Goldstein reported multiple cases of failure to categorise colours in patients that he termed amnesic or anomic aphasics. These patients have a particular difficulty in producing perceptual categories in the absence of other aphasic impairments. We hold that neuropsychological evidence supports the view that the task of colour categorisation is logically impossible without labels.

According to the proponents of Developmental Systems Theory and the Causal Parity Thesis, the privileging of the genome as “first among equals” with respect to the development of phenotypic traits is more a reflection of our own heuristic prejudice than of ontology - the underlying causal structures responsible for that specified development no more single out the genome as primary than they do other broadly “environmental” factors. Parting with the methodology of the popular responses to the Thesis, this paper offers (...) a novel criterion for ‘causal primacy’, one that is grounded in the ontology of the unique causal role of dispositional properties. This paper argues that, if the genome is conceptualised as realising dispositional properties that are “directed toward” phenotypic traits, the parity of ‘causal roles’ between genetic and extra-genetic factors is no longer apparent, and further, that the causal primacy of the genome is both plausible and defensible. (shrink)

This paper proposes that human expression of pain in the presence or absence of caregivers, and the detection of pain by observers, arises from evolved propensities. The function of pain is to demand attention and prioritise escape, recovery, and healing; where others can help achieve these goals, effective communication of pain is required. Evidence is reviewed of a distinct and specific facial expression of pain from infancy to old age, consistent across stimuli, and recognizable as pain by observers. Voluntary control (...) over amplitude is incomplete, and observers can better detect pain that the individual attempts to suppress rather than amplify or simulate. In many clinical and experimental settings, the facial expression of pain is incorporated with verbal and nonverbal vocal activity, posture, and movement in an overall category of pain behaviour. This is assumed by clinicians to be under operant control of social contingencies such as sympathy, caregiving, and practical help; thus, strong facial expression is presumed to constitute an attempt to manipulate these contingencies by amplification of the normal expression. Operant formulations support skepticism about the presence or extent of pain, judgments of malingering, and sometimes the withholding of caregiving and help. To the extent that pain expression is influenced by environmental contingencies, however, could equally plausibly constitute the release of suppression according to evolved contingent propensities that guide behaviour. Pain has been largely neglected in the evolutionary literature and the literature on expression of emotion, but an evolutionary account can generate improved assessment of pain and reactions to it. (shrink)

Philosophers and historians of biology have argued that genes are conceptualized differently in different fields of biology and that these differences influence both the conduct of research and the interpretation of research by audiences outside the field in which the research was conducted. In this paper we report the results of a questionnaire study of how genes are conceptualized by biological scientists at the University of Sydney, Australia. The results provide tentative support for some hypotheses about conceptual differences between different (...) fields of biological research. (shrink)

A central idea of developmental systems theory is ‘parity’ or ‘symmetry’ between genes and non-genetic factors of development. The precise content of this idea remains controversial, with different authors stressing different aspects and little explicit comparisons among the various interpretations. Here I characterise and assess several influential versions of parity.

This article proposes a number of models to examine through which mechanisms a population of autonomous agents could arrive at a repertoire of perceptually grounded categories that is sufficiently shared to allow successful communication. The models are inspired by the main approaches to human categorisation being discussed in the literature: nativism, empiricism, and culturalism. Colour is taken as a case study. Although we take no stance on which position is to be accepted as final truth with respect to human categorisation (...) and naming, we do point to theoretical constraints that make each position more or less likely and we make clear suggestions on what the best engineering solution would be. Specifically, we argue that the collective choice of a shared repertoire must integrate multiple constraints, including constraints coming from communication. Key Words: autonomous agents; colour categorisation; colour naming; connectionism; cultural evolution; genetic evolution; memes; origins of language; self-organisation; semiotic dynamics; symbol grounding. (shrink)

In this paper, I propose two theses, and then examine what the consequences of those theses are for discussions of reduction and emergence. The first thesis is that what have traditionally been seen as robust, reductions of one theory or one branch of science by another more fundamental one are a largely a myth. Although there are such reductions in the physical sciences, they are quite rare, and depend on special requirements. In the biological sciences, these prima facie sweeping reductions (...) fade away, like the body of the famous Cheshire cat, leaving only a smile.... The second thesis is that the "smiles" are fragmentary patchy explanations, and though patchy and fragmentary, they are very important, potentially Nobel-prize winning advances. To get the best grasp of these "smiles," I want to argue that, we need to return to the roots of discussions and analyses of scientific explanation more generally, and not focus mainly on reduction models, though three conditions based on earlier reduction models are retained in the present analysis. I briefly review the scientific explanation literature as it relates to reduction, and then offer my account of explanation. The account of scientific explanation I present is one I have discussed before, but in this paper I try to simplify it, and characterize it as involving field elements and a preferred causal model system abbreviated as FE and PCMS. In an important sense, this FE and PCMS analysis locates an "explanation" in a typical scientific research article. This FE and PCMS account is illustrated using a recent set of neurogenetic papers on two kinds of worm foraging behaviors: solitary and social feeding. One of the preferred model systems from a 2002 Nature article in this set is used to exemplify the FE and PCMS analysis, which is shown to have both reductive and nonreductive aspects. The paper closes with a brief discussion of how this FE and PCMS approach differs from and is congruent with Bickle's "ruthless reductionism" and the recently revived mechanistic philosophy of science of Machamer, Darden, and Craver. (shrink)

Caenorhabditis elegans (C. elegans) is a tiny worm that has become the focus of a large number of worldwide research projects examining its genetics, development, neuroscience, and behavior. Recently several groups of investigators have begun to tie together the behavior of the organism and the underlying genes, neural circuits, and molecular processes implemented in those circuits. Behavior is quintessentially organismal--it is the organism as a whole that moves and mates--but the explanations are devised at the molecular and neurocircuit levels, and (...) tested in populations using protocols that span many levels of aggregation. Following a brief review of the main relevant features of C. elegans, I describe some of these circuits, and then discuss two contrasting approaches in behavioral genetics and neural network analysis of the worm. Finally, I outline the rudiments of a "field and focus" explanation model using the two contrasting approaches. (shrink)

Model organismism—the over-reliance on model organisms without sufficient attention to the adequacy of the models—continues to hobble our understanding of human brains and behaviors. I outline the problem of model organismism in contemporary biology and biomedicine, and discuss the virtues of a genuinely comparative biology for understanding ourselves, our evolutionary history, and our place in nature.

Stem cell scientists and ethicists have focused intently on questions relevant to the developmental stage and developmental capacities of stem cells. Comparably less attention has been paid to an equally important set of questions about the nature of stem cells, their common characteristics, their non‐negligible differences and their possible developmental species specificity. Answers to these questions are essential to the project of justly inferring anything about human stem cell biology from studies in non‐human model systems—and so to the possibility of (...) eventually developing human therapies based on stem cell biology. After introducing and discussing these questions, I conclude with a brief discussion of the creation of novel model systems in stem cell biology: human‐to‐animal embryonic chimeras. Such novel model systems may help to overcome obstacles to extrapolation, but they are also scientifically and ethically contentious. BioEssays 26:1005‐1012, 2004. © 2004 Wiley Periodicals, Inc. (shrink)

This is a critical notice of Evolution's Eye by Susan Oyama, focusing on developmental systems theory primarily in relation to the nature-nurture debates and the explanation of behaviour.

How does a complex organism develop from a relatively simple, homogeneous mass? The usual answer is: through the (context‐dependent) execution of species‐specific genetic instructions specifying the development of that organism. Commentators are sometimes skeptical of this usual answer, but of course not all commentators, and not always for the same reasons. Here I attempt to lay bare the logical structure of the usual answer through an extended analysis of the heuristics and methodological principles at play in the exploration and explanation (...) of development—and also to show a critical ambiguity that renders the usual answer suspect. (shrink)

Many scientists and philosophers of science are troubled by the relative isolation of developmental from evolutionary biology. Reconciling the science of development with the science of heredity preoccupied a minority of biologists for much of the twentieth century, but these efforts were not corporately successful. Mainly in the past fifteen years, however, these previously dispersed integrating programmes have been themselves synthesized and so reinvigorated. Two of these more recent synthesizing endeavours are evolutionary developmental biology and developmental systems theory. While the (...) former is a bourgeoning and scientifically well-respected biological discipline, the same cannot be said of DST, which is virtually unknown among biologists. In this review, we provide overviews of DST and EDB, summarize their key tenets, examine how they relate to one another and to the study of epigenetics, and survey the impact that DST and EDB have had on biological theory and practice. (shrink)

Developmental biology has resurfaced in recent years, often without a clearly central role for the organism. The organism is pulled in divergent directions: on the one hand, there is an important body of work that emphasizes the role of the gene in development, as executing and controlling embryological change; on the other hand, there are more theoretical approaches under which the organism disappears as little more than an instance for testing biological generalizations. I press here for the ineliminability of the (...) organism in developmental biology on explanatory grounds. I examine classical work concerned with growth and development, particularly in Drosophila and C. elegans. Some of this work is suggestive of modular development, and accordingly suggests a level below that of the organism as being explanatory. These are not the only type of case. There are other equally well-established results, which indicate greater integration in the developing organism. Though with a modular organization the organism can be thought of as made up of its constituent traits, and though the explanations of these traits may lie in terms of cells or genes, even with modular development the explanations of "genetic" differences require an appeal to the organism. With non-modular organization the organism has an even more central role. This does not mean that these genetic or cellular contributions are unreal in any way, or that development requires some sort of vitalistic contribution; but the genetic contributions make sense only as constituents of the organism, embedded in a larger organic context. (shrink)

In light of the human genome project, establishing the genetic aetiology of complex human diseases has become a research priority within Western medicine. However, in addition to the identification of disease genes, numerous research projects are also being undertaken to identify genes contributing to the development of human behavioural characteristics, such as cognitive ability and criminal tendency. The permissibility of this research is obviously controversial: will society benefit from this research, or will it adversely affect our conceptions of ourselves and (...) each other? When assessing the permissibility of this research, it is important to consider the nature and deterministic significance of behavioural genetic information. Whilst todate there has been much discussion and debate about the properties of genetic information per se and genetic determinism, this has not been applied to behavioural genetic research and its ethical implications. Therefore, this paper elucidates how behavioural genetic information can be distinguished from other types of genetic and non-genetic information and also synthesises the determinative significance of genetic factors for the development of human behavioural traits. Undertaking this analysis enables the ethical issues raised by this research to be debated in an appropriate context and indicates that separate policy considerations are warranted. (shrink)

In this paper I consider Kenneth Schaffner''s(1998) rendition of ''''developmentalism'''' from the point of viewof bacteriophage biology. I argue that the fact that a viablephage can be produced from purified DNA and host cellularcomponents lends some support to the anti-developmentalist, ifthey first show that one can draw a principled distinctionbetween genetic and environmental effects. The existence ofhost-controlled phage host range restriction supports thedevelopmentalist''s insistence on the parity of DNA andenvironment. However, in the case of bacteriophage, thedevelopmentalist stands on less firm (...) ground than when organismswith nervous systems, such as Schaffner''s C. elegans, areconsidered. (shrink)

In this paper we argue that an operational organism concept can help to overcome the structural deficiency of mathematical models in biology. In our opinion, the structural deficiency of mathematical models lies mainly in our inability to identify functionally relevant biological characters in biological systems, and not so much in a lack of adequate mathematical representations of biological processes. We argue that the problem of character identification in biological systems is linked to the question of a properly formulated organism concept. (...) Lastly, we demonstrate how a decomposition of an organism into independent characters in the context of a specific biological process--such as adaptation by means of natural selection--depends on the dynamical properties and invariance conditions of the equations that describe this process. (shrink)

Minimal genetic pre-formationism is defended, in that primacy is ascribed to DNA in the structuring of molecules through molecular codes. This together with the importance of such codes for stability and variation in living systems makes DNA categorically different from other causal factors. It is argued that post-transcriptional and post-translational processing in protein synthesis does not rob DNA of this structuring role. Notions of structuring causal powers that may vary in degree, of arbitrary molecular codes that are more or less (...) realized, of partial templating and of genetic information as a subspecies of mechanistic information are brought in to support this and to rival causal and semantic notions of information. It is concluded that the primacy of genes in their structuring of molecules goes together with parity between genes and non-genetic causal factors in regulation of living systems. This is seen to hold independently of the radical reconceptualization of organism cum environment that has been suggested in developmental systems theory. (shrink)

It is argued that John Bickle's Ruthless Reductionism is flawed as an account of the practice of neuroscience. Examples from genetics and linguistics suggest, first, that not every mind-brain link or gene-phenotype link qualifies as a reduction or as a complete explanation, and, second, that the higher (psychological) level of analysis is not likely to disappear as neuroscience progresses. The most plausible picture of the evolving sciences of the mind-brain seems a patchwork of multiple connections and partial explanations, linking anatomy, (...) mechanisms and functions across different domains, levels, and grain sizes. Bickle's claim that only the molecular level provides genuine explanations, and higher level concepts are just heuristics that will soon be redundant, is thus rejected. In addition, it is argued that Bickle's recasting of philosophy of science as metascience explicating empirical practices, ignores an essential role for philosophy in reflecting upon criteria for reduction and explanation. Many interesting and complex issues remain to be investigated for the philosophy of science, and in particular the nature of interlevel links found in empirical research requires sophisticated philosophical analysis. (shrink)

This paper questions the form and prospects of “extended theories” which have been simultaneously and independently advocated both in the philosophy of mind and in the philosophy of biology. It focuses on Extend Mind Theory (EMT) and Developmental Systems Theory (DST). It shows first that the two theories vindicate a parallel extension of received views, the former concerning extending cognition beyond the brain, the latter concerned with extending evolution and development beyond the genes. It also shows that both arguments rely (...) on the demonstration of causal parities, which have been undermined by the classical received view. Then I question whether the argument that there is an illegitimate inference from parities or coupling to constitution claims, which has been objected by Adams and Aizawa in The bounds of cognition, (2008) to EMT, also holds against DST. To this aim, I consider two defenses against DST that are parallel to two defenses against EMT, one about intrinsic content, the other about the difference between what’s in principle possible and what happens in practice. I conclude by claiming that the weaknesses and strengths of both theories are different regarding these two kinds of objections. (shrink)

Animal models have received particular attention as key examples of material models. In this paper, we argue that the specificities of establishing animal models—acknowledging their status as living beings and as epistemological tools—necessitate a more complex account of animal models as materialised models. This becomes particularly evident in animal-based models of diseases that only occur in humans: in these cases, the representational relation between animal model and human patient needs to be generated and validated. The first part of this paper (...) presents an account of how disease-specific animal models are established by drawing on the example of transgenic mice models for Alzheimer’s disease. We will introduce an account of validation that involves a three-fold process including from human being to experimental organism; from experimental organism to animal model; and from animal model to human patient. This process draws upon clinical relevance as much as scientific practices and results in disease-specific, yet incomplete, animal models. The second part of this paper argues that the incompleteness of models can be described in terms of multi-level abstractions. We qualify this notion by pointing to different experimental techniques and targets of modelling, which give rise to a plurality of models for a specific disease. (shrink)

This article examines and rejects the claim that 'innateness is canalization'. Waddington's concept of canalization is distinguished from the narrower concept of environmental canalization with which it is often confused. Evidence is presented that the concept of environmental canalization is not an accurate analysis of the existing concept of innateness. The strategy of 'biologicizing the mind' by treating psychological or behavioral traits as if they were environmentally canalized physiological traits is criticized using data from developmental psychobiology. It is concluded that (...) identifying innateness with environmental canalization can only result in adding unhelpful associations from 'folkbiology' to the relatively precise idea of canalization. (shrink)

Alexander Rosenberg recently claimed (1997) that developmental biology is currently being reduced to molecular biology. cite several concrete biological examples that are intended to impugn Rosenberg's claim. I first argue that although Laubichler and Wagner's examples would refute a very strong reductionism, a more moderate reductionism would escape their attacks. Next, taking my cue from the antireductionist's perennial stress on the importance of spatial organization, I describe one form an empirical finding that refutes this moderate reductionism would take. Finally, I (...) point out an actual example, anterior-posterior axis determination in the chick, that challenges the reductionist's belief that all developmental regularities can be explained by molecular biology. In short, I argue that Rosenberg's position can be saved from Laubichler and Wagner's criticisms and putative counter-examples, but it would not survive a different kind of counter-example. (shrink)

The idea that some characteristics of an organism are explained by the organism's intrinsic nature, whilst others reflect the influence of the environment is an ancient one. It has even been argued that this distinction is itself part of the evolved psychology of the human species. The distinction played an important role in the history of philosophy as the locus of the dispute between Rationalism and Empiricism discussed in another entry in this encyclopedia. This entry, however, focuses on twentieth-century accounts (...) of the innate/acquired distinction. These accounts have for the most part been inspired by the sciences of mind and behaviour. (shrink)

Causal selection is the task of picking out, from a field of known causally relevant factors, some factors as elements of an explanation. The Causal Parity Thesis in the philosophy of biology challenges the usual ways of making such selections among different causes operating in a developing organism. The main target of this thesis is usually gene centrism, the doctrine that genes play some special role in ontogeny, which is often described in terms of information-bearing or programming. This paper is (...) concerned with the attempt of confronting the challenge coming from the Causal Parity Thesis by offering principles of causal selection that are spelled out in terms of an explicit philosophical account of causation, namely an interventionist account. I show that two such accounts that have been developed, although they contain important insights about causation in biology, nonetheless fail to provide an adequate reply to the Causal Parity challenge: Ken Waters's account of actual-difference making and Jim Woodward's account of causal specificity. A combination of the two also doesn't do the trick, nor does Laura Franklin-Hall's account of explanation (in this volume). We need additional conceptual resources. I argue that the resources we need consist in a special class of counterfactual conditionals, namely counterfactuals the antecedents of which describe biologically normal interventions. (shrink)

Slightly modified excerpt from the section 13.4 Zusammenfassung und Ausblick (translated into englisch): This chapter is based on an analysis of ethical debates on epigenetics and genome editing, debates, in which ethical arguments relating to future generations and justice play a central role. The analysis aims to contextualize new developments in genetic engineering, such as genome and epigenome editing, ethically. At the beginning, the assumptions of "genetic determinism," on which "genetic essentialism" is based, of "epigenetic determinism" as well as "genetic" (...) and "epigenetic exceptionalism" are analyzed and critically discussed. The remarks on the ethical discourse on epigenetics show that the notion of "epigenetic determinism" can sometimes be discerned not only in popular scientific discourse but also in ethical discourse. Ethical debates on epigenetics, however, have distanced themselves from this deterministic understanding. As a result, the focus in the ethical discourse on epigenetics shifts from responsibility for one's own health and that of subsequent generations to justice. What is meant here is justice, for example, in terms of access to healthy environmental conditions, regardless of whether these contribute to health with or without epigenetic agency. An analysis of the discourse on genome editing reveals that it is primarily germline interventions that are being ethically examined, with a concentration on the aspect of inheritance. The question is whether this is accompanied by an implicit "genetic determinism" or even a "genetic essentialism": the determinism could lie in the centrality of the aspect of heritability, since only genetic information is inherited. Does the aspect of heritability and genome modification play a more decisive role in debates on genome editing than the safety issue? Is the problem of embryos and their potential offspring not being able to consent to germline intervention given such a high priority because it is a genetic intervention? Under such a premise of "strong genetic determinism" supplemented by "epigenetic determinism," not only genome editing but also epigenome editing would be ethically relevant precisely because it too would have an influence on the genome. How this influence of genome editing and epigenome editing is ethically evaluated in each case therefore depends initially on whether the assumptions of "genetic" and "epigenetic determinism" are advocated. These assumptions are increasingly viewed critically in ethical discourse because they cannot be confirmed from a scientific perspective. In popular scientific debates in particular, however, they seem to persist, which ultimately also influences the public discussion. Since a broad public discussion is required especially on genome editing, a reflective approach to the various "-isms" analyzed in this chapter is central. DOI: 10.5771/9783748927242. (shrink)

According to conventional wisdom, local gauge symmetry is not a symmetry of nature, but an artifact of how our theories represent nature. But a study of the so-called theta-vacuum appears to refute this view. The ground state of a quantized non-Abelian Yang-Mills gauge theory is characterized by a real-valued, dimensionless parameter theta—a fundamental new constant of nature. The structure of this vacuum state is often said to arise from a degeneracy of the vacuum of the corresponding classical theory, which degeneracy (...) allegedly arises from the fact that “large” (but not “small”) local gauge transformations connect physically distinct states of zero field energy. If that is right, then some local gauge transformations do generate empirical symmetries. In defending conventional wisdom against this challenge I hope to clarify the meaning of empirical symmetry while deepening our understanding of gauge transformations. I distinguish empirical from theoretical symmetries. Using Galileo’s ship and Faraday’s cube as illustrations, I say when an empirical symmetry is implied by a theoretical symmetry. I explain how the theta-vacuum arises, and how “large” gauge transformations differ from “small” ones. I then present two analogies from elementary quantum mechanics. By applying my analysis of the relation between empirical and theoretical symmetries, I show which analogy faithfully portrays the character of the vacuum state of a classical non-Abelian Yang-Mills gauge theory. The upshot is that “large” as well as “small” gauge transformations are purely formal symmetries of non-Abelian Yang-Mills gauge theories, whether classical or quantized. It is still worth distinguishing between these kinds of symmetries. An analysis of gauge within the constrained-Hamiltonian formalism yields the result that “large” gauge transformations should not be classified as gauge transformations; indeed, nor should “global” gauge transformations. In a theory in which boundary conditions are modeled dynamically, “global” gauge transformations may be associated with physical symmetries, corresponding to translations of these extra dynamical variables. Such translations are symmetries if and only if charge is conserved. But it is hard to argue that these symmetries are empirical, and in any case they do not correspond to any constant phase change in a quantum state. (shrink)

How does a complex organism develop from a relatively simple, homogeneous mass? The usual answer is: through the execution of species-specific genetic instructions specifying the development of that organism. Commentators are sometimes sceptical of this usual answer, but of course not all commentators. Some biologists refer to master control genes responsible for the activation of all the genes responsible for every aspect of organismal development; and some philosophers, most notoriously Rosenberg, buy this claim hook, line, and sinker. Here I explore (...) both the seeming plausibility of the usual position, and also its ultimate inadequacy. (shrink)