Research report presented in partial fulfilment of the requirements for the degree of Master of Business Administration at the University of Stellenbosch.

<p>My essay is an investigation of American Psychos Patrick Bateman. Why is Patrick Batemans identity one so easily described as shallow and superficial? I discuss theese questions from a marxists point of view putting Bateman in the context of Georg Lukács theories of reification. I compare the structure of Patrick Batemans identity with the idea of an reified identity to se how the mechanisms of reification creates the entity that is Patrick Bateman.</p><p>My conclusion is that one answer to Batemans shallowness is the phenomenon of reification. To get a grasp of how shallowness might be understood I combine the theories of Lukács with Bakhtins idea of the aouthorative discourse.</p><p>If one look upon reification as an aouthorative discourse and one also presume that human existence is social and verbal the conclusion is that Patrick Bateman cannot exist because of what he is an example of. Patrick Bateman has only access to one voice, the voice of consumer capitalism and it is the singularity of Bateman that constitutes his ”not thereness”.</p>

My essay is an investigation of American Psychos Patrick Bateman. Why is Patrick Batemans identity one so easily described as shallow and superficial? I discuss theese questions from a marxists point of view putting Bateman in the context of Georg Lukács theories of reification. I compare the structure of Patrick Batemans identity with the idea of an reified identity to se how the mechanisms of reification creates the entity that is Patrick Bateman. My conclusion is that one answer to Batemans shallowness is the phenomenon of reification. To get a grasp of how shallowness might be understood I combine the theories of Lukács with Bakhtins idea of the aouthorative discourse. If one look upon reification as an aouthorative discourse and one also presume that human existence is social and verbal the conclusion is that Patrick Bateman cannot exist because of what he is an example of. Patrick Bateman has only access to one voice, the voice of consumer capitalism and it is the singularity of Bateman that constitutes his ”not thereness”.

This essay focuses on the character Patrick Bateman in American Psycho by Bret Easton Ellis and his unreliability as a narrator and compares it to the unreliable narration of the character Dexter Morgan in Darkly Dreaming Dexter by Jeff Lindsay. These characters' respective unreliability is analyzed from the perspective of six types of unreliability suggested by James Phelan and Mary Patricia Martin: misreporting, misreading, misregarding, underreporting, underreading and underregarding. The result of the analysis is that while Patrick shows proof of being an unreliable narrator with respect to each one of the six types except underreporting and underregarding, Dexter can be connected to three of them (misreading, underreading and underregarding). Even if this might seem like an insignificant difference, the amount and the clarity in the examples of unreliability adhering to Patrick suggests that he is a much more unreliable narrator than Dexter is. This result indicates that characters can be at opposing ends of a spectrum of unreliability, on which Patrick according to this analysis is placed at the highly unreliable end of the spectrum and Dexter somewhere at the low end. / Denna uppsats fokuserar på karaktären Patrick Bateman i American Psycho skriven av Bret Easton Ellis, med tanke på denna karaktärs opålitlighet som berättare. Detta jämförs med karaktären Dexter Morgan från Darkly Dreaming Dexter skriven av Jeff Lindsay och denna karaktärs opålitlighet som berättare. Detta opålitliga berättande analyseras utifrån en modell som består av sex kategorier vilka James Phelan och Mary Patricia Martin har formulerat. Dessa kategorier kallas: ”misreporting”, ”misreading”, ”misregarding”, ”underreporting”, ”underreading” och ”underregarding”. Resultatet av analysen visar på att Patricks berättande kan placeras in i fyra av dessa kategorier (”misreporting”, ”misreading”, ”misregarding” och ”underreading”). Detta i jämförelse med Dexters berättande som kan placeras in i tre av dem (”misreading”, ”underreading” och ”underregarding”). Även fast denna skillnad kan verka obetydlig är det ändå så att de exampel på opålitlighet som Patrick visar upp står att finna i fler och tydligare exempel än hos Dexter vilket innebär att Patrick kan ses som en mer opålitlig berättare än Dexter. Resultatet av analysen indikerar att olika karaktärers berättande kan återfinnas i olika ändar av ett opålitlighetsspektrum. På detta spektrum kan Patrick då placeras in som en mer opålitlig berättare än Dexter som hamnar i den mer pålitliga delen av spektrumet.

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A Conjectura de Bateman-Horn dá condições sobre uma família de polinômios com coeficientes inteiros $f_1(X),\\dots,f_k(X)$ para que hajam infinitos $n \\in \\N$ tais que $f_1(n),\\dots,f_k(n)$ sejam todos primos, e determina qual deve ser o comportamento assintótico de tais inteiros $n$. Neste texto, vamos estudar essa conjectura, assim como um método desenvolvido por Solomon W. Golomb que pode ser usado para demonstrá-la. Veremos que esse cálculo prova a Conjectura de Bateman-Horn a menos da troca de um limite com uma série infinita, que é o único passo ainda não provado desse método. Também estudaremos uma tentativa para solucionar esse problema por meio do uso de teoremas abelianos de regularidade, e provaremos que teoremas tão gerais não são suficientes para provar a troca do limite com a série. / Given a family of polynomials with integer coefficients $f_1(X),\\dots,f_k(X)$, one would like to answer the following question: does there exist infinitely many $n \\in \\N$ such that $f_1(n),\\dots,f_k(n)$ are all primes? Schinzel conjectured that if these polynomials satisfy certain simple conditions, then the answer to this question is affirmative. Assuming these conditions, Bateman and Horn proposed a formula for the asymptotic density of the integers $n \\in \\N$ such that $f_1(n),\\dots,f_k(n)$ are all primes. In this text, we shall study the Bateman-Horn Conjecture, as well as a method proposed by Solomon W. Golomb that may be used to prove this conjecture. We shall see that Golomb\'s $\\Lambda$-method would prove the Bateman-Horn Conjecture, except for a single unproved step, namely, the commutation of a limit with an infinite series.

A Conjectura de Bateman-Horn dá condições sobre uma família de polinômios com coeficientes inteiros $f_1(X),\\dots,f_k(X)$ para que hajam infinitos $n \\in \\N$ tais que $f_1(n),\\dots,f_k(n)$ sejam todos primos, e determina qual deve ser o comportamento assintótico de tais inteiros $n$. Neste texto, vamos estudar essa conjectura, assim como um método desenvolvido por Solomon W. Golomb que pode ser usado para demonstrá-la. Veremos que esse cálculo prova a Conjectura de Bateman-Horn a menos da troca de um limite com uma série infinita, que é o único passo ainda não provado desse método. Também estudaremos uma tentativa para solucionar esse problema por meio do uso de teoremas abelianos de regularidade, e provaremos que teoremas tão gerais não são suficientes para provar a troca do limite com a série. / Given a family of polynomials with integer coefficients $f_1(X),\\dots,f_k(X)$, one would like to answer the following question: does there exist infinitely many $n \\in \\N$ such that $f_1(n),\\dots,f_k(n)$ are all primes? Schinzel conjectured that if these polynomials satisfy certain simple conditions, then the answer to this question is affirmative. Assuming these conditions, Bateman and Horn proposed a formula for the asymptotic density of the integers $n \\in \\N$ such that $f_1(n),\\dots,f_k(n)$ are all primes. In this text, we shall study the Bateman-Horn Conjecture, as well as a method proposed by Solomon W. Golomb that may be used to prove this conjecture. We shall see that Golomb\'s $\\Lambda$-method would prove the Bateman-Horn Conjecture, except for a single unproved step, namely, the commutation of a limit with an infinite series.

Inosine monophosphate dehydrogenase (IMPDH) catalyses the key step in de novo guanine nucleotide biosynthesis at the branch point of GTP and ATP production. Mammals have two ubiquitous, catalytically indistinguishable isoforms, IMPDH type I and type II, and these are considered functionally interchangeable. Each contains a Bateman domain known to serve as energy-sensing / allosteric regulatory modules in a range of unrelated proteins. Mutations in the Bateman domain of type I, which do not affect catalytic activity, cause the retina-degenerative disease, retinitis pigmentosa (RP). The central hypothesis of this thesis is that IMPDH is regulated. In particular, that regulation occurs in an isoform specific manner and that mutations causal to RP affect enzyme regulation. Here we have visualised, including in real-time, the redistribution or clustering of IMPDH into linear macrostructures in a time-dependent manner which appeared to be intimately associated with changes in intracellular nucleotide levels. Data presented suggest the significance of IMPDH clustering is unlikely to be associated with substrate channelling, via interaction with other proteins in the de novo biosynthesis pathway, or enhanced protein stability. Although both isoforms responded similarly to fluctuations in intracellular nucleotide levels, type I had a higher propensity to spontaneously cluster into macrostructures compared to type II. This propensity to cluster was found to be conferred by the N-terminal 244 amino acids, which includes the Bateman domain, using a series of type I / type II chimera proteins. A comparative and novel approach revealed isoform-specific purine nucleotide binding characteristics. Type I bound ATP and type II bound AMP, via a mechanism involving the Bateman domain, resulting in conformational changes in IMPDH. This nucleotide binding was not associated with allosteric activation of IMPDH catalytic activity. The RP-causing mutation, R224P, abolished ATP binding and this correlated with an altered propensity to cluster. Collectively these data (i) show IMPDH distribution is regulated by the intracellular environment (ii) demonstrate that the IMPDH isoforms are modulated in a differential manner by AMP and ATP by a mechanism involving the Bateman domain, (iii) indicate communication between the Bateman domain and the active site and (iv) demonstrate that a RP-causing mutation compromises such regulation. From a broader perspective, this work raises the possibility that the nucleotide sensing properties of the Bateman domain in IMPDH serve to regulate IMPDH and co-ordinate nucleotide homeostasis, thereby giving rise to cellular plasticity in an isoform-specific manner to meet the requirements of the cellular environment.

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