Reading 'On Certainty' through the Lens of Cavell: Scepticism, Dogmatism and the 'Groundlessness of our Believing'

While Cavell is well known for his reinterpretation of the later Wittgenstein, he has never really engaged himself with post-Investigations writings like On Certainty. This collection may, however, seem to undermine the profoundly anti-dogmatic reading of Wittgenstein that Cavell has developed. In addition to apparently arguing against what Cavell calls ‘the truth of skepticism’ – a phrase contested by other Wittgensteinians – On Certainty may seem to justify the rejection of whoever dares to question one’s basic presuppositions. According to On Certainty, or so it seems, the only right response to someone with different certainties is a reproach like ‘Fool!’ or ‘Heretic!’. This article aims to show that On Certainty need not be taken to prove Cavell wrong. It explains that Wittgenstein, in line with the first two parts of The Claim of Reason, does not reject scepticism out of hand but rather questions the sceptic’s self-understanding. Using arguments from Part Three of The Claim, the article moreover argues that a confrontation with divergence calls for self-examination rather than self-righteousness. Precisely because Wittgenstein acknowledges ‘the groundlessness of our believing’ or, in Cavellian terms, ‘the truth of skepticism’, he is not the authoritarian thinker that some have taken him to be

Mycobacterium chelonae, an ‘atypical’ cause of an LVAD driveline infection

We describe the first patient with a left ventricular assist device (LVAD) driveline infection caused by Mycobacterium chelonae presenting with persistent infection despite conventional antibiotics. Treatment was successful with surgical debridement, driveline exit relocation, and a 4-month period of antibiotics. In the case of a culture-negative LVAD driveline infection, non-tuberculous mycobacteria should be considered. This case illustrates tha

Altered fibrin network structure and fibrinolysis in intensive care unit patients with COVID-19, not entirely explaining the increased risk of thrombosis

BACKGROUND: Severe acute respiratory syndrome coronavirus 2 infection is associated with an increased incidence of thrombosis. OBJECTIVES: By studying the fibrin network structure of coronavirus disease 2019 (COVID-19) patients, we aimed to unravel pathophysiological mechanisms that contribute to this increased risk of thrombosis. This may contribute to optimal prevention and treatment of COVID-19 related thrombosis. PATIENTS/METHODS: In this case-control study, we collected plasma samples from intensive care unit (ICU) patients with COVID-19, with and without confirmed thrombosis, between April and December 2020. Additionally, we collected plasma from COVID-19 patients admitted to general wards without thrombosis, from ICU patients with pneumococcal infection, and from healthy controls. Fibrin fiber diameters and fibrin network density were quantified in plasma clots imaged with stimulated emission depletion microscopy and confocal microscopy. Finally, we determined the sensitivity to fibrinolysis. RESULTS: COVID-19 ICU patients (n = 37) and ICU patients with pneumococcal disease (n = 7) showed significantly higher fibrin densities and longer plasma clot lysis times than healthy controls (n = 7). No differences were observed between COVID-19 ICU patients with and without thrombosis, or ICU patients with pneumococcal infection. At a second time point, after diagnosis of thrombosis or at a similar time point in patients without thrombosis, we observed thicker fibers and longer lysis times in COVID-19 ICU patients with thrombosis (n = 19) than in COVID-19 ICU patients without thrombosis (n = 18). CONCLUSIONS: Our results suggest that severe COVID-19 is associated with a changed fibrin network structure and decreased susceptibility to fibrinolysis. Because these changes were not exclusive to COVID-19 patients, they may not explain the increased thrombosis risk