Optimality Models and the Propensity Interpretation of Fitness.

The propensity account of fitness intends to solve the classical tautologicity issue by identifying fitness with a disposition, the ability to survive and reproduce. As proponents recognized early on, this account requires operational independence from actual reproductive success to avoid circularity and vacuousness charges. They suggested that operational independence is achieved by measuring fitness values through optimality models. Our goal in this article is to develop this suggestion. We show that one plausible procedure by which these independent operationalizations could be thought to take place, and which is in accordance with what is said in the optimality literature, is unsound. We provide two independent lines of reasoning to show this. We then provide a sketch of a more adequate account of the role of optimality models in evolutionary contexts and draw some consequences.

Drift as constitutive: conclusions from a formal reconstruction of population genetics.

This article elaborates on McShea and Brandon's idea that drift is unlike the rest of the evolutionary factors because it is constitutive rather than imposed on the evolutionary process. I show that the way they spelled out this idea renders it inadequate and is the reason why it received some (good) objections. I propose a different way in which their point could be understood, that rests on two general distinctions. The first is a distinction between the underlying mathematical apparatus used to formulate a theory and a concept proposed by that theory. With the aid of a formal reconstruction of a population genetic model, I show that drift belongs to the first category. That is, that drift is constitutive of population genetics in the same sense that multiplication is constitutive in classical mechanics, or that circle is constitutive in Ptolemaic astronomy. The second distinction is between eliminating a concept from a theory and setting its value to zero. I will show that even though drift can be set to zero just like the rest of the evolutionary factors (as others have noted in their criticism of McShea and Brandon), eliminating drift is much harder than eliminating those other factors, since it would require changing the entire mathematical apparatus of standard population genetic theory. I conclude by drawing some other implications from the proposed formal reconstruction.

Curative anticoagulation prevents endothelial lesion in COVID-19 patients.

BACKGROUND: Coronavirus disease-2019 (COVID-19) has been associated with cardiovascular complications and coagulation disorders. OBJECTIVES: To explore the coagulopathy and endothelial dysfunction in COVID-19 patients. METHODS: The study analyzed clinical and biological profiles of patients with suspected COVID-19 infection at admission, including hemostasis tests and quantification of circulating endothelial cells (CECs). RESULTS: Among 96 consecutive COVID-19-suspected patients fulfilling criteria for hospitalization, 66 were tested positive for SARS-CoV-2. COVID-19-positive patients were more likely to present with fever (P = .02), cough (P = .03), and pneumonia at computed tomography (CT) scan (P = .002) at admission. Prevalence of D-dimer >500 ng/mL was higher in COVID-19-positive patients (74.2% versus 43.3%; P = .007). No sign of disseminated intravascular coagulation were identified. Adding D-dimers >500 ng/mL to gender and pneumonia at CT scan in receiver operating characteristic curve analysis significantly increased area under the curve for COVID-19 diagnosis. COVID-19-positive patients had significantly more CECs at admission (P = .008) than COVID-19-negative ones. COVID-19-positive patients treated with curative anticoagulant prior to admission had fewer CECs (P = .02) than those without. Interestingly, patients treated with curative anticoagulation and angiotensin-converting-enzyme inhibitors or angiotensin receptor blockers had even fewer CECs (P = .007). CONCLUSION: Curative anticoagulation could prevent COVID-19-associated coagulopathy and endothelial lesion.

Theoricity, observation and homology: a response to Pearson.

An interesting metatheoretical controversy took place during the 1980's and 1990's between pattern and phylogenetic cladists. What was always at stake in the discussion was not how work in systematics should be carried out, but rather how this practice should be metatheoretically interpreted. In this article, we criticize Pearson's account of the metatheoretical factors at play in this discussion. Following him, we focus on the issue of circularity, and on the role that phylogenetic hypotheses play in the determination of "primary homologies". Pearson argues that the recognition of primary homologies cannot be achieved without recourse to previous phylogenetic knowledge, and that to claim otherwise is to state that primary homologies are observable. To show why that view would be inadequate, he appeals to Hanson's views about theory-laden observation, alongside with a specific case study, which allegedly illustrates the more complex relation between observation and theory. We will argue that the pattern cladists' point (at least regarding the issue of homology) is better addressed by taking a quite different approach: instead of thinking in terms of observability, the topic can be tackled by paying attention to the way in which concepts are determined. We will take the notion of T-theoricity from metatheoretical structuralism and show that, once the issue is discussed with the appropriate metatheoretical framework, the alleged counterexample brought up by Pearson is not problematic at all for pattern cladism.

Correction to: Theoricity, observation and homology: a response to Pearson.

Due to an unfortunate turn of events, the family name of the first author was erroneously published as 'RoffÕ' in the original publication (PDF). The correct representation of the first author's family name is listed above and below.