Wesley Fang

I propose a dynamic causal approach to characterizing the notion of a mechanism. Levy and Bechtel, among others, have pointed out several critical limitations of the new mechanical philosophy, and pointed in a new direction to extend this philosophy. Nevertheless, they have not fully fleshed out what that extended philosophy would look like. Based on a closer look at neuroscientific practice, I propose that a mechanism is a dynamic causal system that involves various components interacting, typically nonlinearly, with one another to produce a phenomenon of interest.

This essay considers a mixed-effects modeling practice and its implications for the philosophical debate surrounding reductive explanation. Mixed-effects modeling is a species of the multilevel modeling practice, where a single model incorporates simultaneously two (or even more) levels of explanatory variables to explain a phenomenon of interest. I argue that this practice makes the position of explanatory reductionism held by many philosophers untenable because it violates two central tenets of explanatory reductionism: single-level preference and lower-level obsession.

Polger and Shapiro (2016) claim that unlike human-made artifacts cases of multiple realization in naturally occurring systems are uncommon. Drawing on cases from systems biology, I argue that multiple realization in naturally occurring systems is not as uncommon as Polger and Shapiro initially thought. The relevant cases, which I draw from systems biology, involve generalizable design principles called network motifs which recur in different organisms and species and perform specific functions. I show that network motifs with entirely different underlying causal structures can perform the same function of interest. The article also considers the scope problem of multiple realization.

This essay develops an inferential account of model explanation, based on Mauricio Suárez’s inferential conception of scientific representation and Alisa Bokulich’s counterfactual account of model explanation. It is suggested that the fact that a scientific model can explain is essentially linked to how a modeler uses an established model to make various inferences about the target system on the basis of results derived from the model. The inference practice is understood as a two-step activity, with the first step involving making counterfactual statements about the model itself and the second step involving making hypothetical statements transferring over claims derived from the model onto the target. To illustrate how this two-step activity proceeds, an agent-based simulation model is discussed.

Polger and Shapiro argue that their official recipe, a criterion for judging when the phenomenon of multiple realization exists, renders MR less widespread than its proponents have assumed. I argue that, although Polger and Shapiro’s criterion is a useful contribution, they arrive at their conclusion too hastily. Contrary to Polger and Shapiro, I claim that the phenomenon of multiple realization in the biological world, judged by their criterion, is not as scarce as they suggest. To show this, an updated official recipe, namely a multiple mechanistic realization thesis, integrating Polger and Shapiro’s criterion with a compositional conception of realization, is developed. Then, three examples of varied kinds are examined, showing that cases of MR are not so hard to find in the biological world.

Michael Weisberg’s account of scientific models concentrates on the ways in which models are similar to their targets. He intends not merely to explain what similarity consists in, but also to capture similarity judgments made by scientists. In order to scrutinize whether his account fulfills this goal, I outline one common way in which scientists judge whether a model is similar enough to its target, namely maximum likelihood estimation method. Then I consider whether Weisberg’s account could capture the judgments involved in this practice. I argue that his account fails for three reasons. First, his account is simply too abstract to capture what is going on in MLE. Second, it implies an atomistic conception of similarity, while MLE operates in a holistic manner. Third, Weisberg’s atomistic conception of similarity can be traced back to a problematic set-theoretic approach to the structure of models. Finally, I tentatively suggest how these problems might be solved by a holistic approach in which models and targets are compared in a non-set-theoretic fashion

This book argues for the explanatory autonomy of the biological sciences. It does so by showing that scientific explanations in the biological sciences cannot be reduced to explanations in the fundamental sciences such as physics and chemistry and by demonstrating that biological explanations are advanced by models rather than laws of nature. To maintain the explanatory autonomy of the biological sciences, the author argues against explanatory reductionism and shows that explanation in the biological sciences can be achieved without reduction. Then, he demonstrates that the biological sciences do not have laws of nature. Instead of laws, he suggests that biological models usually do the explanatory work. To understand how a biological model can explain phenomena in the world, the author proposes an inferential account of model explanation. The basic idea of this account is that, for a model to be explanatory, it must answer two kinds of questions: counterfactual-dependence questions that concern the model itself and hypothetical questions that concern the relationship between the model and its target system. The reason a biological model can answer these two kinds of questions is due to the fact that a model is a structure, and the holistic relationship between the model and its target warrants the hypothetical inference from the model to its target and thus helps to answer the second kind of question. The Explanatory Autonomy of the Biological Sciences will be of interest to researchers and advanced students working in philosophy of science, philosophy of biology and metaphysics.

In this essay I propose that what design principles in systems biology and systems neuroscience do is to present abstract characterizations of mechanisms, and thereby facilitate mechanistic explanation. To show this, one design principle in systems neuroscience, i.e., the multilayer perceptron, is examined. However, Braillard (2010) contends that design principles provide a sort of non-mechanistic explanation due to two related reasons: they are very general and describe non-causal dependence relationships. In response to this, I argue that, on the one hand, all mechanisms are more or less general (or abstract), and on the other, many (if not all) design principles are causal systems.