Ce texte a déjà paru dans la revue Théâtre/public, octobre-décembre 2017, n° 226, p. 17-22. Nous remercions Olivier Neveux de nous avoir autorisé à le reproduire ici. Une partie des chorégraphies mentionnées ci-dessous est visible dans la section GALERIE DE DANSE. Socialement et individuellement, l'homme est un animal rythmique. Marcel Mauss Quelques chorégraphies de Maguy Marin. Quelques notes prises à la volée. MAY B Au début, une scansion d'ahans, de corps trottinant. La marche hébétée - Danse, théâtre et (...) spectacle vivant – GALERIE – Nouvel article. (shrink)

Philosophy of Experimental Biology explores some central philosophical issues concerning scientific research in experimental biology, including genetics, biochemistry, molecular biology, developmental biology, neurobiology, and microbiology. It seeks to make sense of the explanatory strategies, concepts, ways of reasoning, approaches to discovery and problem solving, tools, models and experimental systems deployed by scientific life science researchers and also integrates developments in historical scholarship, in particular the New Experimentalism. It concludes that historical explanations of scientific change that are based on local laboratory (...) practice need to be supplemented with an account of the epistemic norms and standards that are operative in science. This book should be of interest to philosophers and historians of science as well as to scientists. (shrink)

I present a reconstruction of F.H.C. Crick's two 1957 hypotheses "Sequence Hypothesis" and "Central Dogma" in terms of a contemporary philosophical theory of causation. Analyzing in particular the experimental evidence that Crick cited, I argue that these hypotheses can be understood as claims about the actual difference-making cause in protein synthesis. As these hypotheses are only true if restricted to certain nucleic acids in certain organisms, I then examine the concept of causal specificity and its potential to counter claims about (...) causal parity of DNA and other cellular components. I first show that causal specificity is a special kind of invariance under interventions, namely invariance of generalizations that range over finite sets of discrete variables. Then, I show that this notion allows the articulation of a middle ground in the debate over causal parity. (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)

Griffiths et al. (2015) have proposed a quantitative measure of causal specificity and used it to assess various attempts to single out genetic causes as being causally more specific than other cellular mechanisms, for example, alternative splicing. Focusing in particular on developmental processes, they have identified a number of important challenges for this project. In this discussion note, I would like to show how these challenges can be met.

Economics is dominated by model building, therefore a comprehension of how such models work is vital to understanding the discipline. This book provides a critical analysis of the economist's favourite tool, and as such will be an enlightening read for some, and an intriguing one for others.

Experimental modeling in biology involves the use of living organisms (not necessarily so-called "model organisms") in order to model or simulate biological processes. I argue here that experimental modeling is a bona fide form of scientific modeling that plays an epistemic role that is distinct from that of ordinary biological experiments. What distinguishes them from ordinary experiments is that they use what I call "in vivo representations" where one kind of causal process is used to stand in for a physically (...) different kind of process. I discuss the advantages of this approach in the context of evolutionary biology. (shrink)

John Searle has argued that functions owe their existence to the value that we put into life and survival. In this paper, I will provide a critique of Searle’s argument concerning the ontology of functions. I rely on a standard analysis of functional predicates as relating not only a biological entity, an activity that constitutes the function of this entity and a type of system but also a goal state. A functional attribution without specification of such a goal state has (...) no truth-value. But if completed with a goal state, functional attributions understood as four-place relations attain a truth-value. The truth conditions of all attributions of function involve a dependence claim of the goal state on the function bearer’s activity. The nature of this dependence may differ; I consider five different possibilities: causality, mechanistic constitution, mereology, supervenience and metaphysical grounding. If these dependency relations are objective, Searle’s central ontological thesis fails. What he ought to have said is that our valuing survival or other goal states may be the reason why biology seeks functional knowledge, but this has nothing to do with ontology. I will show further that Searle also raised an interesting challenge concerning the relationship of functional and causal truths, but it does not threaten the objectivity of functions either. At best, it could show that functional vocabulary is eliminable. However, I will show that functional vocabulary is not so eliminable. (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)

The study explains the perception of the nation in the political thinking of Svetozár Hurban Vajanský, which is founded on primordialist starting points and has a holistic character. In this context, the relationship between the nationally conscious elite and the people is analysed in more detail. The ambivalence of Vajanský’s political thinking is evident in the fact that, in many ways, he formally promotes Ľudovít Štúr’s original idea of unity, but, within Slovak political discourse, he promotes the idea of programme (...) uniformity. Subsequently, this becomes a source of cultural and political isolationism. This fact is complemented in parallel by reflecting the primary acculturation importance of the national elite in developing the national consciousness of the population. Vajanský also incorporated the idea of Slavic mutuality into the national emancipation concept of developing Slovak national identity. Its content is in line with Štúr’s ethnic romanticism. The historicist concept of the development of Slavs under Russian protection also appears in his thinking. Vajanský’s Russophilism was, thus, loosely tied to the ideas of Russian Slavophiles and the idealising perspective of the Slavs’ civilisational mission, who were to form a new, more spiritual and culturally advanced, civilisation circle compared with the morally declining nations of the West. (shrink)

Going back at least to Duhem, there is a tradition of thinking that crucial experiments are impossible in science. I analyse Duhem's arguments and show that they are based on the excessively strong assumption that only deductive reasoning is permissible in experimental science. This opens the possibility that some principle of inductive inference could provide a sufficient reason for preferring one among a group of hypotheses on the basis of an appropriately controlled experiment. To be sure, there are analogues to (...) Duhem's problems that pertain to inductive inference. Using a famous experiment from the history of molecular biology as an example, I show that an experimentalist version of inference to the best explanation (IBE) does a better job in handling these problems than other accounts of scientific inference. Furthermore, I introduce a concept of experimental mechanism and show that it can guide inferences from data within an IBE-based framework for induction. 1. Introduction2. Duhem on the Logic of Crucial Experiments3. ‘The Most Beautiful Experiment in Biology’4. Why Not Simple Elimination?5. Severe Testing6. An Experimentalist Version of IBE 6.1. Physiological and experimental mechanisms6.2. Explaining the data6.3. IBE and the problem of untested auxiliaries6.4. IBE-turtles all the way down7. Van Fraassen's ‘Bad Lot’ Argument8. IBE and Bayesianism9. Conclusions. (shrink)

Environmental pollution and greenhouse gas emissions that contribute to climate change have adverse impacts on global health. Somewhat paradoxically, health care systems that aim to prevent and cure disease are themselves major emitters and polluters. In this paper we develop a justification for the claim that solidaristic health care systems should include sustainability as one of the criteria for determining which health interventions are made available or reimbursed – and which not. There is however a complication: most adverse health effects (...) due to climate change do occur elsewhere in the world. If solidarity would commit us to take care of everyone’s health, worldwide, it might imply that solidaristic health system cannot justifiably restrict universal access to their own national populations. In response we explain health solidarity is to be considered as a moral ideal. Such an ideal does not specify what societies owe to whom, but it does have moral implications. We argue that ignoring sustainability in political decision making about what health care is to be offered, would amount to betrayal of the ideal of solidarity. (shrink)

Biological modalities, i.e., biologically possible, impossible, or necessary states of affairs have not received much attention from philosophers. Yet, it is widely agreed that there are biological constraints on physically possible states of affairs, such that not everything that is physically possible is also biologically possible, even if everything that is biologically possible is also physically possible. Furthermore, biologists use concepts that appear to be modal in nature, such as the concept of evolvability in evolutionary developmental biology, or “evo-devo.” The (...) present chapter investigates what kind of modality underlies the concept of evolvability. This concept tries to capture the capacity of an organism or a lineage to sustain genetic changes that enable it to evolve or to evolve adaptively. The basic idea of the proposed approach is to construe evolvability as a kind of accessibility in a modal space. The difficult part is to specify this modal space and the relevant accessibility relation. While there may not be a general way of defining such a relation, there exist model systems for which it is possible, e.g., evolving small RNAs. The modal space in such cases turns out to be quite distinct from those constructed by philosophers, e.g., David Lewis’s similarity metric for possible worlds. Even though the biological case examined here is quite special, attending to the way in which biological possibilities are modeled in this case harbors some general lessons about biological modalities, in particular their dependence on the explanatory goals of the models modeling modality. (shrink)

The history of developmental biology is interwoven with debates as to whether mechanistic explanations of development are possible or whether alternative explanatory principles or even vital forces need to be assumed. In particular, the demonstrated ability of embryonic cells to tune their developmental fate precisely to their relative position and the overall size of the embryo was once thought to be inexplicable in mechanistic terms. Taking a causal perspective, this Element examines to what extent and how developmental biology, having turned (...) molecular about four decades ago, has been able to meet the vitalist challenge. It focuses not only on the nature of explanations but also on the usefulness of causal knowledge – including the knowledge of classical experimental embryology – for further scientific discovery. It also shows how this causal perspective allows us to understand the nature and significance of some key concepts, including organizer, signal and morphogen. This title is also available as Open Access on Cambridge Core. (shrink)

Psychologists and neuroscientists extensively rely on computational models for studying and analyzing the human mind. Traditionally, such computational models have been hand-designed by expert researchers. Two prominent examples are cognitive architectures and Bayesian models of cognition. Although the former requires the specification of a fixed set of computational structures and a definition of how these structures interact with each other, the latter necessitates the commitment to a particular prior and a likelihood function that – in combination with Bayes' rule – (...) determine the model's behavior. In recent years, a new framework has established itself as a promising tool for building models of human cognition: the framework of meta-learning. In contrast to the previously mentioned model classes, meta-learned models acquire their inductive biases from experience, that is, by repeatedly interacting with an environment. However, a coherent research program around meta-learned models of cognition is still missing to date. The purpose of this article is to synthesize previous work in this field and establish such a research program. We accomplish this by pointing out that meta-learning can be used to construct Bayes-optimal learning algorithms, allowing us to draw strong connections to the rational analysis of cognition. We then discuss several advantages of the meta-learning framework over traditional methods and reexamine prior work in the context of these new insights. (shrink)

Some screening tests for donor blood that are used by blood services to prevent transfusion-transmission of infectious diseases offer relatively few health benefits for the resources spent on them. Can good ethical arguments be provided for employing these tests nonetheless? This paper discusses—and ultimately rejects—three such arguments. According to the ‘rule of rescue’ argument, general standards for cost-effectiveness in healthcare may be ignored when rescuing identifiable individuals. The argument fails in this context, however, because we cannot identify beforehand who will (...) benefit from additional blood screening tests. On the ‘imposed risk’ argument, general cost-effectiveness standards do not apply when healthcare interventions impose risks on patients. This argument ignores the fact that imposing risks on patients is inevitable in healthcare and that these risks can be countered only within reasonable limits. Finally, the ‘manufacturing standard’ argument premises that general cost-effectiveness standards do not apply to procedures preventing the contamination of manufactured medical products. We contend that while this argument seems reasonable insofar as commercially manufactured medical products are concerned, publicly funded blood screening tests should respect the standards for general healthcare. We conclude that these particular arguments are unpersuasive, and we offer directions to advance the debate. (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)

Historians of biology have argued that much of the dynamics of experimental disciplines such as genetics or molecular biology can be understood from studying experimental systems and model organisms alone . Such accounts contrast sharply with more traditional philosophies of science which viewed scientific research essentially as a process of inventing and testing theories. I present a case from the history of biochemistry which can be viewed from both the experimental systems perspective and from the methodology of theory testing. I (...) argue that not only are the two perspectives fully compatible, but they are both necessary for a complete account of the research process. (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)

In this chapter, we discuss a specific kind of progress in economics, namely, progress that is pushed by the repeated use of mathematical models in most sub-branches of economics today. We adopt a functional account of progress to argue that progress in economics occurs via the use of what we call ‘common recipes’ and the use of model templates to define and solve problems of relevance for economists. We support our argument by discussing the case of twentieth-century business cycle research. (...) By presenting this case study in detail, we show how model templates are not only re-applied to different phenomena. We also show how scientists come up with them in the first place and how – once they are considered less useful – they are replaced with new ones. Finally, our case also illustrates that it is not only the mathematical structure that is re-used but that such a re-use also requires a shared conceptual vision of core properties of the phenomenon. If that vision is not shared anymore among economists, a model template can become useless and has to be replaced – sometimes through overcoming resistance – with a different one. (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)

It is shown that the 3-stratifiable sentences are equivalent in $\mathit{NFU}$ to truth-functional combinations of sentences about objects, sets of objects, sets of sets of objects, and sentences stating that there are at least $n$ urelements. This is then used to characterize the closed 3-stratifiable theorems of $\mathit{NFU}$ with an externally infinite number of urelements, as those that can be nearly proved in $\mathit{TTU}$ with an externally infinite number of urelements. As a byproduct we obtain a rather simple demonstration of (...) the consistency of 3-stratifiable extensions of $\mathit{NFU}$. (shrink)

The rule of rescue holds that special weight should be given to protecting the lives of assignable individuals in need, implying that less weight is given to considerations of cost-effectiveness. This is sometimes invoked as an argument for funding or reimbursing life-saving treatment in public healthcare even if the costs of such treatment are extreme. At first sight one might assume that an individualist approach to ethics—such as Scanlon’s contractualism—would offer a promising route to justification of the rule of rescue. (...) In this chapter I argue that contractualism cannot endorse the rule of rescue, whereas a collectivist approach that appeals to group solidarity would offer support for rescue cases. The argument, however, has its limitations, and though solidarity is of central concern in shaping public healthcare, there are good reasons for not endorsing the rule of rescue as a moral basis for allocating scarce resources in clinical care. (shrink)

Several authors have used the notion of causal specificity in order to defend non-parity about genetic causes (Waters 2007, Woodward 2010, Weber 2017, forthcoming). Non-parity in this context is the idea that DNA and some other biomolecules that are often described as information-bearers by biologists play a unique role in life processes, an idea that has been challenged by Developmental Systems Theory (e.g., Oyama 2000). Indeed, it has proven to be quite difficult to state clearly what the alleged special role (...) of genetic causes consists in. In this paper, I show that the set of biomolecules that are normally considered to be information-bearers (DNA, mRNA) can be shown to be the most specific causes of protein primary structure, provided that causal specificity is measured over a relevant space of biological possibilities, disregarding physical as well as logically possible states of the causal variables. (shrink)

The title of the article in the initial online publication was mixed up with copy editing information. The original article has been corrected.

Ich rekonstruiere und kritisiere Hans Drieschs Argumentation für die Behauptung, daß biologischen Prozessen nur eine substanzdualistische Ontologie der belebten Materie (Vitalismus) gerecht werden kann. Meine Diagnose lautet, daß Drieschs Argumentation zwar logisch schlüssig ist bzw. durch leichte Modifikationen in eine logisch gültige Form gebracht werden kann, aber von empirisch unbegründeten, metaphysischen Prämissen über die Möglichkeiten eines energieumwandelnden Mechanismus ausgeht.

I examine the adequacy of the causal graph-structural equations approach to causation for modeling biological mechanisms. I focus in particular on mechanisms with complex dynamics such as the PER biological clock mechanism in Drosophila. I show that a quantitative model of this mechanism that uses coupled differential equations – the well-known Goldbeter model – cannot be adequately represented in the standard causal graph framework, even though this framework does permit causal cycles. The reason is that the model contains dynamical information (...) about the mechanism that concerns causal properties but that does not correspond to variables that could be subject to independent interventions. Thus, a representation of the mechanisms as a causal structural model necessarily suppresses causally relevant information. (shrink)