History and Philosophy of the Life Sciences最新文献

Cell biologists, including those seeking molecular mechanistic explanations of cellular phenomena, frequently rely on experimental strategies focused on identifying the cellular context relevant to their investigations. We suggest that such practices can be understood as a guided decomposition strategy, where molecular explanations of phenomena are defined in relation to natural contextual (cell) boundaries. This "top-down" strategy contrasts with "bottom-up" reductionist approaches where well-defined molecular structures and activities are orphaned by their displacement from actual biological functions. We focus on the central role of microscopic imaging in cell biology to uncover possible constraints on the system. We show how identified constraints are used heuristically to limit possible mechanistic explanations to those that are biologically meaningful. Historical examples of this process described here include discovery of the mechanism of oxidative phosphorylation in mitochondria, molecular explanation of the first steps in protein secretion, and identification of molecular motors. We suggest that these instances are examples of a form of downward causation or, more specifically, constraining relations, where higher-level structures and variables delimit and enable lower-level system states. The guided decomposition strategy in our historical cases illustrates the irreducibility of experimentally identified constraints in explaining biological activities of cells. Rather than viewing decomposition and recomposition as separate epistemic activities, we contend that they need to be iteratively integrated to account for the ontological complexity of multi-level systems.

The diagnosis of childhood schizophrenia was widely employed in the U.S. from the 1930s to the late 1970s. In this paper I will provide a history of the diagnosis. Some of the earliest publications on childhood schizophrenia outlined the notion that childhood schizophrenia had different types. I will outline the development of these types, outlining differing symptoms and causes associated with various types. I outline how different types of childhood schizophrenia were demarcated from one another primarily on age of onset and the type of psychosis which was believed to be present. I will outline how various child psychiatrists viewed the types of childhood schizophrenia posited by other child psychiatrists. I will outline the process of abandoning childhood schizophrenia. I use my history to challenge what I believe are misconceptions about childhood schizophrenia. Also, I will use my history to draw lessons for thinking about modern notions of autism. It shows potential problems around formulating psychiatric diagnoses around causes and how compromises might be needed to prevent those problems. Additionally, childhood schizophrenia shows that psychiatrists could formulate subtypes that are not based upon functioning levels and that we can conceive of subtypes as dynamic whereby someone can change which subtype they exhibit over time.

Comparative to the commonplace focus onto developments in mathematics and physics, the life sciences appear to have received relatively sparse attention within the early history of analytic philosophy. This paper addresses two related aspects of this phenomenon. On the one hand, it asks: to the extent that the significance of the life sciences was indeed downplayed by early analytic philosophers, why was this the case? An answer to this question may be found in Bertrand Russell's 1914 discussions of the relation between biology and philosophy. Contrary to received views of the history of analytic philosophy, Russell presented his own 'logical atomism' in opposition not only to British Idealism, but also to 'evolutionism'. On the other hand, I will question whether this purported neglect of the life sciences does indeed accurately characterise the history of analytic philosophy. In answering this, I turn first to Susan Stebbing's criticisms of Russell's overlooking of biology, her influence on J.H. Woodger, and her critical discussion of T.H. Huxley's and C.H. Waddington's application of evolutionary views to philosophical questions. I then discuss the case of Moritz Schlick, whose evolutionist philosophy has been overlooked within recent debates concerning Logical Empiricism's relation to the philosophy of biology.

Drawing on institutional historical records, interviews and student theses, this article charts the intersection of hospital acquired illness, the emergence of antimicrobial resistance (AMR), environments of armed conflict, and larger questions of social governance in the specific case of the American University of Beirut Medical Center (AUBMC) in Lebanon. Taking a methodological cue from approaches in contemporary scientific work that understand non-clinical settings as a fundamental aspect of the history and development of AMR, we treat the hospital as not just nested in a set of social and environmental contexts, but frequently housing within itself elements of social and environmental history. AMR in Lebanon differs in important ways from the settings in which global protocols for infection control or rubrics for risk factor identification for resistant nosocomial outbreaks were originally generated. While such differences are all too often depicted as failures of low and middle-income countries (LMIC) to maintain universal standards, the historical question before us is quite the reverse: how have the putatively universal rubrics of AMR and hospital infection control failed to take account of social and environmental conditions that clearly matter deeply in the evolution and spread of resistance? Focusing on conditions of war as an organized chaos in which social, environmental and clinical factors shift dramatically, on the social and political topography of patient transfer, and on a missing "meso" level of AMR surveillance between the local and global settings, we show how a multisectoral One Health approach to AMR could be enriched by an answering multisectoral methodology in history, particularly one that unsettles a canonical focus on the story of AMR in the Euro-American context.

Since the completion of the Human Genome Project (HGP), biomedical sciences have moved away from a gene-centred view and towards a multi-factorial one in which environment, broadly speaking, plays a central role in the determination of human health and disease. Environmental exposures have been shown to be highly prevalent in disease causation. They are considered as complementary to genetic factors in the etiology of diseases, hence the introduction of the concept of the "exposome" as encompassing the totality of human environmental exposures, from conception onwards (Wild in Cancer Epidemiol Biomark Prev 14:1847-1850, 2005), and the launch of the Human Exposome Project (HEP) which aims to complement the HGP. At first sight, and seen as complementary to the genome, the exposome could thus appear as contributing to the rise of novel postgenomic deterministic narratives which place the environment at their core. Is this really the case? If so, what sort of determinism is at work in exposomics research? Is it a case of environmental determinism, and if so, in what sense? Or is it a new sort of deterministic view? In this paper, we first show that causal narratives in exposomics are still very similar to gene-centred deterministic narratives. They correspond to a form of Laplacian determinism and, above all, to what Claude Bernard called the "determinism of a phenomenon". Second, we introduce the notion of "reversed heuristic determinism" to characterize the specific deterministic narratives present in exposomics. Indeed, the accepted sorts of external environmental exposures conceived as being at the origins of diseases are determined, methodologically speaking, by their identifiable internal and biological markers. We conclude by highlighting the most relevant implications of the presence of this heuristic determinism in exposomics research.

In their anthology Everything Flows: Towards a Processual Philosophy of Biology, Daniel J. Nicholson and John Dupré argue that modern theories of biology imply that the fundamental structure of reality is processual at its core. In the present work, I first examine the implicit and explicit metaphysical presuppositions the editors make in order to allow for such an inference from scientific theory to ontology. After showing the difficulties of a naïve transfer of theoretical entities to fundamental ontology, I argue that the editors can nevertheless extend their claims beyond the mere articulation of different domain ontologies. This leads to the idea of a scientifically informed induction base for an ontology of processes.