Content & Watkins's account of natural axiomatizations

This paper briefly recounts the importance of the notion of natural axiomatizations for explicating hypothetico-deductivism, empirical significance, theoretical reduction, and organic fertility. Problems for the account of natural axiomatizations developed by John Watkins in Science and Scepticism and the revised account developed by Elie Zahar are demonstrated. It is then shown that Watkins's account can be salvaged from various counter-examples in a principled way by adding the demand that every axiom of a natural axiomatization should be part of the content of the theory being axiomatized. The crucial point here is that content cannot simply be identified with the set of logical consequences of a theory, but must be restricted to a proper subset of the consequence set. It is concluded that the revised Watkins account has certain advantages over the account of natural axiomatizations offered in Gemes (1993)

Ad Hoc Hypotheses and the Monsters within

Science is increasingly becoming automated. Tasks yet to be fully automated include the conjecturing, modifying, extending and testing of hypotheses. At present scientists have an array of methods to help them carry out those tasks. These range from the well-articulated, formal and unexceptional rules to the semi-articulated and variously understood rules-of-thumb and intuitive hunches. If we are to hand over at least some of the aforementioned tasks to machines, we need to clarify, refine and make formal, not to mention computable, even the more obscure of the methods scientists successfully employ in their inquiries. The focus of this essay is one such less-than-transparent methodological rule. I am here referring to the rule that ad hoc hypotheses ought to be spurned. This essay begins with a brief examination of some notable conceptions of ad hoc-ness in the philosophical literature. It is pointed out that there is a general problem afflicting most such conceptions, namely the intuitive judgments that are supposed to motivate them are not universally shared. Instead of getting bogged down in what ad hoc-ness exactly means, I shift the focus of the analysis to one undesirable feature often present in alleged cases of ad hoc-ness. I call this feature the ‘monstrousness’ of a hypothesis. A fully articulated formal account of this feature is presented by specifying what it is about the internal constitution of a hypothesis that makes it monstrous. Using this account, a monstrousness measure is then proposed and somewhat sketchily compared with the minimum description length approach

Humour in Nietzsche's style

Nietzsche's writing style is designed to elicit affective responses in his readers. Humour is one of the most common means by which he attempts to engage his readers' affects. In this article, I explain how and why Nietzsche uses humour to achieve his philosophical ends. The article has three parts. In part 1, I reject interpretations of Nietzsche's humour on which he engages in self‐parody in order to mitigate the charge of decadence or dogmatism by undermining his own philosophical authority. In part 2, I look at how Nietzsche uses humour and laughter as a critical tool in his polemic against traditional morality. I argue that one important way in which Nietzsche uses humour is as a vehicle for enhancing the effectiveness of his ad hominem arguments. In part 3, I show how Nietzsche exploits humour's social dimension in order to find and cultivate what he sees as the right kinds of readers for his works

STIM2 regulates PKA-dependent phosphorylation and trafficking of AMPARs

STIMs (STIM1 and STIM2 in mammals) are transmembrane proteins that reside in the endoplasmic reticulum (ER) and regulate store-operated Ca2+ entry (SOCE). The function of STIMs in the brain is only beginning to be explored, and the relevance of SOCE in nerve cells is being debated. Here we identify STIM2 as a central organizer of excitatory synapses. STIM2, but not its paralogue STIM1, influences the formation of dendritic spines and shapes basal synaptic transmission in excitatory neurons. We further demonstrate that STIM2 is essential for cAMP/PKA-dependent phosphorylation of the AMPA receptor (AMPAR) subunit GluA1. cAMP triggers rapid migration of STIM2 to ER–plasma membrane (PM) contact sites, enhances recruitment of GluA1 to these ER-PM junctions, and promotes localization of STIM2 in dendritic spines. Both biochemical and imaging data suggest that STIM2 regulates GluA1 phosphorylation by coupling PKA to the AMPAR in a SOCE-independent manner. Consistent with a central role of STIM2 in regulating AMPAR phosphorylation, STIM2 promotes cAMP-dependent surface delivery of GluA1 through combined effects on exocytosis and endocytosis. Collectively our results point to a unique mechanism of synaptic plasticity driven by dynamic assembly of a STIM2 signaling complex at ER-PM contact sites