The presence and role of microbes in human cancers has come full circle in the last century. Tumors are no longer considered aseptic, but implications for cancer biology and oncology remain underappreciated. Opportunities to identify and build translational diagnostics, prognostics, and therapeutics that exploit cancer's second genome—the metagenome—are manifold, but require careful consideration of microbial experimental idiosyncrasies that are distinct from host‐centric methods. Furthermore, the discoveries of intracellular and intra‐metastatic cancer bacteria necessitate fundamental changes in describing clonal evolution (...) and selection, reflecting bidirectional interactions with non‐human residents. Reconsidering cancer clonality as a multispecies process similarly holds key implications for understanding metastasis and prognosing therapeutic resistance while providing rational guidance for the next generation of bacterial cancer therapies. Guided by these new findings and challenges, this Review describes opportunities to exploit cancer's metagenome in oncology and proposes an evolutionary framework as a first step towards modeling multispecies cancer clonality. Also see the video abstract here: https://youtu.be/-WDtIRJYZSs. (shrink)

From carrots to frogs to sheep and finally to humans, the history of cloning is a fascinating study of the interplay between science and popular culture. Imagination and discovery provide mutual impetus in the evolving science and cultural phenomenon of cloning. Its history is a paradigm of science unfiction: What once belonged unequivocally on the pages of science fiction is now emerging in flesh and blood. Writers, movie producers, ethicists, and all manner of social commentators, no less than scientists, have (...) all participated in the creation of the human clone as an idea and as a biological entity. While the clone stands apart as having only one genetic parent, it truly is a brainchild of multifarious origins. (shrink)

The clonal evolution model and the cancer stem cell model are two independent models of cancers, yet recent data shows intersections between the two models. This article explores the impacts of the CSC model on the CE model. I show that CSC restriction, which depends on CSC frequency in cancer cell populations and on the probability of dedifferentiation of cancer non-stem cells into CSCs, can favor or impede some patterns of evolution and some processes of evolution. (...) Taking CSC restriction into account for the CE model thus has implications for the way in which we understand the patterns and processes of evolution, and can also provide new leads for therapeutic interventions. (shrink)

Originating in the work of Ernst Haeckel and Wilhelm Preyer, and advanced by a Prussian embryologist, Wilhelm Roux, the idea of struggle for existence between body parts helped to establish a framework, in which population cell dynamics rather than a predefined harmony guides adaptive changes in an organism. Intended to provide a causal-mechanical view of functional adjustments in body parts, this framework was also embraced later by early pioneers of immunology to address the question of vaccine effectiveness and pathogen resistance. (...) As an extension of these early efforts, Elie Metchnikoff established an evolutionary vision of immunity, development, pathology, and senescence, in which phagocyte-driven selection and struggle promote adaptive changes in an organism. Despite its promising start, the idea of somatic evolution lost its appeal at the turn of the twentieth century giving way to a vision, in which an organism operates as a genetically uniform, harmonious entity. (shrink)

All surviving jawed vertebrate representatives achieve diversity in immunoglobulin‐based B and T cell receptors for antigen recognition through recombinatorial rearrangement of V(D)J segments. However, the extant jawless vertebrates, lampreys and hagfish, instead generate three types of variable lymphocyte receptors (VLRs) through a template‐mediated combinatorial assembly of different leucine‐rich repeat (LRR) sequences. The clonally diverse VLRB receptors are expressed by B‐like lymphocytes, while the VLRA and VLRC receptors are expressed by lymphocyte lineages that resemble αβ and γδ T lymphocytes, respectively. These (...) findings suggest that three basic types of lymphocytes, one B‐like and two T‐like, are an essential feature of vertebrate adaptive immunity. Around 500 million years ago, a common ancestor of jawed and jawless vertebrates evolved a genetic program for the development of prototypic lymphoid cells as a foundation for an adaptive immune system. This acquisition preceded the convergent evolution of alternative types of clonally diverse receptors for antigens in all vertebrates, as reviewed in this article. (shrink)

Few topics have intrigued biologists as much as the evolution of sex. Understanding why sex persists despite its costs requires not just rigorous theoretical study, but also empirical data on related fundamental issues, including the nature of genetic variance for fitness, patterns of genetic interactions, and the dynamics of adaptation. The increasing feasibility of examining genomes in an experimental context is now shedding new light on these problems. Using this approach, McDonald et al. recently demonstrated that sex uncouples beneficial (...) and deleterious mutations, allowing selection to proceed more effectively with sex than without. Here we discuss the insights provided by this study, along with other recent empirical work, in the context of the major theoretical models for the evolution of sex. (shrink)

Cancers rely on multiple, heterogeneous processes at different scales, pertaining to many biomedical fields. Therefore, understanding cancer is necessarily an interdisciplinary task that requires placing specialised experimental and clinical research into a broader conceptual, theoretical, and methodological framework. Without such a framework, oncology will collect piecemeal results, with scant dialogue between the different scientific communities studying cancer. We argue that one important way forward in service of a more successful dialogue is through greater integration of applied sciences (experimental and clinical) (...) with conceptual and theoretical approaches, informed by philosophical methods. By way of illustration, we explore six central themes: (i) the role of mutations in cancer; (ii) the clonal evolution of cancer cells; (iii) the relationship between cancer and multicellularity; (iv) the tumour microenvironment; (v) the immune system; and (vi) stem cells. In each case, we examine open questions in the scientific literature through a philosophical methodology and show the benefit of such a synergy for the scientific and medical understanding of cancer. (shrink)

The extent to which normal (nonmalignant) cells of the body can evolve through mutation and selection during the lifetime of the organism has been a major unresolved issue in evolutionary and developmental studies. On the one hand, stable multicellular individuality seems to depend on genetic homogeneity and suppression of evolutionary conflicts at the cellular level. On the other hand, the example of clonal selection of lymphocytes indicates that certain forms of somatic mutation and selection are concordant with the organism-level (...) fitness. Recent DNA sequencing and tissue physiology studies suggest that in addition to adaptive immune cells also neurons, epithelial cells, epidermal cells, hematopoietic stem cells and functional cells in solid bodily organs are subject to evolutionary forces during the lifetime of an organism. Here we refer to these recent studies and suggest that the expanding list of somatically evolving cells modifies idealized views of biological individuals as radically different from collectives. (shrink)

Recent studies of prostate cancer and other tumor types have revealed significant support, as well as unexpected complexities, for the application of concepts from normal stem cell biology to cancer. In particular, the cell of origin and cancer stem cell models have been proposed to explain the heterogeneity of tumors during the initiation, propagation, and evolution of cancer. Thus, a basis of intertumor heterogeneity has emerged from studies investigating whether stem cells and/or non‐stem cells can serve as cells of (...) origin for cancer and give rise to tumor subtypes that vary in disease outcome. Furthermore, analyses of putative cancer stem cells have revealed the genetically diverse nature of cancers and expanded our understanding of intratumor heterogeneity and clonal evolution. Overall, the principles that have emerged from these stem cell studies highlight the challenges to be surmounted to develop effective treatment strategies for cancer. (shrink)

Clonal disease is often regarded as almost synonymous with cancer. However, it is becoming increasingly clear that our bodies harbor numerous mutant clones that are not tumors, and mostly give rise to no disease at all. Here we discuss three somatic mutations arising within the hematopoietic system: BCR‐ABL, characteristic of chronic myeloid leukemia; mutations of the PIG‐A gene, characteristic of paroxysmal nocturnal hemoglobinuria; the V617F mutation in the JAK2 gene, characteristic of myeloproliferative diseases. The population frequencies of these three (...) blood disorders fit well with a hierarchical model of hematopoiesis. The fate of any mutant clone will depend on the target cell and on the fitness advantage, if any, that the mutation confers on the cell. In general, we can expect that only a mutation in a hematopoietic stem cell will give long‐term disease; the same mutation taking place in a cell located more downstream may produce just a ripple in the hematopoietic ocean. (shrink)

Ecological fitness has been suggested to provide a unifying definition of fitness. However, a metric for this notion of fitness was in most cases unavailable except by proxy with differential reproductive success. In this article, I show how differential persistence of lineages can be used as a way to assess ecological fitness. This view is inspired by a better understanding of the evolution of some clonal plants, colonial organisms, and ecosystems. Differential persistence shows the limitation of an ensemblist (...) noncausal understanding of evolution. Causal explanations are necessary to understand the evolution by natural selection of these biological systems. †To contact the author write to: Department of Philosophy, University of Montreal, P.O. Box 6128, Station Centre‐Ville, Montreal, Quebec, H3C 3J7 Canada; e‐mail: [email protected]. (shrink)

Here I advance two related evolutionary propositions. (1) Natural selection is most often considered to require competition between reproducing “individuals”, sometimes quite broadly conceived, as in cases of clonal, species or multispecies-community selection. But differential survival of non-competing and non-reproducing individuals will also result in increasing frequencies of survival-promoting “adaptations” among survivors, and thus is also a kind of natural selection. (2) Darwinists have challenged the view that the Earth’s biosphere is an evolved global homeostatic system. Since there is (...) only one biosphere, reproductive competition cannot have been involved in selection for such survival-promoting adaptations, they claim. But natural selection through survival could reconcile Gaia with evolutionary theory. (shrink)

Cancer is generally defined as uncontrollable growth of cells caused by genetic aberrations and/or environmental factors. Yet contagious cancers also occur. The recent emergence of a contagious cancer in Tasmanian devils has reignited interest in transmissible cancers. Two naturally occurring transmissible cancers are known: devil facial tumour disease and canine transmissible venereal tumour. Both cancers evolved once and have then been transmitted from one individual to another as clonal cell lines. The dog cancer is ancient; having evolved more than (...) 6,000 years ago, while the devil disease was first seen in 1996. In this review I will compare and contrast the two diseases focusing on the life histories of the clonal cell lines, their evolutionary trajectories and the mechanisms by which they have achieved immune tolerance. A greater understanding of these contagious cancers will provide unique insights into the role of the immune system in shaping tumour evolution and may uncover novel approaches for treating human cancer. (shrink)

In multicellular organisms, cells are frequently programmed to die. This makes good sense: cells that fail to, or are no longer playing important roles are eliminated. From the cell’s perspective, this also makes sense, since somatic cells in multicellular organisms require the cooperation of clonal relatives. In unicellular organisms, however, programmed cell death poses a difficult and unresolved evolutionary problem. The empirical evidence for PCD in diverse microbial taxa has spurred debates about what precisely PCD means in the case (...) of unicellular organisms. In this article, we survey the concepts of PCD in the literature and the selective pressures associated with its evolution. We show that definitions of PCD have been almost entirely mechanistic and fail to separate questions concerning what PCD fundamentally is from questions about the kinds of mechanisms that realize PCD. We conclude that an evolutionary definition is best able to distinguish PCD from closely related phenomena. Specifically, we define “true” PCD as an adaptation for death triggered by abiotic or biotic environmental stresses. True PCD is thus not only an evolutionary product but must also have been a target of selection. Apparent PCD resulting from pleiotropy, genetic drift, or trade-offs is not true PCD. We call this “ersatz PCD.”. (shrink)

The risk of cigarette smoking plays a pivotal role in increasing the incidence rates of lung cancer. This paper sheds new light on modeling the impact of cigarette smoking on lung cancer evolution, especially genetic instability and the number of gene mutations in the genome of stem cells. To handle this issue, we have set up stochastic multi-stage models to fit the data set of the probabilities of current and former smokers from the Nurses’ Health Study cohort of females (...) and the Health Professionals Follow up Study cohort of men. Throughout this paper, we consider both mutation rates and clonal expansion rates as parameters in each compartment. For current and former smokers, three-driver mutations are most likely to take place in the progression of lung cancer under smoking risk. For current smokers, our findings reveal that two to sixteen gene mutations are required to obtain a cancerous cell among men and women in US. Moreover, two to six cancer-mutations are available in the pathway to lung cancer among former smokers who have quit smoking for more than ten years for both male and female patients. This highlights that cigarette smoking stimulates the number of driver mutations during lung tumorigenesis in both sexes. It is very crucial to examine the role of cigarette smoking in determining whether genomic instability is an early stage or late stage in the process of lung carcinogenesis. (shrink)

B‐cell acute lymphoblastic leukaemia (B‐ALL) is a clonal malignant disease originated in a single cell and characterized by the accumulation of blast cells that are phenotypically reminiscent of normal stages of B‐cell differentiation. B‐ALL origin has been a subject of continuing discussion, given the fact that human disease is diagnosed at late stages and cannot be monitored during its natural evolution from its cell of origin, although most B‐ALLs probably start off with chromosomal changes in haematopoietic stem cells. (...) However, the cells responsible for maintaining the disease appear to differ between the different types of B‐ALLs and this remains an intriguing and exciting topic of research, since these cells have been posited to be responsible for resistance to conventional therapies, recurrence and dissemination. During the last years this problem has been addressed primarily by transplantation of purified subpopulations of human B‐ALL cells into immunodeficient mice. The results from these different reconstitution experiments and their interpretations are compared in this review in the context of normal B‐cell developmental plasticity. While the results from different research groups might appear mutually exclusive, we discuss how they could be reconciled with the biology of normal B‐cells and propose research avenues for addressing these issues in the future. (shrink)

Bacteria do many things as organized populations. We have recently learned much about the molecular basis of intercellular communication among prokaryotes. Colonies display bacterial capacities for multicellular coordination which can be useful in nature where bacteria predominantly grow as films, chains, mats and colonies. E. coli colonies are organized into differentiated non-clonal populations and undergo complex morphogenesis. Multicellularity regulates many aspects of bacterial physiology, including DNA rearrangement systems. In some bacterial species, colony development involves swarming (active migration of cell (...) groups). Swarm colony development displays precise geometrical controls and periodic phenomena. Motile E. coli cells in semi-solid media form organized patterns due to chemotactic autoaggregation. On poor media, B. subtilis forms branched colonies using group motility and long-range chemical signalling. The significances of bacterial colony patterns thus reside in a deeper understanding of prokaryotic biology and evolution and in experimental systems for studying self-organization and morphogenesis. (shrink)

Variation or rearrangement of regulatory genes is responsible for cellular malignant change. These types of chromosomal variations also produce heterochrony or paedomorphic evolution at the organismal level. Analogously, neoplasia represents a cellular macroevolutionary event, and a tumour can be said to be an evolved population of cells. To understand this cellular evolution to malignancy, it may be necessary to go beyond a clonal selection (adaptationist) explanation of neoplastic alteration. In the pericellular environment natural selection consists of the (...) organizational restraints of surrounding cells as well as the host's immunological surveillance and non-specific monocyte-macrophage systems. Indirect evidence suggests that success for the neoplasm depends not upon clonal selection, but solely upon a genetic methodology—the function of which is to elude selection.The author has coined the term cellular heterochrony to illustrate analogic similarities in the molecular modes of speciation between anaplastic cancer cells and the heterochronic evolution of organisms. By reverting to a juvenile (embryonic) repertoire of cellular behaviour a tumour secures its own tenure or niche by usurping the host's armamentarium of selection forces, employing many of the same or similar methods by which implanting and invading tissues of the mammalian embryo forestall maternal detection and rejection. A number of ways by which the tumour blocks, subverts or evades selection are discussed. (shrink)

The current mainstream in cancer research favours the idea that malignant tumour initiation is the result of a genetic mutation. Tumour development and progression is then explained as a sort of micro-evolutionary process, whereby an initial genetic alteration leads to abnormal proliferation of a single cell that leads to a population of clonally derived cells. It is widely claimed that tumour progression is driven by natural selection, based on the assumption that the initial tumour cells acquire some properties that endow (...) such cells with a selective advantage over the normal cells from which the tumour cells are derived. The standard view assumes that the transformed bodily cell somehow acquires "responsiveness" to natural selection independently of the whole organism to which the cell belongs. Yet, it is never explained where such an acquired capacity to respond to natural selection by the individual bodily cell comes from. This situation poses many difficult questions that so far have been left unanswered. For example, there is no explanation why some cells belonging to an organised whole and as such having no independent capacity for survival, apparently become 'independent' entities, able to respond to selective pressures in an autonomous fashion and then to be evaluated by natural selection. Hereunder it is argued that such a qualitative change cannot be the consequence of specific genetic mutations. Moreover, it is shown that natural selection is unlikely to be acting within the organism during tumour development and progression and that tumour evolution is a random, non-adaptive process, driven by no fundamental biological principle. Thus, mutations in the so-called oncogenes and tumour suppressor genes observed in epithelial cancers (that constitute more than 90% of all cancers) are not the result of selection for better cellular growth or survival under restrictive conditions. Instead, here it is suggested that they are the consequence of genetic drift acting upon gene functions that become non-relevant, either for the individual or the species fitness, once the organism is past its reproductive prime and as such, they also become superfluous for cell survival in the short term. It is proposed that the origin of cancer is epigenetic and it is a consequence of the need for a continued turnover of the individuals that constitute a species. (shrink)

The male gametes of most organisms lack cytoplasm. Consequently, most cytoplasmic genetic elements are maternally inherited: they cannot be transmitted patrilinnearly. The evolutionary interests of cytoplasmic elements therefore lie in transmission through the female. These elements may thus be in evolutionary conflict with nuclear genes which are transmitted by both sexes. This conflict is manifested in observations of cytoplasmically induced biased sex‐ratios. Some cytoplasmic genes avoid this fate by biasing the primary sex ratio towards females, or by inducing parthenogenesis. Others (...) kill male hosts, and either achieve transmission via dispersal, or benefit their clonal relatives in the dead male's female siblings. Still others cause the failure of zygotes resulting from pairings between males carrying specific microbes and females lacking them, causing an increase in the microbes through the sterilisation of non‐bearing females. Many, but not all, of these ‘ultra‐selfish’ microbes are closely related. Investigations of the significance of their phylogenetic affinities, or lack of them, their adaptability in terms of the methods by which they avoid, or ameliorate, the adverse effects of being in male hosts, and their importance as selective agents in the evolution of invertebrate sex determination systems, provide fertile spheres for future research. (shrink)

The vertebrate adaptive immune system has well defined functions in maintaining tolerance to self‐tissues. Suppression of autoreactive T cells is dependent on the regulatory cytokine transforming growth factor‐β (TGF‐β) and regulatory T (Treg) cells, a distinct T cell lineage specified by the transcription factor Foxp3. Although TGF‐β promotes thymic Treg (tTreg) cell development by repressing T cell clonal deletion and peripheral Treg cell differentiation by inducing Foxp3 expression, a recent study shows that TGF‐β suppresses autoreactive T cells independent of (...) Foxp3+ Treg cells. These findings imply that as an ancestral growth factor family member, TGF‐β may have been co‐opted as a T cell‐intrinsic mechanism of self‐tolerance control to assist the evolutionary transition of vertebrate adaptive immunity. Later, perhaps in placental mammals upon their acquisition of a TGF‐β regulatory element in the Foxp3 locus, the TGF‐β pathway is further engaged to induce peripheral Treg cell differentiation and expand the scope of T cell tolerance control to innocuous foreign antigens. (shrink)

According to a once influential view of selection, it consists of repeated cycles of replication and interaction. It has been argued that this view is wrong: replication is not necessary for evolution by natural selection. I analyze the nine most influential arguments for this claim and defend the replication–interaction conception of selection against these objections. In order to do so, however, the replication–interaction conception of selection needs to be modified significantly. My proposal is that replication is not the copying (...) of an entity, the replicator, but the copying of a property. Thus, we can have a replication process without there being a replicator that is being copied. (shrink)

Here, we propose that the heterogeneity of mutational types in populations underpins alternative pathways of evolutionary adaptation. Point mutations, deletions, insertions, transpositions and duplications cause different biological effects and provide distinct adaptive possibilities. Experimental evidence for this notion comes from the mutational origins of adaptive radiations in large, clonal bacterial populations. Independent sympatric lineages with different phenotypes arise from distinct genetic events including gene duplication, different insertion sequence movements and several independent point mutations. The breadth of the mutational spectrum (...) in the ancestral population should be viewed as a form of bet‐hedging, reducing the risk of evolutionary dead ends and complementing the phenotypic and epigenetic heterogeneities that improve the survival capabilities of a population. Different mutational events arise from distinct cellular processes and are subject to separate environmental impacts, so the availability of any particular type of mutation may constrain or promote adaptive pathways in populations. (shrink)

In the Preface of Animal Species and Evolution (1963), I wrote that it was "an attempt to summarize and review critically what we know about the biology and genetics of animal species and their role in evolution." The result was a volume of XIV ...

Robert Boyd*†, Herbert Gintis‡, Samuel Bowles§, and Peter J. Richerson¶.

Since Darwin, the idea of psychological continuity between humans and other animals has dominated theory and research in investigating the minds of other species. Indeed, the field of comparative psychology was founded on two assumptions. First, it was assumed that introspection could provide humans with reliable knowledge about the causal connection between specific mental states and specific behaviors. Second, it was assumed that in those cases in which other species exhibited behaviors similar to our own, similar psychological causes were at (...) work. In this paper. we show how this argument by analogy is flowed with respect to the case of second-order mental states. As a test case, we focus on the question of how other species conceive of visual attention, and in particular whether chimpanzees interpret seeing as a mentalistic event involving internal states of perception, attention, and belief. We conclude that chimpanzees do not reason about seeing in this manner, and indeed, there is considerable reason to suppose that they do not harbor representations of mental states in general. We propose a reinterpretation model in which the majority of the rich social behaviors that humans and other primates share in common emerged long before the human lineage evolved the psychological means of interpreting those behaviors in mentalistic terms. Although humans, chimpanzees, and most other species may be said to possess mental states, humans alone may have evolved a cognitive specialization for reasoning about such states. (shrink)

Evolutionary theory relevant to the question of human cooperation is reviewed and compared to other theoretical perspectives. A compound explanation is distilled as a plausible account of human cooperation and selfishness. This account leans heavily on group selection on cultural variation but also includes lower-level forces driven by both micro-scale cooperation and purely selfish motives. It is proposed that innate aspects of human social psychology coevolved with group-selected cultural institutions to produce just the kinds of social and moral faculties originally (...) proposed by Darwin. This is termed the “tribal social instincts” hypothesis. The account is systemic in the sense that human social systems are functionally differentiated, conflicted, and diverse. A successful explanation of human cooperation has to account for these complexities. For example, a tribal-scale cultural group selection process alone cannot account for human patterns of cooperation because, on one hand, much conflict exists within tribes and, on the other, people have proven able to organize cooperation on a much larger scale than tribes. Multilevel selection and gene-culture coevolution effects are included to account for some of these complexities and empirical tests of the resulting hypotheses are discussed. In particular, it is argued that strong support for the tribal social instincts hypothesis comes from the structure of modern social institutions. These institutions have conspicuous “work-arounds” that shed light on the underlying instincts. (shrink)

In this ground-breaking book, a renowned bioethicist argues that the political left must radically revise its outdated view of human nature. He shows how the insights of modern evolutionary theory, particularly on the evolution of cooperation, can help the left attain its social and political goals. Singer explains why the left originally rejected Darwinian thought and why these reasons are no longer viable. He discusses how twentieth-century thinking has transformed our understanding of Darwinian evolution, showing that it is (...) compatible with cooperation as well as competition, and that the left can draw on this modern understanding to foster cooperation for socially desirable ends. A Darwinian left, says Singer, would still be on the side of the weak, poor, and oppressed, but it would have a better understanding of what social and economic changes would really work to benefit them. It would also work toward a higher moral status for nonhuman animals and a less anthropocentric view of our dominance over nature. (shrink)

Michael Ruse, a leading expert on Charles Darwin, presents a fictional dialogue among characters with sharply contrasting positions regarding the tensions between science and religious belief.

Sir John Eccles, a distinguished scientist and Nobel Prize winner who has devoted his scientific life to the study of the mammalian brain, tells the story of how we came to be, not only as animals at the end of the hominid evolutionary line, but also as human persons possessed of reflective consciousness.

In den Aufsätzen dieses Bandes präsentiert Anton Friedrich Koch Hegels theoretische Philosophie als diejenige Nichtstandard-Metaphysik, in der sich die Metaphysik, nicht aber die Philosophie vollendet. Jenseits von Hegels Evolutionstheorie des Absoluten gilt es von einem Standpunkt der Endlichkeit aus neu zu philosophieren.

Evolutionary theodicies are attempts to explain how the enormous amounts of suffering, premature death and extinction inherent in the evolutionary process can be reconciled with belief in a loving and almighty God. A common strategy in this area is to argue that certain very valuable creaturely attributes could only be exemplified by creatures that are produced by a partly random and uncontrolled process of evolution. Evolution, in other words, was the only possible way for God to create these (...) kinds of creatures. This article presents and examines two versions of the “only way”-argument. The anthropocentric version tries to justify God’s use of evolution by reference to the value of human freedom, and argues that freedom presupposes that God lets go of full control over the process of creation . The non-anthropocentric version presents a similar argument with respect to more inclusive creaturely properties, such as that of being “truly other” than God, or of being a “creaturely self” with a certain degree of autonomy in relation to God . With the help of a number of thought-experiments of the “Twin-Earth”-type, the author argues that both the anthropocentric and the non-anthropocentric only way-arguments fail. (shrink)

Brackets and tables, circles and maps, 1554-1872 -- Early botanical networks and trees, 1766-1815 -- The first evolutionary tree, 1786-1820 -- Diverse and unusual trees of the early nineteenth century, 1817-1834 -- The rule of five, 1819-1854 -- Pre-Darwinian branching diagrams, 1828-1858 -- Evolution and the trees of Charles Darwin, 1837-1868 -- The trees of Ernst Haeckel, 1866-1905 -- Post-Darwinian nonconformists, 1868-1896 -- More late-nineteenth-century trees, 1874-1897 -- Trees of the early twentieth century, 1901-1930 -- The trees of Alfred (...) Sherwood Romer, 1933-1966 -- Additional trees of the mid-twentieth century, 1931-1943 -- The trees of William King Gregory, 1938-1951 -- Hints of new approaches, 1954-1969 -- Phenograms and cladograms, 1958-1966 -- Early molecular trees, 1962-1987 -- Notable trees of the past four decades, 1970-2010 -- Primeval branches and universal trees of life, 1997-2010. (shrink)

_Examines John Dewey’s ideas in the context of evolutionary theory._.

Darwinian evolutionary theory has two key terms, variations and biological selection, which finally lead to survival of the fittest variant. With the rise of molecular genetics, variations were explained as results of error replications out of the genetic master templates. For more than half a century, it has been accepted that new genetic information is mostly derived from random error-based events. But the error replication narrative has problems explaining the sudden emergence of new species, new phenotypic traits, and genome innovations (...) as a sudden single event. Meanwhile, it is recognized that errors cannot explain the evolution of genetic information, genetic novelty, and complexity. Now, empirical evidence establishes the crucial role of non-random genetic content editors, such as viruses, diversity generating retroelements, and other RNA networks, to produce new genetic information, complex regulatory control, inheritance vectors, genetic identity, immunity, new sequence space, evolution of complex organisms, and evolutionary transitions. (shrink)

Sir John Eccles, a distinguished scientist and Nobel Prize winner who has devoted his scientific life to the study of the mammalian brain, tells the story of how we came to be, not only as animals at the end of the hominid evolutionary line, but also as human persons possessed of reflective consciousness.

Examines the relations between logic and philosophy over the last 150 years. Logic underwent a major renaissance beginning in the nineteenth century. Cantor almost tamed the infinite, and Frege aimed to undercut Kant by reducing mathematics to logic. These achievements were threatened by the paradoxes, like Russell's. This ferment generated excellent philosophy by excellent philosophers up to World War II. This book provides a selective, critical history of the collaboration between logic and philosophy during this period. After World War II, (...) mathematical logic became a recognized subdiscipline in mathematics departments, and consequently but unfortunately philosophers have lost touch with its monuments. This book aims to make four of them more accessible to philosophers, making available the tools necessary for modern scholars of philosophy to renew a productive dialogue between logic and philosophy. (shrink)