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  1. Holly Andersen (2013). When to Expect Violations of Causal Faithfulness and Why It Matters. Philosophy of Science Supplement (5):672-683.
    I present three reasons why philosophers of science should be more concerned about violations of causal faithfulness (CF). In complex evolved systems, mechanisms for maintaining various equilibrium states are highly likely to violate CF. Even when such systems do not precisely violate CF, they may nevertheless generate precisely the same problems for inferring causal structure from probabilistic relationships in data as do genuine CF-violations. Thus, potential CF-violations are particularly germane to experimental science when we rely on probabilistic information to uncover (...)
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  2. Christopher J. Austin (2014). The Dispositional Genome: Primus Inter Pares. Biology and Philosophy:1-20.
    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 (...)
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  3. Tudor M. Baetu (2012). Mechanistic Constraints on Evolutionary Outcomes. Philosophy of Science 79 (2):276-294.
  4. Alain L. Bardou, Pierre M. Auger, Jean-Luc Chasse & Renaud Seigneuric (1997). Theoretical Study of Cardiac Transient Conduction Blocks on Reentries Induction. Applications to Antiarrhythmic Drugs. Acta Biotheoretica 45 (3-4).
    Limitations of antiarrhythmic drugs on cardiac sudden death prevention appeared since the early 80's. The "Cardiac Arrhythmia Suppression Trial"(CAST) showed more recently that mortality was significantly higher inpatients treated with some particular antiarrhythmic drugs than in non-treated patients. In this field, our group recently demonstrated that a bolus of a Class 1B antiarrhythmic drug was able to trigger a ventricular fibrillation due to transient blocks induction. The aim of the present work was to systematically study, by use of the van (...)
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  5. David A. Baum (2013). Developmental Causation and the Problem of Homology. Philosophy and Theory in Biology 5.
    While it is generally agreed that the concept of homology refers to individuated traits that have been inherited from common ancestry, we still lack an adequate account of trait individuation or inheritance. Here I propose that we utilize a counterfactual criterion of causation to link each trait with a developmental-causal (DC) gene. A DC gene is made up of the genetic information (which might or might not be physically contiguous in the genome) that is needed for the production of the (...)
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  6. Brett Calcott (2013). Why How and Why Aren't Enough: More Problems with Mayr's Proximate-Ultimate Distinction. Biology and Philosophy 28 (5):767-780.
    Like Laland et al., I think Mayr’s distinction is problematic, but I identify a further problem with it. I argue that Mayr’s distinction is a false dichotomy, and obscures an important question about evolutionary change. I show how this question, once revealed, sheds light on some debates in evo-devo that Laland et al.’s analysis cannot, and suggest that it provides a different view about how future integration between biological disciplines might proceed.
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  7. Brett Calcott (2013). Why the Proximate–Ultimate Distinction Is Misleading, and Why It Matters for Understanding the Evolution of Cooperation. In Kim Sterelny, Richard Joyce, Brett Calcott & Ben Fraser (eds.), Cooperation and its Evolution. MIT Press. 249.
  8. Gustavo Caponi (2010). La regla de Darwin. Principia 4 (1):27-78.
    Taking as a starting point Brandon's account of the principle of natural selection, we argue that it is possible to consider such a principle as bearing the same status of the principle of causation, to wit, that of a methodological rule whose function would be to introduce a "teleological mode of inquiring the living". This way of understanding the principle of natural selection will drive us into an interpretation of Darwinism that is close to that one argued for by Daniel (...)
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  9. Gustavo Caponi, Claude Bernard, Charles Darwin y los dos modos fundamentales de interrogar lo viviente.
    Research in modern biology has largely been developed according to two main ways of inquiry, as they were outlined by Charles Darwin and Claude Bernard. Each stands for a specific approach to the living corresponding to two different methodological rules: the principle of natural selection and the principle of causation.
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  10. A. Charles Catania (2001). Selection as a Cause Versus the Causes of Selection. Behavioral and Brain Sciences 24 (3):533-533.
    Hull et al. rightly point out the special character of selection as a causal mode, but ironically they seem to force selection back into traditional causal modes by decomposing it into replication, variation, and environmental interaction. Many processes are selective, and a taxonomy of a broad range of kinds of selection may be preferable to narrowing the applicability of the term.
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  11. Hsiang-Ke Chao, Szu-Ting Chen & Roberta L. Millstein (2013). Mechanism and Causality in Biology and Economics. Springer.
    This volume addresses fundamental issues in the philosophy of science in the context of two most intriguing fields: biology and economics. Written by authorities and experts in the philosophy of biology and economics, Mechanism and Causality in Biology and Economics provides a structured study of the concepts of mechanism and causality in these disciplines and draws careful juxtapositions between philosophical apparatus and scientific practice. By exploring the issues that are most salient to the contemporary philosophies of biology and economics and (...)
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  12. Hsiang-Ke Chao, Szu-Ting Chen & Roberta L. Millstein (2013). Towards the Methodological Turn in the Philosophy of Science. In Hsiang-Ke Chao, Szu-Ting Chen & Roberta L. Millstein (eds.), Mechanism and Causality in Biology and Economics. Springer.
    This chapter provides an introduction to the study of the philosophical notions of mechanisms and causality in biology and economics. This chapter sets the stage for this volume, Mechanism and Causality in Biology and Economics, in three ways. First, it gives a broad review of the recent changes and current state of the study of mechanisms and causality in the philosophy of science. Second, consistent with a recent trend in the philosophy of science to focus on scientific practices, it in (...)
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  13. Ken Cheng (2001). Generalization and Tinbergen's Four Whys. Behavioral and Brain Sciences 24 (4):660-661.
    Shepard's exponential law provides a functional explanation of generalization. The account complements the more common mechanistic models. The elegant and powerful analyses answer one of Tinbergen's (1963) four whys of behavior: a benefit conferred on the animal by generalizing in this way. A complete account might address evolutionary and developmental questions in addition to mechanistic and functional ones. [Shepard].
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  14. Brendan Clarke (2012). Causation in Medicine. In Wenceslao J. Gonzalez (ed.), Conceptual Revolutions: from Cognitive Science to Medicine. Netbiblo.
    In this paper, I offer one example of conceptual change. Specifically, I contend that the discovery that viruses could cause cancer represents an excellent example of branch jumping, one of Thagard’s nine forms of conceptual change. Prior to about 1960, cancer was generally regarded as a degenerative, chronic, non-infectious disease. Cancer causation was therefore usually held to be a gradual process of accumulating cellular damage, caused by relatively non-specific component causes, acting over long periods of time. Viral infections, on the (...)
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  15. Brendan Clarke (2011). Causality in Medicine with Particular Reference to the Viral Causation of Cancers. Dissertation, University College London
    In this thesis, I give a metascientific account of causality in medicine. I begin with two historical cases of causal discovery. These are the discovery of the causation of Burkitt’s lymphoma by the Epstein-Barr virus, and of the various viral causes suggested for cervical cancer. These historical cases then support a philosophical discussion of causality in medicine. This begins with an introduction to the Russo- Williamson thesis (RWT), and discussion of a range of counter-arguments against it. Despite these, I argue (...)
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  16. John Collier (1983). Frequency-Dependent Causation: A Defense of Giere. Philosophy of Science 50 (4):618-625.
    Ronald Giere's analysis of causal effectiveness in populations involves the comparison of two hypothetical populations, one in which every individual has the suspected causal factor, and the other in which none do. Elliott Sober has argued that in cases where causal effectiveness depends on relative population sizes, Giere's analysis breaks down. I take issue with this claim, and argue to the contrary that Giere's analysis can help provide insight into these cases.
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  17. Carl F. Craver & William Bechtel (2007). Top-Down Causation Without Top-Down Causes. Biology and Philosophy 22 (4):547-563.
    We argue that intelligible appeals to interlevel causes (top-down and bottom-up) can be understood, without remainder, as appeals to mechanistically mediated effects. Mechanistically mediated effects are hybrids of causal and constitutive relations, where the causal relations are exclusively intralevel. The idea of causation would have to stretch to the breaking point to accommodate interlevel causes. The notion of a mechanistically mediated effect is preferable because it can do all of the required work without appealing to mysterious interlevel causes. When interlevel (...)
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  18. T. E. Dickins & R. A. Barton (2013). Reciprocal Causation and the Proximate–Ultimate Distinction. Biology and Philosophy 28 (5):747-756.
    Laland and colleagues have sought to challenge the proximate–ultimate distinction claiming that it imposes a unidirectional model of causation, is limited in its capacity to account for complex biological phenomena, and hinders progress in biology. In this article the core of their argument is critically analyzed. It is claimed that contrary to their claims Laland et al. rely upon the proximate–ultimate distinction to make their points and that their alternative conception of reciprocal causation refers to phenomena that were already accounted (...)
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  19. Michael R. Dietrich & Roberta L. Millstein (2008). The Role of Causal Processes in the Neutral and Nearly Neutral Theories. Philosophy of Science 75 (5):548-559.
    The neutral and nearly neutral theories of molecular evolution are sometimes characterized as theories about drift alone, where drift is described solely as an outcome, rather than a process. We argue, however, that both selection and drift, as causal processes, are integral parts of both theories. However, the nearly neutral theory explicitly recognizes alleles and/or molecular substitutions that, while engaging in weakly selected causal processes, exhibit outcomes thought to be characteristic of random drift. A narrow focus on outcomes obscures the (...)
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  20. John Dupré (2013). Living Causes. Aristotelian Society Supplementary Volume 87 (1):19-37.
    This paper considers the applicability of standard accounts of causation to living systems. In particular it examines critically the increasing tendency to equate causal explanation with the identification of a mechanism. A range of differences between living systems and paradigm mechanisms are identified and discussed. While in principle it might be possible to accommodate an account of mechanism to these features, the attempt to do so risks reducing the idea of a mechanism to vacuity. It is proposed that the solution (...)
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  21. L. R. Franklin-Hall (forthcoming). Explaining Causal Selection with Explanatory Causal Economy: Biology and Beyond. In P.-A. Braillard & C. Malaterre (eds.), Explanation in Biology: An Enquiry into the Diversity of Explanatory Patterns in the Life Sciences. Springer.
    Among the factors necessary for the occurrence of some event, which of these are selectively highlighted in its explanation and labeled as causes — and which are explanatorily omitted, or relegated to the status of background conditions? Following J. S. Mill, most have thought that only a pragmatic answer to this question was possible. In this paper I suggest we understand this ‘causal selection problem’ in causal-explanatory terms, and propose that explanatory trade-offs between abstraction and stability can provide a principled (...)
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  22. Andy Gardner (2013). Ultimate Explanations Concern the Adaptive Rationale for Organism Design. Biology and Philosophy 28 (5):787-791.
    My understanding is that proximate explanations concern adaptive mechanism and that ultimate explanations concern adaptive rationale. Viewed in this light, the two kinds of explanation are quite distinct, but they interact in a complementary way to give a full understanding of biological adaptations. In contrast, Laland et al. (2013)—following a literal reading of Mayr (Science 134:1501–1506, 1961)—have characterized ultimate explanations as concerning any and all mechanisms that have operated over the course of an organism’s evolutionary history. This has unfortunate consequences, (...)
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  23. Jean Gayon (2005). Chance, Explanation, and Causation in Evolutionary Theory. History and Philosophy of the Life Sciences 27 (3/4):395 - 405.
    Chance comes into plays at many levels of the explanation of the evolutionary process; but the unity of sense of this category is problematic. The purpose of this talk is to clarify the meaning of chance at various levels in evolutionary theory: mutations, genetic drift, genetic revolutions, ecosystems, macroevolution. Three main concepts of chance are found at these various levels: luck (popular concept), randomness (probabilistic concept), and contingency relative to a given theoretical system (epistemological concept). After identifying which concept(s) of (...)
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  24. Alexander Gebharter & Marie I. Kaiser (2014). Causal Graphs and Biological Mechanisms. In Marie I. Kaiser, Oliver Scholz, Daniel Plenge & Andreas Hüttemann (eds.), Explanation in the special sciences: The case of biology and history. Springer. 55-85.
    Modeling mechanisms is central to the biological sciences – for purposes of explanation, prediction, extrapolation, and manipulation. A closer look at the philosophical literature reveals that mechanisms are predominantly modeled in a purely qualitative way. That is, mechanistic models are conceived of as representing how certain entities and activities are spatially and temporally organized so that they bring about the behavior of the mechanism in question. Although this adequately characterizes how mechanisms are represented in biology textbooks, contemporary biological research practice (...)
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  25. Peter Gildenhuys (2010). Causal Equations Without Ceteris Paribus Clauses. Philosophy of Science 77 (4):608-632.
    Some writers have urged that evolutionary theory produces generalizations that hold only ceteris paribus, that is, provided “everything else is equal.” Others have claimed that all laws in the special sciences, or even all laws in science generally, hold only ceteris paribus. However, if we lack a way to determine when everything else really is equal, hedging generalizations with the phrase ceteris paribus renders those generalizations vacuous. I propose a solution to this problem for the case of causal equations from (...)
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  26. Brian C. Goodwin (1985). Problems and Paradigms: What Are the Causes of Morphogenesis? Bioessays 3 (1):32-36.
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  27. James R. Griesemer (1988). Causal Explanation in Laboratory Ecology: The Case of Competitive Indeterminacy. PSA: Proceedings of the Biennial Meeting of the Philosophy of Science Association 1988:337 - 344.
    This paper characterizes the role of the experimenter in causal explanations of laboratory phenomena. Causal explanation rests on appeals to the experimenter's efficacy as a causal agent. I contrast "demographic" and "genetic" explanations of stochastic outcomes in a set of competition experiments in ecology. The demographic view ascribes causes to the experimenter's agency in setting up the experiment and to events within the experimental set-up. The genetic view ascribes causes to an unrecognized effect of the experimenter's sampling process prior to (...)
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  28. David Guez (2009). A Bio-Logical Theory of Animal Learning. Biological Theory 4 (2):148-158.
    This article provides the foundation for a new predictive theory of animal learning that is based upon a simple logical model. The knowledge of experimental subjects at a given time is described using logical equations. These logical equations are then used to predict a subject’s response when presented with a known or a previously unknown situation. This new theory suc- cessfully anticipates phenomena that existing theories predict, as well as phenomena that they cannot. It provides a theoretical account for phenomena (...)
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  29. D. Lynn Holt (1988). Teleological Explanation: A Species of Causal Explanation. Philosophical Psychology 1 (3):313-325.
    Abstract The thesis that teleological explanations are best understood as causal explanations is defended (contra Valentine). I shift the focus of debate from behavior simpliciter to allegedly rational behavior. Teleological explanation, in the case of rational agents, involves reason?giving; and the reasons agents give for acting must be causative of that action if those agents are to be rational in practice. I argue initially that to abandon the claim that reasons are causes of action is to abandon that which renders (...)
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  30. Sui Huang (2014). When Correlation and Causation Coincide. Bioessays 36 (1):1-2.
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  31. Harmon R. Holcomb Iii (1986). Causes, Ends, and the Units of Selection. Philosophy Research Archives 12:519-539.
    This paper inquires into the very possibility of the units of selection debate’s origin in the problem of altruism, function in articulating the evolutionary synthesis, and philosophical status as a problem in clarifying what makes something a level or unit of selection. What makes the debate possible? In terms of origins, there are a number of logically possible ways to deviate from the model of Darwinian individual selection to explain evolved traits. In terms of function, adherence to the evolutionary synthesis (...)
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  32. Michael Joffe (2013). The Concept of Causation in Biology. Erkenntnis 78 (2):179-197.
    This paper sets out to analyze how causation works by focusing on biology, as represented by epidemiology and by scientific information on how the body works (“physiology”). It starts by exploring the specificity of evolved physiological systems, in which evolutionary, developmental and proximal causes all fit together, and the concept of function is meaningful; in contrast, this structure does not apply in epidemiology (or outside biology). Using these two contrasting branches of biology, I examine the role both of mechanism and (...)
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  33. David M. Johnson (1990). Can Abstractions Be Causes? Biology and Philosophy 5 (1):63-77.
    The Empiricist or Lockean view says natural kinds do not exist objectively in nature but are practical categories reflecting use of words. The Modern, Ostensive view says they do exist, and one can refer to such a kind by ostention and recursion, assuming his designation of it is related causally to the kind itself. However, this leads to a problem: Kinds are abstract repeatables, and it seems impossible that abstractions could have causal force. In defence of the Modern view, I (...)
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  34. Jonathan Michael Kaplan (2013). “Relevant Similarity” and the Causes of Biological Evolution: Selection, Fitness, and Statistically Abstractive Explanations. Biology and Philosophy 28 (3):405-421.
    Matthen (Philos Sci 76(4):464–487, 2009) argues that explanations of evolutionary change that appeal to natural selection are statistically abstractive explanations, explanations that ignore some possible explanatory partitions that in fact impact the outcome. This recognition highlights a difficulty with making selective analyses fully rigorous. Natural selection is not about the details of what happens to any particular organism, nor, by extension, to the details of what happens in any particular population. Since selective accounts focus on tendencies, those factors that impact (...)
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  35. Tarja Knuuttila & Andrea Loettgers (2011). Causal Isolation Robustness Analysis: The Combinatorial Strategy of Circadian Clock Research. Biology and Philosophy 26 (5):773-791.
    This paper distinguishes between causal isolation robustness analysis and independent determination robustness analysis and suggests that the triangulation of the results of different epistemic means or activities serves different functions in them. Circadian clock research is presented as a case of causal isolation robustness analysis: in this field researchers made use of the notion of robustness to isolate the assumed mechanism behind the circadian rhythm. However, in contrast to the earlier philosophical case studies on causal isolation robustness analysis (Weisberg and (...)
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  36. Y. H. Krikorian (1949). Teleology and Causality. Review of Metaphysics 2 (8):35 - 46.
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  37. Kevin N. Laland, John Odling-Smee, William Hoppitt & Tobias Uller (2013). More on How and Why: Cause and Effect in Biology Revisited. Biology and Philosophy 28 (5):719-745.
    In 1961, Ernst Mayr published a highly influential article on the nature of causation in biology, in which he distinguished between proximate and ultimate causes. Mayr argued that proximate causes (e.g. physiological factors) and ultimate causes (e.g. natural selection) addressed distinct ‘how’ and ‘why’ questions and were not competing alternatives. That distinction retains explanatory value today. However, the adoption of Mayr’s heuristic led to the widespread belief that ontogenetic processes are irrelevant to evolutionary questions, a belief that has (1) hindered (...)
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  38. Kevin N. Laland, John Odling-Smee, William Hoppitt & Tobias Uller (2013). More on How and Why: A Response to Commentaries. Biology and Philosophy 28 (5):793-810.
    We are grateful to the commentators for taking the time to respond to our article. Too many interesting and important points have been raised for us to tackle them all in this response, and so in the below we have sought to draw out the major themes. These include problems with both the term ‘ultimate causation’ and the proximate-ultimate causation dichotomy more generally, clarification of the meaning of reciprocal causation, discussion of issues related to the nature of development and phenotypic (...)
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  39. Gisela Loeck (1991). Aristotle's Technical Simulation and its Logic of Causal Relations. History and Philosophy of the Life Sciences 13 (1):3 - 32.
    The paper investigates Aristotle's simulation of the embryo (zygote) by a gear wheel mechanism. By this technical simulation of a natural thing Aristotle pursues an epistemic end, viz. to gain information on the efficient cause of embryonal development. Aristotle verifies the conjectured, yet unknown efficient cause of this natural process by means of a distinctive mapping of the artifact onto the embryo. The paper aims to show that Aristotle, to achieve this verification, tackles a calculus of relations with a semantics (...)
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  40. A. H. Louie (2008). Functional Entailment and Immanent Causation in Relational Biology. Axiomathes 18 (3):289-302.
    I explicate the crucial role played by efficient cause in Robert Rosen’s characterization of life, by elaborating on the topic of Aristotelian causality, and exploring the many alternate descriptions of causal and inferential entailments. In particular, I discuss the concepts of functional entailment and immanent causation, and examine how they fit into Robert Rosen’s relational-biology universe of living, anticipatory, and complex systems.
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  41. Kevin MacDonald (1999). What About Sex Differences? An Adaptationist Perspective on “the Lines of Causal Influence” of Personality Systems. Behavioral and Brain Sciences 22 (3):530-531.
    The evolutionary theory of sex implies a theoretically principled account of the causal mechanisms underlying personality systems in which males pursue a relatively high-risk strategy compared to females and are thus higher on traits linked to sensation seeking and social dominance. Females are expected to be lower on these traits but higher on traits related to nurturance and attraction to long-term relationships. The data confirm this pattern of sex differences. It is thus likely that these traits have (...)
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  42. Maximiliano Martinez & Maurizio Esposito (2014). Multilevel Causation and the Extended Synthesis. Biological Theory 9.
    In this article we argue that the classical—linear and bottom-up directed—models of causation in biology, and the ‘‘proximate/ultimate’’ dichotomy, are inappropriate to capture the complexity inherent to biological processes. We introduce a new notion of ‘‘multilevel causation’’ where old dichotomies such as proximate/ultimate and bottom-up/ top-down are reinterpreted within a multilevel, web-like, approach. In briefly reviewing some recent work on complexity, EvoDevo, carcinogenesis, autocatalysis, comparative genomics, animal regeneration, phenotypic plasticity, and niche construction, we will argue that such reinterpretation is a (...)
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  43. Maximiliano Martínez & Andrés Moya (2011). Natural Selection and Multi-Level Causation. Philosophy and Theory in Biology 3 (20130604).
    In this paper, using a multilevel approach, we defend the positive role of natural selection in the generation of organismal form. Despite the currently widespread opinion that natural selection only plays a negative role in the evolution of form, we argue, in contrast, that the Darwinian factor is a crucial (but not exclusive) factor in morphological organization. Analyzing some classic arguments, we propose incorporating the notion of ‘downward causation’ into the concept of ‘natural selection.’ In our opinion, this kind of (...)
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  44. Mohan Matthen & André Ariew (2009). Selection and Causation. Philosophy of Science 76 (2):201-224.
    We have argued elsewhere that: (A) Natural selection is not a cause of evolution. (B) A resolution-of-forces (or vector addition) model does not provide us with a proper understanding of how natural selection combines with other evolutionary influences. These propositions have come in for criticism recently, and here we clarify and defend them. We do so within the broad framework of our own “hierarchical realization model” of how evolutionary influences combine.
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  45. Mohan Matthen & André Ariew (2009). Selection and Causation. Philosophy of Science 76 (2):201-224.
    We have argued elsewhere that: (A) Natural selection is not a cause of evolution. (B) A resolution-of-forces (or vector addition) model does not provide us with a proper understanding of how natural selection combines with other evolutionary influences. These propositions have come in for criticism recently, and here we clarify and defend them. We do so within the broad framework of our own “hierarchical realization model” of how evolutionary influences combine.
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  46. Mohan Matthen & André Ariew (2002). Two Ways of Thinking About Fitness and Natural Selection. Journal of Philosophy 99 (2):55-83.
    How do fitness and natural selection relate to other evolutionary factors like architectural constraint, mode of reproduction, and drift? In one way of thinking, drawn from Newtonian dynamics, fitness is one force driving evolutionary change and added to other factors. In another, drawn from statistical thermodynamics, it is a statistical trend that manifests itself in natural selection histories. It is argued that the first model is incoherent, the second appropriate; a hierarchical realization model is proposed as a basis for a (...)
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  47. Mohan Matthen & Edwin Levy (1984). Teleology, Error, and the Human Immune System. Journal of Philosophy 81 (7):351-372.
    The authors attempt to show that certain forms of behavior of the human immune system are illuminatingly regarded as errors in that system's operation. Since error-ascription can occur only within the context of an intentional/teleological characterization of the system, it follows that such a characterization is illuminating. It is argued that error-ascription is objective, non-anthropomorphic, irreducible to any purely causal form of explanation of the same behavior, and further that it is wrong to regard all errors of the immune system (...)
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  48. Armand Maurer (2004). Darwin, Thomists, and Secondary Causality. Review of Metaphysics 57 (3):491 - 514.
  49. Ernst Mayr (1993). Proximate and Ultimate Causations. Biology and Philosophy 8 (1):93-94.
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  50. Alexander Mebius (2014). A Weakened Mechanism is Still a Mechanism: On the Causal Role of Absences in Mechanistic Explanation. Studies in History and Philosophy of Science Part C: Studies in History and Philosophy of Biological and Biomedical Sciences 45:43-48.
    Much contemporary debate on the nature of mechanisms centers on the issue of modulating negative causes. One type of negative causability, which I refer to as “causation by absence,” appears difficult to incorporate into modern accounts of mechanistic explanation. This paper argues that a recent attempt to resolve this problem, proposed by Benjamin Barros, requires improvement as it overlooks the fact that not all absences qualify as sources of mechanism failure. I suggest that there are a number of additional types (...)
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