Geophysical investigation into the geology, geometry and geochronology of the South African Pilanesberg Complex and the Pilanesberg dyke system

A dissertation submitted to the Faculty of Science, University of the Witwatersrand, Johannesburg, in fulfilment of the requirements for the degree of Master of Science. Johannesburg, 2016The Mesoproterozoic Pilanesberg Complex, South Africa, is the world’s largest alkaline intrusive complex. Mapped geological field relationships suggest the Complex has circular inward dipping layers. However, it is unclear how the dipping layers extend at depth. As a result, the 3D geometry of the Pilanesberg Complex is unknown. Modelling of the Pilanesberg Complex uses 2D forward models as well as 3D forward and inversion, gravity and magnetic data models, to set limits on the 3D geometry of the Pilanesberg Complex. The 2D Bouguer gravity models and geology maps indicate that some of the Bushveld Complex Main Zone shifted to the west of the Pilanesberg Complex during emplacement. This, and a highly faulted country rock, accounts for a portion of how the host rock was able to accommodate the Pilanesberg Complex intrusion. The geometry of the Complex is explored with test gravity models where the model of outward dipping and vertically dipping cylinders are unable to match the Bouguer gravity signal over the Complex, but the inward dipping model matched the data to provide a possible solution for the geometry of the Complex. The Pilanesberg Complex geometry is modelled with 3D magnetic inversion, 3D forward gravity models and 2.5D gravity test profiles that were all constrained by the surface geology. The different models correlate so that best data fit for the Complex is represented by an overall inward dipping structure. Surface geological measurements indicate that the northern edge of the Complex dip out to the north. The 3D forward modelling was able to produce a positive solution that matched the gravity data with a northward dipping northern edge. The dipping northern edge is also observed on the University of British Columbia, UBC, 3D gravity inversion and the Euler deconvolution gravity profile solutions. The depth of the Pilanesberg Complex from 3D forward gravity modelling is estimated to be between 5 and 6 km. The Complex is suggested to have undergone block movement where the northern block and southern block are separated by the 30 km long Vlakfontein fault, which bisects the Complex from the north-east to the south-west. The image processing contact depth, Euler deconvolution solutions and the 3D Voxi inversion model suggest that the fresh bedrock is closer to surface in the north, while the southern block appears to be approximately 1km deeper than the northern block. The northern dip and block movement are explained by complicated structural events that include trap door graben settling which hinged on the northern edge as well as faulting and external block movement during a regional lateral extensional event. The Pilanesberg Complex intruded during a larger system of alkaline intrusions, known as the Pilanesberg Alkaline Province. The intrusions are associated with the Province due to their ages and chemical affinity. This Province includes two dyke swarms that radiate to the north-west and south of the Pilanesberg Complex, as well as smaller circular clinopyroxenite intrusions throughout the Bushveld Complex. The Pilanesberg dyke system and the circular clinopyroxenite intrusions are reversely magnetised with IGRF corrected values ranging between -150 to -320 nT compared to the normally magnetised 166 to 330 nT values of the Pilanesberg Complex. This suggests that a magnetic reversal occurred between the emplacement of the Pilanesberg Complex and the dyke System. The age data of the Complex and dyke Swarm suggest a magnetic reversal could have occurred between the emplacement of the Pilanesberg Complex and the Pilanesberg dyke System. The Complex is dated at 1602 ± 38 Ma and 1583 ± 10 Ma, from two white foyaite samples from the southern edge (using 40Ar/39Ar amphibole spectrum analysis). These ages are vastly different from previously reported ages, which ranged between 1200 Ma and 1450 Ma (Harmer R., 1992; Hansen et al., 2006). The error analysis has improved considerably from the published dates making the proposed dates plausible for the intrusion of the Pilanesberg Complex as the first and main intrusion of the Pilanesberg Alkaline Province. The Pilanesberg dyke System intruded much later between 1219 ± 6 Ma to 1268 ± 10 Ma for the red syenite dyke samples (using 40Ar/39Ar on feldspars spectrum analysis) and 1139 ± 18 Ma obtained for the grey syenite dyke (using 40Ar/39Ar on amphiboles inverse isochronal analysis). The dyke Swarm dates are significantly younger than the previously published ages for the dykes, which were between 1290 Ma and 1330 Ma (Van Niekerk, 1962; Emerman, 1991).LG201

The Iowa Homemaker vol.35, no.7

New England by Garfield, Mary Vandecar, page 5 Where else but at college?, Ruth Abbott, page 6 Kitchen formula #1: recipes, Pat McBride, page 7 Our Des Moines apartment, Marilyn Martin, page 8 Our near-campus apartment, Barbara Culver, page 9 Practice makes prize-winning pies, Sally Rosenquist Bennett, page 10 New life for the landings, Lee Klinzman, page 12 What’s New, Mary Anne Larson, page 13 Trends – Scandinavian art, Donna Danielson, page 1

Influence of neighbourhood socioeconomic position on the transition to type II diabetes in older Mexican Americans: the Sacramento Area Longitudinal Study on Aging

To examine the influence of neighbourhood socioeconomic position (NSEP) on development of diabetes over time

No father required? The welfare assessment in the Human Fertilisation and Embryology Act 2008

Of all the changes to the Human Fertilisation and Embryology Act 1990 that were introduced in 2008 by legislation of the same name, foremost to excite media attention and popular controversy was the amendment of the so-called welfare clause. This clause forms part of the licensing conditions which must be met by any clinic before offering those treatment services covered by the legislation. The 2008 Act deleted the statutory requirement that clinicians consider the need for a father of any potential child before offering a woman treatment, substituting for it a requirement that clinicians must henceforth consider the child’s need for “supportive parenting”. In this paper, we first briefly recall the history of the introduction of s 13(5) in the 1990 Act, before going on to track discussion of its amendment through the lengthy reform process that preceded the introduction of the 2008 Act. We then discuss the meaning of the phrase “supportive parenting” with reference to guidance regarding its interpretation offered by the Human Fertilisation and Embryology Authority. While the changes to s 13(5) have been represented as suggesting a major change in the law, we suggest that the reworded section does not represent a significant break from the previous law as it had been interpreted in practice. This raises the question of why it was that an amendment that is likely to make very little difference to clinical practice tended to excite such attention (and with such polarising force). To this end, we locate debates regarding s 13(5) within a broader context of popular anxieties regarding the use of reproductive technologies and, specifically, what they mean for the position of men within the family

The Rise and Fall, and the Rise (Again) of Feminist Research in Music: 'What Goes Around Comes Around'

This article reports from a two-phase study that involved an analysis of the extant literature followed by a three-part survey answered by seventy-one women composers. Through these theoretical and empirical data, the authors explore the relationship between gender and music’s symbolic and cultural capital. Bourdieu’s theory of the habitus is employed to understand the gendered experiences of the female composers who participated in the survey. The article suggests that these female composers have different investments in gender but that, overall, they reinforce the male habitus given that the female habitus occupies a subordinate position in relation to that of the male. The findings of the study also suggest a connection between contemporary feminism and the attitudes towards gender held by the participants. The article concludes that female composers classify themselves, and others, according to gendered norms and that these perpetuate the social order in music in which the male norm dominates

A case report and brief review of the literature on bilateral retinal infarction following cardiopulmonary bypass for coronary artery bypass grafting

Postoperative visual loss is a devastating perioperative complication. The commonest aetiologies are anterior ischaemic optic neuropathy (AION), posterior ischaemic optic neuropathy (PION), and central retinal artery occlusion (CRAO). These appear to be related to certain types of operation, most commonly spinal and cardiac bypass procedures; with the rest divided between: major trauma causing excessive blood loss; head/neck and nasal or sinus surgery; major vascular procedures (aortic aneurysm repair, aorto-bifemoral bypass); general surgery; urology; gynaecology; liposuction; liver transplantation and duration of surgery. The non-surgical risk factors are multifactorial: advanced age, prolonged postoperative anaemia, positioning (supine v prone), alteration of venous drainage of the retina, hypertension, smoking, atherosclerosis, hyperlipidaemia, diabetes, hypercoagulability, hypotension, blood loss and large volume resuscitation. Other important cardiac causes are septic emboli from bacterial endocarditis and emboli caused by atrial myxomata. The majority of AION cases occur during CPB followed by head/neck surgery and prone spine surgery. CPB is used to allow coronary artery bypass grafting on a motionless heart. It has many side-effects and complications associated with its use and we report here a case of bilateral retinal infarction during routine coronary artery bypass grafting in a young male patient with multiple risk factors for developing this complication despite steps to minimise its occurrence

Pan-cancer Alterations of the MYC Oncogene and Its Proximal Network across the Cancer Genome Atlas

Although theMYConcogene has been implicated incancer, a systematic assessment of alterations ofMYC, related transcription factors, and co-regulatoryproteins, forming the proximal MYC network (PMN),across human cancers is lacking. Using computa-tional approaches, we define genomic and proteo-mic features associated with MYC and the PMNacross the 33 cancers of The Cancer Genome Atlas.Pan-cancer, 28% of all samples had at least one ofthe MYC paralogs amplified. In contrast, the MYCantagonists MGA and MNT were the most frequentlymutated or deleted members, proposing a roleas tumor suppressors.MYCalterations were mutu-ally exclusive withPIK3CA,PTEN,APC,orBRAFalterations, suggesting that MYC is a distinct onco-genic driver. Expression analysis revealed MYC-associated pathways in tumor subtypes, such asimmune response and growth factor signaling; chro-matin, translation, and DNA replication/repair wereconserved pan-cancer. This analysis reveals insightsinto MYC biology and is a reference for biomarkersand therapeutics for cancers with alterations ofMYC or the PMN

Pan-Cancer Analysis of lncRNA Regulation Supports Their Targeting of Cancer Genes in Each Tumor Context

Long noncoding RNAs (lncRNAs) are commonly dys-regulated in tumors, but only a handful are known toplay pathophysiological roles in cancer. We inferredlncRNAs that dysregulate cancer pathways, onco-genes, and tumor suppressors (cancer genes) bymodeling their effects on the activity of transcriptionfactors, RNA-binding proteins, and microRNAs in5,185 TCGA tumors and 1,019 ENCODE assays.Our predictions included hundreds of candidateonco- and tumor-suppressor lncRNAs (cancerlncRNAs) whose somatic alterations account for thedysregulation of dozens of cancer genes and path-ways in each of 14 tumor contexts. To demonstrateproof of concept, we showed that perturbations tar-geting OIP5-AS1 (an inferred tumor suppressor) andTUG1 and WT1-AS (inferred onco-lncRNAs) dysre-gulated cancer genes and altered proliferation ofbreast and gynecologic cancer cells. Our analysis in-dicates that, although most lncRNAs are dysregu-lated in a tumor-specific manner, some, includingOIP5-AS1, TUG1, NEAT1, MEG3, and TSIX, synergis-tically dysregulate cancer pathways in multiple tumorcontexts

Oncogenic BRAF mutation induces DNA methylation changes in a murine model for human serrated colorectal neoplasia

Colorectal cancer is a major cause of cancer death and approximately 20% arises within serrated polyps, which are under-recognized and poorly understood. Human serrated colorectal polyps frequently exhibit both oncogenic BRAF mutation and widespread DNA methylation changes, which are important in silencing genes restraining neoplastic progression. Here, we investigated whether in vivo induction of mutant Braf is sufficient to result in coordinated promoter methylation changes for multiple cancer-related genes. The BrafV637E mutation was induced in murine intestine on an FVB;C57BL/6J background and assessed for morphological and DNA methylation changes at multiple time points from 10 days to 14 months. Extensive intestinal hyperplasia developed by 10 days post-induction of the mutation. By 8 months, most mice had murine serrated adenomas with dysplasia and invasive cancer developed in 40% of mice by 14 months. From 5 months onwards, Braf mutant mice showed extensive, gene-specific increases in DNA methylation even in hyperplastic mucosa without lesions. This demonstrates that persistent oncogenic Braf signaling is sufficient to induce widespread DNA methylation changes. This occurs over an extended period of time, mimicking the long latency followed by rapid progression of human serrated neoplasia. This study establishes for the first time that DNA methylation arises slowly in direct response to prolonged oncogenic Braf signaling in serrated polyps; this finding has implications both for chemoprevention and for understanding the origin of DNA hypermethylation in cancer generally.Catherine E. Bond, Cheng Liu, Futoshi Kawamata, Diane M. McKeone, Winnie Fernando, Saara Jamieson, Sally-Ann Pearson, Alexandra Kane, Susan L. Woods, Tamsin R.M. Lannagan, Roshini Somashekar, Young Lee, Troy Dumenil, Gunter Hartel, Kevin J. Spring, Jennifer Borowsky, Lochlan Fennell, Mark Bettington, Jason Lee, Daniel L. Worthley, Barbara A. Leggett and Vicki L.J. Whitehal