On having bad persons as friends

Intuitively, one who counts a morally bad person as a friend has gone wrong somewhere. But it is far from obvious where exactly they have gone astray. Perhaps in cultivating a friendship with a bad person, one extends to them certain goods that they do not deserve. Or perhaps the failure lies elsewhere; one may be an abettor to moral transgressions. Yet another option is to identify the mistake as a species of imprudence—one may take on great personal risk in counting a bad person as a friend. In this paper, I argue that none of these intuitive explanations are entirely convincing; for many such proposals run contrary to widely accepted features of friendship. However, they do point us in the direction of a more satisfying explanation—one which concerns a person’s moral priorities. An individual who counts a morally bad person as a friend is, I propose, one who betrays a distinct kind of defect in her values

Evolutionary Hypotheses and Moral Skepticism

Proponents of evolutionary debunking arguments aim to show that certain genealogical explanations of our moral faculties, if true, undermine our claim to moral knowledge. Criticisms of these arguments generally take the debunker’s genealogical explanation for granted. The task of the anti-debunker is thought to be that of reconciling the (supposed) truth of this hypothesis with moral knowledge. In this paper, I shift the critical focus instead to the debunker’s empirical hypothesis and argue that the skeptical strength of an evolutionary debunking argument is dependent upon the evidence for that hypothesis—evidence which, upon further inspection, proves far from compelling. Following that, however, I suggest that the same considerations which spell trouble for the empirical hypotheses of traditional debunking arguments can also be taken to give rise to an alternative—and better supported—style of debunking argument

Cardiotoxicity and other adverse events associated with mitoxantrone treatment for MS(e–Pub ahead of print)

Background: Mitoxantrone is used for aggressive multiple sclerosis (MS), but concerns about safety, including cardiotoxicity and other laboratory measures, prevail. Objective: To evaluate the incidence and potential predictors of adverse events associated with mitoxantrone at the MS Clinic, University of British Columbia, Canada. Methods: Retrospective review of patients treated with mitoxantrone by standard protocol; maximum cumulative dose = 120 mg/m(2). Left ventricular ejection fraction (LVEF) was measured with regular multiple-gated acquisition (MUGA) scans; blood cell counts and biochemical liver tests were performed before infusions. Generalized estimating equations were used to examine potential predictors of adverse events (graded according to the Common Toxicity Criteria, version 4) in patients with normal baseline and >= 1 follow-up MUGA or laboratory assessment. Results: All 163 patients (58% women) treated with mitoxantrone from 1999 to 2007 were reviewed. Mean baseline age was 41.9 (SD 10.8) years, cumulative dose was 59.7 (SD 26.0) mg/m2, and median follow-up duration was 14 months (maximum 6.5 years). By study end, 14% developed de novo cardiotoxicity (grade >= 2) as measured by decreased LVEF, 27% neutropenia (grade >= 1), 15% anemia (grade >= 1), and 15% liver toxicity (grade >= 1). Possible predictors of adverse events included sex, age, disease duration, and cumulative dose; only women exposed to a higher cumulative dose were at a greater risk of anemia (adjusted odds ratio 1.26, 95% confidence interval 1.08-1.48 per 10 mg/m(2)). Conclusions: Based on cardiac and laboratory assessments, mitoxantrone was reasonably well tolerated. However, cardiotoxicity was evident after doses well below current maximum recommended levels. A dose-response effect was not apparent. Findings emphasize the importance of monitoring; the long-term effects of mitoxantrone in multiple sclerosis require investigation. Neurology(R) 2010;74:1822-182

Prevalence and associated clinical characteristics of exercise-induced ST-segment elevation in lead aVR

10.1371/journal.pone.0160185PLoS ONE117e016018