Do Ethicists and Political Philosophers Vote More Often Than Other Professors?

If philosophical moral reflection improves moral behavior, one might expect ethics professors to behave morally better than socially similar non-ethicists. Under the assumption that forms of political engagement such as voting have moral worth, we looked at the rate at which a sample of professional ethicists—and political philosophers as a subgroup of ethicists—voted in eight years’ worth of elections. We compared ethicists’ and political philosophers’ voting rates with the voting rates of three other groups: philosophers not specializing in ethics, political scientists, and a comparison group of professors specializing in neither philosophy nor political science. All groups voted at about the same rate, except for the political scientists, who voted about 10–15% more often. On the face of it, this finding conflicts with the expectation that ethicists will behave more responsibly than non-ethicists

Aplasia cutis congenita in surviving co-twin after propylthiouracil exposure in utero

Aim: Aplasia cutis congenita (ACC) has been observed after fetal exposure to the antithyroid drug methimazole (MMI), but not reported after propylthiouracil (PTU), the current antithyroid drug of choice during pregnancy. This occurrence has implications for patient information and causal research. Case report: We describe a surviving term co-twin to a mother with hyperthyroidism exposed to PTU from conception to 34 weeks of gestation presenting with ACC at birth. Discussion: The association between PTU exposure and ACC is clinically relevant and allows speculation on the etiology. A similar mechanism to the classical MMI-induced ACC is postulated, unless a vascular etiology suggested by a vanishing twin or maternal hyperthyroidism itself is causal. Coincidence of PTU exposure and ACC seems unlikely. Conclusion: ACC in a newborn after PTU exposure during pregnancy hitherto observed only after MMI strongly encourages further reports of similar cases that may remain clinically underdiagnosed or unreported. Such confirmation could have significant implications for maternal treatment of hyperthyroidism, common in women of childbearing ag

Expression of neurogenin3 reveals an islet cell precursor population in the pancreas

Differentiation of early gut endoderm cells into the endocrine cells forming the pancreatic islets of Langerhans depends on a cascade of gene activation events controlled by transcription factors including the basic helix-loop-helix (bHLH) proteins. To delineate this cascade, we began by establishing the position of neurogenin3, a bHLH factor found in the pancreas during fetal development. We detect neurogenin3 immunoreactivity transiently in scattered ductal cells in the fetal mouse pancreas, peaking at embryonic day 15.5. Although not detected in cells expressing islet hormones or the islet transcription factors Isl1, Brn4, Pax6 or PDX1, neurogenin3 is detected along with early islet differentiation factors Nkx6.1 and Nkx2.2, establishing that it is expressed in immature cells in the islet lineage. Analysis of transcription factor-deficient mice demonstrates that neurogenin3 expression is not dependent on neuroD1/BETA2, Mash1, Nkx2.2, Nkx6.1, or Pax6. Furthermore, early expression of neurogenin3 under control of the Pdx1 promoter is alone sufficient to drive early and ectopic differentiation of islet cells, a capability shared by the pancreatic bHLH factor, neuroD1/BETA2, but not by the muscle bHLH factor, MyoD. However, the islet cells produced in these transgenic experiments are overwhelmingly α cells, suggesting that factors other than the bHLH factors are required to deviate from a default α cell fate. These data support a model in which neurogenin3 acts upstream of other islet differentiation factors, initiating the differentiation of endocrine cells, but switching off prior to final differentiation. The ability to uniquely identify islet cell precursors by neurogenin3 expression allows us to determine the position of other islet transcription factors in the differentiation cascade and to propose a map for the islet cell differentiation pathway

In Defence of Modest Doxasticism About Delusions

Here I reply to the main points raised by the commentators on the arguments put forward in my Delusions and Other Irrational Beliefs (OUP, 2009). My response is aimed at defending a modest doxastic account of clinical delusions, and is articulated in three sections. First, I consider the view that delusions are in-between perceptual and doxastic states, defended by Jacob Hohwy and Vivek Rajan, and the view that delusions are failed attempts at believing or not-quite-beliefs, proposed by Eric Schwitzgebel and Maura Tumulty. Then, I address the relationship between the doxastic account of delusions and the role, nature, and prospects of folk psychology, which is discussed by Dominic Murphy, Keith Frankish, and Maura Tumulty in their contributions. In the final remarks, I turn to the continuity thesis and suggest that, although there are important differences between clinical delusions and non-pathological beliefs, these differences cannot be characterised satisfactorily in epistemic terms. \u

Nietzsche’s Epistemic Perspectivism

Nietzsche offers a positive epistemology, and those who interpret him as a skeptic or a mere pragmatist are mistaken. Instead he supports what he calls per- spectivism. This is a familiar take on Nietzsche, as perspectivism has been analyzed by many previous interpreters. The present paper presents a sketch of the textually best supported and logically most consistent treatment of perspectivism as a first- order epistemic theory. What’s original in the present paper is an argument that Nietzsche also offers a second-order methodological perspectivism aimed at enhancing understanding, an epistemic state distinct from knowledge. Just as Descartes considers and rejects radical skepticism while at the same time adopting methodological skepticism, one could consistently reject perspectivism as a theory of knowledge while accepting it as contributing to our understanding. It is argued that Nietzsche’s perspectivism is in fact two-tiered: knowledge is perspectival because truth itself is, and in addition there is a methodological perspectivism in which distinct ways of knowing are utilized to produce understanding. A review of the manner in which understanding is conceptualized in contemporary epistemology and philosophy of science serves to illuminate how Nietzsche was tackling these ideas

Against dispositionalism: belief in cognitive science

Dispositionalism about belief has had a recent resurgence. In this paper we critically evaluate a popular dispositionalist program pursued by Eric Schwitzgebel. Then we present an alternative: a psychofunctional, representational theory of belief. This theory of belief has two main pillars: that beliefs are relations to structured mental representations, and that the relations are determined by the generalizations under which beliefs are acquired, stored, and changed. We end by describing some of the generalizations regarding belief acquisition, storage, and change

Are intuitions about moral relevance susceptible to framing effects?

Various studies have reported that moral intuitions about the permissibility of acts are subject to framing effects. This paper reports the results of a series of experiments which further examine the susceptibility of moral intuitions to framing effects. The main aim was to test recent speculation that intuitions about the moral relevance of certain properties of cases might be relatively resistent to framing effects. If correct, this would provide a certain type of moral intuitionist with the resources to resist challenges to the reliability of moral intuitions based on such framing effects. And, fortunately for such intuitionists, although the results can’t be used to mount a strident defence of intuitionism, the results do serve to shift the burden of proof onto those who would claim that intuitions about moral relevance are problematically sensitive to framing effects

Prenatal nicotine exposure alters early pancreatic islet and adipose tissue development with consequences on the control of body weight and glucose metabolism later in life. Endocrinology 149

ABSTRACT Despite medical advice, 20% to 30% of female smokers continue to smoke during pregnancy. Epidemiological studies have associated maternal smoking with increased risk of obesity and type-2 diabetes in the offspring. In the present study, we investigated the impact of prenatal nicotine exposure (3mg/kg in Sprague-Dawley rats via osmotic Alzet minipumps) on the early endocrine pancreas and adipose tissue development in rat pups before weaning. Body weight, fat deposition, food intake and food efficiency, cold tolerance, spontaneous physical activity, glucose utilization and insulin sensitivity were also examined at adulthood. Prenatal nicotine exposure led to a decrease in endocrine pancreatic islet size and number at 7 days of life (PND7) which corroborates with a decrease in gene expression of specific transcription factors such as Pdx-1, Pax-6, Nkx6.1 and of hormones such as insulin and glucagon. The prenatal nicotine exposure also led to an increase in epididymal white adipose tissue (eWAT) weight at weaning (PND21), and marked hypertrophy of adipocytes, with increased gene expression of proadipogenic transcription factors such as C/EBP-α, PPAR-γ and SREBP-1C. These early tissue alterations led to significant metabolic consequences, as shown by increased body weight and fat deposition, increased food efficiency on high fat diet, cold intolerance, reduced physical activity, glucose intolerance combined with insulin resistance observed at adulthood. These results prove a direct association between fetal nicotine exposure and offspring metabolic syndrome with early signs of dysregulations of adipose tissue and pancreatic development

Pancreatic Transcription Factors Containing Protein Transduction Domains Drive Mouse Embryonic Stem Cells towards Endocrine Pancreas

Protein transduction domains (PTDs), such as the HIV1-TAT peptide, have been previously used to promote the uptake of proteins into a range of cell types, including stem cells. Here we generated pancreatic transcription factors containing PTD sequences and administered these to endoderm enriched mouse embryonic stem (ES) cells under conditions that were designed to mimic the pattern of expression of these factors in the developing pancreas. The ES cells were first cultured as embryoid bodies and treated with Activin A and Bone morphogenetic protein 4 (BMP4) to promote formation of definitive endoderm. Cells were subsequently plated as a monolayer and treated with different combinations of the modified recombinant transcription factors Pdx1 and MafA. The results demonstrate that each transcription factor was efficiently taken up by the cells, where they were localized in the nuclei. RT-qPCR was used to measure the expression levels of pancreatic markers. After the addition of Pdx1 alone for a period of five days, followed by the combination of Pdx1 and TAT-MafA in a second phase, up-regulation of insulin 1, insulin 2, Pdx1, Glut2, Pax4 and Nkx6.1 was observed. As assessed by immunocytochemistry, double positive insulin and Pdx1 cells were detected in the differentiated cultures. Although the pattern of pancreatic markers expression in these cultures was comparable to that of a mouse transformed β-cell line (MIN-6) and human islets, the expression levels of insulin observed in the differentiated ES cell cultures were several orders of magnitude lower. This suggests that, although PTD-TFs may prove useful in studying the role of exogenous TFs in the differentiation of ES cells towards islets and other pancreatic lineages, the amount of insulin generated is well below that required for therapeutically useful cells