Original sin: divine and symbolic violence in the turn to the Apostle Paul

When we take a step back from the imposing figure of physical violence, it becomes possible to examine other structurally violent forces that constantly shape our cultural and political landscapes. One of the driving interests in the “turn to Paul” in recent continental philosophy stems from wrestling with questions about the real nature of contemporary violence. Paul is positioned as a thinker whose messianic experience began to cut through the violent masquerade of the existing order. The crucifixion and resurrection of the Messiah (a slave and a God co-existing in one body) exposed the empty grounding upon which power resided. The Christ-event signifies a moment of violent interruption in the existing order which Paul enjoins the Gentiles to participate in through a dedication of love for the neighbour. This divine violence aims to reveal and subvert the “powers,” epitomised in the Roman Empire, in order to fulfil the labour of the Messianic now-time which had arrived. The impetus behind this research comes from a typically enigmatic and provocative section of text by the Slovene philosopher, cultural critic, and Christian atheist Slavoj Žižek. He claims that 'the notion of love should be given here all its Paulinian weight: the domain of pure violence… is the domain of love' (2008a, 173). In this move he links Paul’s idea of love to that of Walter Benjamin’s divine violence; the sublime and the cataclysmic come together in this seemingly perverse notion. At stake here is the way in which uncovering violent forces in the “zero-level” of our narrative worldviews aids the diagnosis of contemporary political and ethical issues. It is not enough to imagine Paul’s encounter with the Christ-event as non-violent. This Jewish apocalyptic movement was engaged in a violent struggle within an existing order that God’s wrath will soon dismantle. Paul’s weak violence, inspired by his fidelity to the Christ-event, places all responsibility over creation in the role of the individual within the collective body. The centre piece of this re-imagined construction of the Pauline narrative comes in Romans 13: the violent dedication to love understood in the radical nature of the now-time. 3 This research examines the role that narratives play in the creation and diagnosis of these violent forces. In order to construct a new genealogy of violence in Christianity it is crucial to understand the role of the slave of Christ (the revolutionary messianic subject). This turn in the Symbolic is examined through creating a literary structure in which we can approach a radical Nietzschean shift in Pauline thought. The claim here, a claim which is also central to Paul’s letters, is that when the symbolic violence which manipulates our worldviews is undone by a divine violence, if even for a moment, new possibilities are created in the opening for a transvaluation of values. Through this we uncover the nature of original sin: the consequences of the interconnected reality of our actions. The role of literature is vital in the construction of this narrative; starting with Cormac McCarthy’s No Country for Old Men, and continuing through works such as Melville’s Bartleby the Scrivener, this thesis draws upon the power of literature in the shaping of our narrative worlds. Typical of the continental philosophy at the heart of this work, a diverse range of illustrations and inspirations from fiction is pulled into its narrative to reflect the symbolic universe that this work was forged through. What this work attempts to do is give this theory a greater grounding in Paul’s letters by demonstrating this radical kenotic power at the heart of the Christ-event. Romans 13 reveals, in a way that has not yet been picked up by Critchley, Žižek, and others, that Paul opposed the biopolitical power of the Roman Empire through the weak violence of love that is the labour of the slaves of Christ on the “now-time” that had arrived.

Antiplatelet therapy and clinical outcomes in cardiovascular diseases

Cardiovascular diseases (CVD) is a leading cause of death in the world. Despite effective treatment regimens for ischaemic heart disease (IHD) and ischaemic stroke, mortality and recurrence rates remain high. Antiplatelet therapy is on effective treatment and reduces the risk of recurrent heart attack and stroke. Nevertheless, there are patients who stopped or interrupted their antiplatelet therapy for certain reasons or some patients may be resistant or poor responders to antiplatelet therapy. Furthermore, there is evidence of rebound effect in platelet activity after antiplatelet cessation and this may associate with increased risk of cardiovascular event. This thesis is divided into five main chapters (chapters 3 to 7) which attempt to provide data to help resolve the uncertainty. Chapter 1 highlights the background of cardiovascular diseases and the global burden of cardiovascular and cerebrovascular diseases. The metabolism of platelets, antiplatelet therapy and current antiplatelet therapy guidelines are described, followed by discussion of the risk of cardiovascular event and changes in antiplatelet therapy. Chapter 2 describes the data source from Virtual International Stroke Trial Archive (VISTA) and National Health Service Greater Glasgow and Clyde (NHSGGC) Safe Haven, followed by definition of outcome measures. In chapter 3, Virtual International Stroke Trial Archive (VISTA) data was examined to test whether continue with the same antiplatelet therapy or changing to a new antiplatelet regimen reduces the risk of subsequent events in patients who experience a stroke whilst taking antiplatelet therapy. The findings indicate that subjects who switch to a new antiplatelet regimen after stroke did not have a lower early recurrence rate than subjects who continued with the same antiplatelet therapy. Observations on bleeding complications were similar in both groups. However, changing antiplatelet regimen after stroke was associated with more favourable functional outcome across a full scale modified Rankin Scale (mRS) at 90 days. In chapter 4, association between early or later initiation of antiplatelet with a recurrent ischaemic stroke and bleeding complications was assessed using VISTA data. The findings indicate that there was no association between a recurrent ischaemic stroke and timing of initiation of antiplatelet drug after stroke. However, early initiation was associated with increased risk of bleeding. In terms of functional outcomes, this study demonstrated that the mid-time and late initiation of antiplatelet therapy after acute stroke are associated with better functional outcomes compared with early initiation. In chapter 5, a nested case-control study was performed to explore the rate of antiplatelet cessation and interruption in a sample of patients with recent ischaemic stroke and to assess the risk of cardiovascular events associated with cessation and interruption of antiplatelet. It was found that there was no increased risk of cardiovascular event among patients who had early cessation or interrupted/stopped antiplatelet therapy within 90 days following acute ischaemic stroke. In chapter 6, the incidence and predictors of cardiovascular events after DAPT cessation were evaluated. The incidence of cardiovascular event while taking DAPT and following discontinuation of DAPT was 15.7% and 16.7% respectively. This study found that increasing age was associated with an increased risk of cardiovascular event, whereas, revascularization-treated patients and longer duration of DAPT, were each associated with a decreased risk. The duration of DAPT six months and less was associated a significantly higher risk for cardiovascular event. In chapter 7, an untargeted metabolomics analysis was performed while on DAPT (aspirin plus ticagrelor) and once they stopped ticagrelor to identify metabolite changes associated with cardiovascular events after stopping DAPT. Ten ACS patients were recruited in this study and data were analysed for seven patients. Three hundred eleven putative metabolites were identified. This study found 16 putative metabolites significantly altered following ticagrelor cessation. Of these, seven metabolites were from lipid pathway and down-regulated some up to 3-fold. On the other hand, adenosine, from nucleotide metabolism was upregulated up to 2.6-fold. It concluded that there are changes in numerous pathways following DAPT discontinuation and whether these changes differ in patients who have cardiovascular event after stopping DAPT warrant further investigation. In chapter 8, a summary of the findings of this thesis are presented as well as the future directions of research in this area.