaitent un cadre complet à jour pour le comportement humain de la vue moderne de deuxemssyst peuvent consulter mon livre 'The Logical Structure of Philosophy, Psychology, Mind and Language in Ludwig Wittgenstein et John Searle' 2nd ed (2019). Ceux qui s’intéressent à plus de mes écrits peuvent voir «Talking Monkeys --Philosophie, Psychologie, Science, Religion et Politique sur une planète condamnée --Articles et revues 2006-2017' 3rd ed (2019) et autres. (shrink)

Many moral debunking arguments are driven by the idea that the correlation between our moral beliefs and the moral truths is a big coincidence, given a robustly realist conception of morality.One influential response is that the correlation is not a coincidence because there is a common explainer of our moral beliefs and the moral truths. For example, the reason that I believe that I should feed my child is because feeding my child helps them to survive, and natural selection instills (...) in me beliefs and dispositions that help my children survive since that is conductive to my genes continuing through the generations. Similarly, the reason that it's morally good to feed my child is because it helps them to survive, and survival is morally valuable.But if we look at some cases from scientific practice, and from everyday life, we can see, I argue, why this response fails. A correlation can be coincidental even if there is a common explainer. I give an account of the nature of coincidence that draws upon recent literature on scientific explanation and argue that the correlation between moral belief and moral truth is a coincidence, even given such common explainers. And I use this to defend a certain form of debunking argument. (shrink)

The co-evolutionary concept of three-modal stable evolutionary strategy of Homo sapiens is developed. The concept based on the principle of evolutionary complementarity of anthropogenesis: value of evolutionary risk and evolutionary path of human evolution are defined by descriptive (evolutionary efficiency) and creative-teleological (evolutionary correctness) parameters simultaneously, that cannot be instrumental reduced to other ones. Resulting volume of both parameters define the vectors of biological, social, cultural and techno-rationalistic human evolution by two gear mechanism — genetic and cultural co-evolution and techno-humanitarian (...) balance. Explanatory model and methodology of evaluation of creatively teleological evolutionary risk component of NBIC technological complex is proposed. Integral part of the model is evolutionary semantics (time-varying semantic code, the compliance of the biological, socio-cultural and techno-rationalist adaptive modules of human stable evolutionary strategy). (shrink)

I distinguish two roles for a fitness concept in the context of explaining cumulative adaptive evolution: fitness as a predictor of gene frequency change, and fitness as a criterion for phenotypic improvement. Critics of inclusive fitness argue, correctly, that it is not an ideal fitness concept for the purpose of predicting gene-frequency change, since it relies on assumptions about the causal structure of social interaction that are unlikely to be exactly true in real populations, and that hold as (...) approximations only given a specific type of weak selection. However, Hamilton took this type of weak selection, on independent grounds, to be responsible for cumulative assembly of complex adaptations. In this special context, I argue that inclusive fitness is distinctively valuable as a criterion for improvement and a standard for optimality. Yet to call inclusive fitness a criterion for improvement and a standard for optimality is not to make any claim about the frequency with which inclusive fitness optimization actually occurs in nature. This is an empirical question that cannot be settled by theory alone. I close with some reflections on the place of inclusive fitness in the long running clash between ‘causalist’ and ‘statisticalist’ conceptions of fitness. (shrink)

Philosophical discussions of species have focused on multicellular, sexual animals and have often neglected to consider unicellular organisms like bacteria. This article begins to fill this gap by considering what species concepts, if any, apply neatly to the bacterial world. First, I argue that the biological species concept cannot be applied to bacteria because of the variable rates of genetic transfer between populations, depending in part on which gene type is prioritized. Second, I present a critique of phylogenetic (...) bacterial species, arguing that phylogenetic bacterial classification requires a questionable metaphysical commitment to the existence of essential genes. I conclude by considering how microbiologists have dealt with these biological complexities by using more pragmatic and not exclusively evolutionary accounts of species. I argue that this pragmatism is not borne of laziness but rather of the substantial conceptual problems in classifying bacteria based on any evolutionary standard. (shrink)

The biomedical literature makes extensive use of the concept of a genetic program. So far, however, the nature of genetic programs has received no satisfactory elucidation from the standpoint of computer science. This unsettling omission has led to doubts about the very existence of genetic programs, on the grounds that gene regulatory networks lack a predetermined schedule of execution, which may seem to contradict the very idea of a program. I show, however, that we can make perfect sense of (...) genetic programs, if only we abandon the preconception that all computers have a von Neumann architecture. Instead, genetic programs instantiate the computational architecture of Post–Newell Production Systems. That is, genetic programs are unordered sets of conditional instructions, instructions that fire independently when their conditions are matched. For illustration I present a paradigm Production System that regulates the functioning of the well-known lac operon of E. coli. On close reflection it turns out that not only genes, but also proteins encode instructions. I propose, therefore, to rename genetic programs to biomolecular programs. Biomolecular and/or genetic programs, and the cellular computers than run them, are to be understood not as von Neumann computers, but as Post–Newell production systems. (shrink)

We discuss the role of perceptron (or threshold) connectives in the context of Description Logic, and in particular their possible use as a bridge between statistical learning of models from data and logical reasoning over knowledge bases. We prove that such connectives can be added to the language of most forms of Description Logic without increasing the complexity of the corresponding inference problem. We show, with a practical example over the Gene Ontology, how even simple instances of perceptron connectives (...) are expressive enough to represent learned, complex concepts derived from real use cases. This opens up the possibility to import concepts learnt from data into existing ontologies. (shrink)

The organism is neither a discovery like the circulation of the blood or the glycogenic function of the liver, nor a particular biological theory like epigenesis or preformationism. It is rather a concept which plays a series of roles – sometimes overt, sometimes masked – throughout the history of biology, and frequently in very normative ways, also shifting between the biological and the social. Indeed, it has often been presented as a key-concept in life science and the ‘theorization’ of Life, (...) but conversely has also been the target of influential rejections: as just an instrument of transmission for the selfish gene, but also, historiographically, as part of an outdated ‘vitalism’. Indeed, the organism, perhaps because it is experientially closer to the ‘body’ than to the ‘molecule’, is often the object of quasi-affective theoretical investments presenting it as essential, sometimes even as the pivot of a science or a particular approach to nature, while other approaches reject or attack it with equal force, assimilating it to a mysterious ‘vitalist’ ontology of extra-causal forces, or other pseudo-scientific doctrines. This paper does not seek to adjudicate between these debates, either in terms of scientific validity or historical coherence; nor does it return to the well-studied issue of the organism-mechanism tension in biology. Recent scholarship has begun to focus on the emergence and transformation of the concept of organism, but has not emphasized so much the way in which organism is a shifting, ‘go-between’ concept – invoked as ‘natural’ by some thinkers to justify their metaphysics, but then presented as value-laden by others, over and against the natural world. The organism as go-between concept is also a hybrid, a boundary concept or an epistemic limit case, all of which partly overlap with the idea of ‘nomadic concepts’. Thereby the concept of organism continues to function in different contexts – as a heuristic, an explanatory challenge, a model of order, of regulation, etc. – despite having frequently been pronounced irrelevant and reduced to molecules or genes. Yet this perpetuation is far removed from any ‘metaphysics of organism’, or organismic biology. (shrink)