Knowledge in Accounting: Using a threshold concept lens to identify knowledge of financial instruments in an Accounting course, as experienced by students at a South African university

This qualitative research aims to identify the threshold concepts in financial instruments using Meyer and Land's Threshold Concept Framework (2005) and applies the dimension of Semantics and Legitimation Code Theory (Maton, 2014) to analyse whether semantic gravity and semantic density are stronger or weaker in the threshold concepts. The analysis points to five threshold concepts in the financial instruments module. It further aims to explore whether African, Coloured and Indian students' exposure to these threshold concepts results in troublesome knowledge and/or transformation in understanding and thinking in a second-year Accounting course at a South African university. Triangulation is used to confirm the authenticity and consistency of the data emerging from the identification of the threshold concepts. Using Semantics, this research illustrates that the five threshold concepts possess weaker semantic gravity due to the abstract nature of the threshold concepts and stronger semantic density is present due to the complex and dense terminology inherent in financial instruments. Evidence from a general survey, interviews and summative assessments conducted with students registered for an Accounting course shows that exposure to the threshold concepts resulted in troublesome knowledge and/or transformed understanding. Identifying the threshold concepts could make specialised Accounting knowledge more explicit to students and exploring the knowledge experienced as troublesome and the transformed understanding experienced provides room for debate around pedagogy and curriculum reform

A molecular investigation of the novel gene underlying autosomal dominant retinitis pigmentosa in a South African family

The inherited retinal degenerative disorders are a common cause of severe visual handicap in the W estem world. Retinitis pigmentosa (RP) is a group of retinopathies in which a primary feature is a progressive loss of photoreceptor and retinal pigment epithelium function. Over the last decade, investigations into the patho-physiology of RP have identified numerous disease-causing genes and loci (for a current listing refer to the web site http://www.sph.uth.tmc.edu/Retnet/). A study of a South African family with an autosomal dominant form of RP (adRP) forms the basis of this dissertation. In this family, comprising 44 individuals, the first manifestation of visual disturbance is usually evident between 20 and 30 years of age. Subsequently, another South African adRP family, consisting of 25 members, was also incorporated into this investigation. Genetic linkage analysis facilitated the mapping of the disease phenotype in the two South African adRP families to a 10 cM interval on chromosome 17q22. This novel locus, designated RP17, is the eighth identified for adRP. Haplotype construction in the two kindreds, in conjunction with multipoint analyses subsequently fine mapped RP17 to a 1 cM region between microsatellite markers D17S1604 and D17S948. Although the two families are from ethnically diverse population groups, they share the same disease-associated haplotype spanning 12 cM, which suggests that the disorder may be caused by the same pathogenic mutation in the same gene. The positional cloning approach was utilised in an endeavour to identify the RP17 gene and an attempt was made to construct a physical map of the 1 cM critical region. A contig consisting of seven yeast artificial chromosome (YAC) clones was assembled using sequence-tagged-site (STS) content mapping. In order to close a gap in the YAC contig, a bacterial artificial chromosome (BAC) library was screened and the vectorette PCR technique was used to verify overlapping sequences. This contig should provide a useful tool for the purpose of isolating genes or transcription units within the RP17 critical interval. In this regard, purified YAC DNA was isolated using pulsed-field gel electrophoresis and the cDNA selection technique was employed to generate a transcription map. This approach was applied to YAC 75Ic12 using a foetal brain cDNA library, and two rounds of selection were performed to create a sub-library for enriched cDNAs derived from this clone. Screening for the presence of contaminating sequences in the 480 transformants revealed that (i) approximately 7% of the selected clones contain COT-1 DNA and (ii) none of the clones were contaminated with yeast AB1380 DNA. Ten randomly chosen clones were sequenced and subjected to BLASTN analysis, which revealed the presence of a 23 bp contaminant, known genes as well as novel transcripts. In order to optimise efforts to isolate the adRP gene, four positional candidates residing on 17q were screened for evidence implicating them in the adRP phenotype in the two 17q22-linked families. The genes investigated were: PDEG (gamma subunit of rod phosphodiesterase), TIMP2 (tissue inhibitor of metalloproteinases-2), PKCA (protein kinase C alpha) and retinal fascin. These candidates were chosen on the basis of (i) mapping to 17q, (ii) expression in the retina and/or (iii) potential involvement in the rod phototransduction pathway. Recombination events between the adRP locus and a single strand conformation polymorphism (SSCP) in PDEG, and a restriction fragment length polymorphism (RFLP) in TIMP2 provided evidence for the exclusion of these candidate genes. A novel SSCP detected in the promoter region of retinal fascin was genotyped in the two adRP families and showed a lack of co-segregation with the disease locus. Furthermore, direct DNA sequencing of the coding regions as well as the promoter region of retinal fascin in RP affected family members did not reveal any pathogenic mutations. In addition, data is provided which suggests that PKCA does not reside on any of the YACs and BACs encompassing the RP17 critical interval. This gene is therefore unlikely to be responsible for the adRP phenotype in the two RP17-linked families. Ultimately, the work reported in this thesis may contribute to the body of knowledge on inherited retinal degenerative disorders. Moreover, this investigation should provide the basis for further study of the aetiology of RP in all families linked to the RP17 locus on chromosome 17q22. The immediate application of these molecular findings is the potential for pre-symptomatic testing of at-risk members from the two adRP kindreds

Fiction, ideology and history : a critical examination of Hans Grimm's novel 'Kaffernland'

Bibliography: pages 186-197.This dissertation aims to place Hans Grimm's uncompleted epic, Kaffernland, eine deutsche Sage (Kaffraria, a German Legend) within the context of the historical discourse of the nineteenth-century as it has been challenged by presentday critical historiography. Central to Grimm's text is the problematic relationship between fiction and historical reality. It reproduces historical documents and relies on the scientific aura of a bourgeois realist discourse to present itself as having reference to an extra-textual reality. These truth-claims are examined with Roland Barthes' structuralist techniques. I locate Grimm's text within an intertext dominated by the ideologies of German nationalism, colonial space and fate. His portrayal of mid-nineteenth century political questions is shown as a contradictory amalgam of partisanship for both the bourgeoisie and the small peasantry, of romantic anti-capitalism and pro-imperialism. The authoritarian narrative discourse affirms Britain's colonial subjugation of the Xhosa and negates Xhosa resistance. I focus on speaking positions in the text and the power of the colonizer's practice of designating and signifying. The rhetoric of the text is seen as a continuation of politics against Britain's exploitation of the British German Legion and of German missionary work in British Kaffraria. Grimm reproduces and embellishes the mythology of the German Legion as saviours of Kaffraria and Germany. He inverts history to re-make the negative record of the German Military Settlement. I show how mythic signs and a moralizing discourse stimulate an envisaged pre-World War I readership to recognize Kaffraria as a German colony and to reflect on how, in its own times, Germany can be regenerated through acquiring colonial space. The mythological discourse is also viewed in the light of the text's attempts to manifest the external factual reliability and inner truth of bourgeois realism. While Grimm deploys the literary conventions of the modern novel, as an epigone he draws on the forms of legend, saga and epic cultivated in the nineteenth century. He alludes to the Icelandic saga also to legitimize a claim to Xhosaland. This first book of the epic, presented as complete, attains a measure of cohesion through techniques of parallelism and contiguity. The text parallels the fate of the German and Xhosa nations and simultaneously signifies the Xhosa as destroyers of Xhosaland and the cattle-killing movement of 1856-57 as a diabolical plan. I see this mythologization of history as the ideological justification for the expropriation of the Xhosa and show that Grimm's colonialist fiction is in fact a colonizing discourse

Clinical findings and genetic screening for copy number variation mutations in a cohort of South African patients with Parkinson’s disease

Background. Parkinson’s disease (PD), with a prevalence of up to 4% in Western countries, appears to be less common in Africa, possibly in part because of genetic factors. African studies investigating the genetic causation of PD are limited.Objective. To describe the clinical and genetic findings in a group of black South African patients with PD.Methods. All black African patients with PD from a tertiary hospital neurology clinic were examined. Symptoms were scored according to the Unified Parkinson’s Disease Rating Scale (UPDRS), and patients were classified according to motor features. Genomic DNA was extracted and multiplex ligation-dependent probe amplification was used for detection of copy number variation (CNV) mutations in the known PD-causing genes.Results. Sixteen patients were identified (ages 56 - 82 years). Three had a family history of PD. Classification into motor subtypes showed 44% mixed, 31% akinetic-rigid, and 25% tremor-dominant subtypes. UPDRS scores ranged from 7 to 88, with dementia in 20%. No patient had G2019S LRRK2 and A30P SNCA mutations, and all except one had no CNV mutations in the known PD-causing genes. A female patient (age of onset 50 years, no family history) had a parkin gene heterozygous deletion of exon 4. She had hyperreflexia, bilateral Hoffmann’s reflexes, normal plantar responses and no dystonia.Conclusion. This group of black African patients showed similar characteristics to patients in Western studies, possibly with a higher proportion having tremor dominant disease. Genetic analysis showed one parkin gene mutation. The limited knowledge on PD-causing genes and mutations in black populations warrants further studies involving next-generation sequencing approaches

The lived experience of health sciences students’ participation in an interprofessional community-based stroke class

Background. Collaborative approaches in healthcare contexts may provide better care for patients. Interprofessional circuit-based group therapy could counter profession-specific tribalism. There is no evidence on interprofessional education (IPE) community-based interventions on student learning in the health professions. Objective. To explore undergraduate health sciences students’ experience of being involved in community-based interprofessional circuit-based group therapy. Methods. Semi-structured interviews were inductively analysed exploring undergraduate health sciences students’ experience of involvement in an IPE community-based stroke intervention. Results. A total of 12 final-year students participated, with representation from physiotherapy, occupational therapy and speech therapy. This IPE opportunity beneficially impacted students’ collaborative competencies in knowledge, attitudes, skills and behaviours. This community-based rotation immersed students in a service-delivery environment where patient management was co-ordinated by a multiprofessional rehabilitation team. The integrated stroke circuit group activity aimed to enhance further interconnectedness between student participants. Students who were exposed to this clinical activity reported an understanding of (i) patients’ unique contexts; (ii) role development and complementary overlap between health professions; and (iii) the value of joint interventions to both patients and rehabilitation teams in resource-constrained settings. Conclusion. These students have been primed in their practice-readiness as healthcare professionals for the 21st century who will promote quality care, and embrace collaborative professional practice and person-centredness

The role of genetics in racial categorisation of humans

CITATION: Bardien-Kruger, S. & Muller-Nedebock, A. 2020. The role of genetics in racial categorisation of humans, in Jansen, J. & Walters, C. (eds). 2020. Fault lines : a primer on race, science and society. Stellenbosch: SUN PReSS, doi:10.18820/9781928480495/01.The original publication is available at https://africansunmedia.store.it.si/zaOnly very recently in the history of modern humans have we learned how to read the stories hidden in our DNA. The ability to read and interpret DNA has revealed that many things are not as they are perceived to be. For instance, physical features between two people may be strikingly different and therefore be taken to mean that the individuals are fundamentally different, when in fact the DNA of any two humans is almost identical (99.9% the same) on a genetic level. Given the physical differences apparent between populations, much research has gone into studying what makes them different. This type of research, no matter how well intentioned, has led to the pseudoscientific arguments used to justify movements such as the slave trade, the eugenics movement and apartheid in South Africa. Scientists at Stellenbosch University have also played a significant role in highlighting the ‘racial’ differences in the South African population. One such study is the nowretracted Sport Science article.1 In this study, the authors, albeit unwittingly, reinforce racial stereotyping by concluding that so‑called ‘coloured’ women in South Africa have lower cognitive functioning when compared to American age-standardised norms, and that this is due to exposure to a variety of factors with known negative effects on cognitive function. In an attempt to shed some light on the inaccuracies of the assumptions on which this article is based, this chapter will provide some background to racial categorisation from a genetic perspective. It will start with basic concepts in genetics and then expand into some of the more complex concepts and theories supporting the fact that there is no genetic basis for race in humans.Publisher's versio

Aminoglycoside-induced hearing loss: South Africans at risk

South Africa is currently experiencing a TB epidemic with an estimated incidence of 940/100 000 population/year, and the country has been ranked 4th among the 22 high-burden TB countries worldwide by the World Health Organization (WHO). A potentially devastating threat to TB control is the emergence of multidrug-resistant TB (MDR-TB) and, more recently, extensively drug-resistant TB (XDR-TB), mainly as a result of poor drug adherence by TB patients and incorrect management or treatment regimens by health providers; however, direct transmission of drug-resistant strains also plays an important role. The MDR/XDR-TB strains necessitate prolonged chemotherapy for up to 2 years or more, and the use of more toxic second-line drugs including the aminoglycoside (streptomycin, kanamycin and amikacin) and polypeptide (capreomycin) antibiotics. In South Africa, in accordance with WHO guidelines, streptomycin is used for retreatment of TB while kanamycin, amikacin and capreomycin are used to treat MDR/XDR-TB

Mitochondrial DNA variation in Parkinson’s disease: Analysis of “out-of-place” population variants as a risk factor

Mitochondrial DNA (mtDNA), a potential source of mitochondrial dysfunction, has been implicated in Parkinson’s disease (PD). However, many previous studies investigating associations between mtDNA population variation and PD reported inconsistent or contradictory findings. Here, we investigated an alternative hypothesis to determine whether mtDNA variation could play a significant role in PD risk. Emerging evidence suggests that haplogroup-defining mtDNA variants may have pathogenic potential if they occur “out-of-place” on a different maternal lineage. We hypothesized that the mtDNA of PD cases would be enriched for out-of-place variation in genes encoding components of the oxidative phosphorylation complexes. We tested this hypothesis with a unique dataset comprising whole mitochondrial genomes of 70 African ancestry PD cases, two African ancestry control groups (n = 78 and n = 53) and a replication group of 281 European ancestry PD cases and 140 controls from the Parkinson’s Progression Markers Initiative cohort. Significantly more African ancestry PD cases had out-of-place variants than controls from the second control group (P < 0.0125), although this association was not observed in the first control group nor the replication group. As the first mtDNA study to include African ancestry PD cases and to explore out-of-place variation in a PD context, we found evidence that such variation might be significant in this context, thereby warranting further replication in larger cohorts

Arrhythmogenic right ventricular cardiomyopathy type 6 (ARVC6): support for the locus assignment, narrowing of the critical region and mutation screening of three candidate genes

BACKGROUND: Arrhythmogenic right ventricular cardiomyopathy (ARVC) is a heritable disorder characterized by progressive degeneration of right ventricular myocardium, arrhythmias and an increased risk of sudden death at a young age. By linkage analysis, ARVC type 6 was previously mapped to a 10.6 cM region on chromosome 10p12-p14 in a large North American kindred. To date, the genetic defect that causes ARVC6 has not been identified. METHODS: We identified a South African family of 13 members with ARVC segregating as an autosomal dominant disorder. The diagnosis of ARVC was based on international diagnostic criteria. All available family members were genotyped with microsatellite markers at six known ARVC loci, and positional candidate gene screening was performed. RESULTS: Genetic linkage and haplotype analysis provided lod scores that are highly suggestive of linkage to the ARVC6 locus on chromosome 10p12-p14, and the narrowing of the critical region to ~2.9 Mb. Two positional candidate genes (ITG8 and FRMD4A) were screened in which defects could possibly disrupt cell-cell adhesion. A non-positional candidate gene with apoptosis inducing properties, LAMR1P6 (laminin receptor 1 pseudogene 6) was also screened. Direct sequencing of DNA from affected individuals failed to detect disease-causing mutations in the exonic sequences of the three genes investigated. CONCLUSION: The narrowing of the ARVC6 critical region may facilitate progress towards the identification of the gene that is involved in ARVC. Identification of the causative genes for ARVC will contribute to the understanding of the pathogenesis and management of this poorly understood condition