Marcel Weber

Dieser Aufsatz untersucht die Vergleichbarkeit metaphysischer Systeme an einem historischen Fallbeispiel, Leibniz' Kritik an Locke. Die zentrale Frage ist, wie weit es Leibniz gelingt, Lockes Thesen zu widerlegen ohne dabei einfach Behauptungen aus seinem eigenen System vorauszusetzen. Es wird gezeigt, dass Leibniz dies nur bei der Frage nach der Existenz eingeborener Ideen gelingt, nicht aber bei der Denkfähigkeit der Materie oder der Existenz unbewusster mentaler Vorgänge. Die Quellen dieser Unvergleichbarkeit werden mittels des wissenschaftstheoretischen Begriffs der semantischen Inkommensurabilität analysiert

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.

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.

This article examines the role of experimental generalizations and physical laws in neuroscientific explanations, using Hodgkin and Huxley’s electrophysiological model from 1952 as a test case. I show that the fact that the model was partly fitted to experimental data did not affect its explanatory status, nor did the false mechanistic assumptions made by Hodgkin and Huxley. The model satisfies two important criteria of explanatory status: it contains invariant generalizations and it is modular (both in James Woodward’s sense). Further, I argue that there is a sense in which the explanatory heteronomy thesis holds true for this case. †To contact the author, please write to: SNF‐Professorship for Philosophy of Science, University of Basel, Missionsstrasse 21, 4003 Basel, Switzerland; e‐mail: [email protected].

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.

I present an attempt at an explication of the ecological theory of interspecific competition, including its explanatory role in community ecology and evolutionary biology. The account given is based on the idea that law-like statements play an important role in scientific theories of this kind. I suggest that the principle of competitive exclusion is such a law, and that it is evolutionarily invariant. The principle's empirical status is defended and implications for the ongoing debates on the existence of biological laws are discussed

I examine some philosophical arguments as well as current empirical research in molecular neurobiology in order to throw some new light on the question of whether neurological processes are deterministic or indeterministic. I begin by showing that the idea of an autonomous biological indeterminism violates the principle of the supervenience of biological properties on physical properties. If supervenience is accepted, quantum mechanics is the only hope for the neuro-indeterminist. But this would require that indeterministic quantum-mechanical effects play a role in the functioning of the nervous system. I examine several candidates of molecular processes where this could, in theory, be the case. It turns out that there is good news from recent work on ion channels. Unfortunately (for the indeterminist), this good news is neutralised at once by bad news.

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.

Recent discussion of the statistical character of evolutionary theory has centered around two positions: (1) Determinism combined with the claim that the statistical character is eliminable, a subjective interpretation of probability, and instrumentalism; (2) Indeterminism combined with the claim that the statistical character is ineliminable, a propensity interpretation of probability, and realism. I point out some internal problems in these positions and show that the relationship between determinism, eliminability, realism, and the interpretation of probability is more complex than previously assumed in this debate. Furthermore, I take some initial steps towards a more adequate account of the statistical character of evolutionary theory

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

I defend the view that single experiments can provide a sufficient reason for preferring one among a group of hypotheses against the widely held belief that “crucial experiments” are impossible. My argument is based on the examination of a historical case from molecular biology, namely the Meselson-Stahl experiment. “The most beautiful experiment in biology”, as it is known, provided the first experimental evidence for the operation of a semi-conservative mechanism of DNA replication, as predicted by Watson and Crick in 1953. I use a mechanistic account of explanation to show that this case is best construed as an inference to the best explanation (IBE). Furthermore, I show how such an account can deal with Duhem's well-known arguments against crucial experiments as well as Van Fraassen's “bad lot” argument against IBE.

This paper examines how experimental scientists choose theoretical frameworks as well as their experimental systems for doing research. I start out with Kuhn's claim that there are no algorithms that could determine the coices made by individual scientists. Samir Okasha has recently provided an argument for this claim in terms of social choice theory, which I briefly discuss. Then, I show why this problem is not relevant in an experimental science. There are social mechanisms in place that make sure the community chooses the best framework and a matching experimental system. As historical evidence for this claim, I present the case of classical genetics.

It has been claimed that the intentional stance is necessary to individuate behavioral traits. This thesis, while clearly false, points to two interesting sets of problems concerning biological explanations of behavior: The first is a general in the philosophy of science: the theory-ladenness of observation. The second problem concerns the principles of trait individuation, which is a general problem in philosophy of biology. After discussing some alternatives, I show that one way of individuating the behavioral traits of an organism is by a special use of the concept of biological function, as understood in an enriched causal role (not selected effect) sense. On this view, a behavioral trait is essentially a special kind of regularity, namely a regularity that is produced by some regulatory mechanism. Regulatory mechanisms always require goal states, which can only be provided by functional considerations. As an example from actual (as opposed to folk) science, I examine the case of social behavior in nematodes. I show that the attempt to explain this phenomenon actually transformed it. This supports the view that scientific explanation does not explain an explanandum phenomenon that is given prior to the explanation; rather, the explanandum is changed by the explanation. This means that there could be a plurality of stances that have some heuristic value initially, but which will be abandoned in favor of a functional characterization eventually.

Incommensurability of scientific theories, as conceived by Thomas Kuhnand Paul Feyerabend, is thought to be a major or even insurmountable obstacletothe empirical comparison of these theories. I examine this problem in light ofaconcrete case from the history of experimental biology, namely the oxidativephosphorylation controversy in biochemistry (ca. 1961-1977). After a briefhistorical exposition, I show that the two main competing theories which werethe subject of the ox-phos controversy instantiate some of the characteristicfeatures of incommensurable theories, namely translation failure,non-corresponding predictions, and different claims about what kinds ofentitiesexist in the world. By examining how the controversy was eventually resolved, Ithen show that at least this pair of incommensurable theories couldneverthelessbe empirically compared.

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.