Photorealistic visualisation of urban greening in a low-cost high- density housing settlement.

Thesis (M.Sc.)-University of KwaZulu-Natal, Pietermaritzburg, 2005.Apartheid housing policies of the pre-1994 South African government, and the low-cost highdensity housing programmes of the post-1994 government, has given rise to numerous urban environmental problems, some of which could be addressed in a cost-effective and sustainable manner through urban greening, while simultaneously promoting biodiversity. Public participation in the planning of urban greening has been identified as being of vital importance, without which urban greening projects run a high, and expensive, risk of failure. Previous studies indicate that the greening priorities of residents in low-cost high-density housing settlements may differ considerably from those of managers and experts tasked with the protection and extension of the natural environment resource base. A system of participatory decision support is therefore required to reconcile the greening requirements of the community, and the ecological benefits of biodiversity. If language, literacy, map literacy and numeracy difficulties are to be avoided, and a sense of place or belonging is to be invoked, such a participatory decision support system should, ideally, be visually based, and capable of generating realistic eye-level depictions of the urban landscape. New computer-based landscape visualisation applications, which can directly utilise GIS, CAD and DEM data to produce detailed photo-realistic viewsheds, were deemed better suited to the task of visualising urban greening than existing GIS based mapping systems, CAD and traditional landscape visualisation methods. This dissertation examines the process of constructing a 3D computer model of the Mount Royal low-cost high-density housing settlement, situated in the eThekwini Municipality, KwaZulu-Natal, South Africa. Visualisations including terrain, natural features, indigenous vegetation, houses and roads were produced and submitted, with a questionnaire, to experts from different disciplines, Mount Royal residents and neighbors. Results from the expert survey indicate moderate support for visualisation in professional decision-making. However, both experts and residents expressed strong support for the accuracy and credibility ofthe visualisations, as well as for their potential in a participatory decision support system

Bi-allelic Loss-of-Function CACNA1B Mutations in Progressive Epilepsy-Dyskinesia.

The occurrence of non-epileptic hyperkinetic movements in the context of developmental epileptic encephalopathies is an increasingly recognized phenomenon. Identification of causative mutations provides an important insight into common pathogenic mechanisms that cause both seizures and abnormal motor control. We report bi-allelic loss-of-function CACNA1B variants in six children from three unrelated families whose affected members present with a complex and progressive neurological syndrome. All affected individuals presented with epileptic encephalopathy, severe neurodevelopmental delay (often with regression), and a hyperkinetic movement disorder. Additional neurological features included postnatal microcephaly and hypotonia. Five children died in childhood or adolescence (mean age of death: 9 years), mainly as a result of secondary respiratory complications. CACNA1B encodes the pore-forming subunit of the pre-synaptic neuronal voltage-gated calcium channel Cav2.2/N-type, crucial for SNARE-mediated neurotransmission, particularly in the early postnatal period. Bi-allelic loss-of-function variants in CACNA1B are predicted to cause disruption of Ca2+ influx, leading to impaired synaptic neurotransmission. The resultant effect on neuronal function is likely to be important in the development of involuntary movements and epilepsy. Overall, our findings provide further evidence for the key role of Cav2.2 in normal human neurodevelopment.MAK is funded by an NIHR Research Professorship and receives funding from the Wellcome Trust, Great Ormond Street Children's Hospital Charity, and Rosetrees Trust. E.M. received funding from the Rosetrees Trust (CD-A53) and Great Ormond Street Hospital Children's Charity. K.G. received funding from Temple Street Foundation. A.M. is funded by Great Ormond Street Hospital, the National Institute for Health Research (NIHR), and Biomedical Research Centre. F.L.R. and D.G. are funded by Cambridge Biomedical Research Centre. K.C. and A.S.J. are funded by NIHR Bioresource for Rare Diseases. The DDD Study presents independent research commissioned by the Health Innovation Challenge Fund (grant number HICF-1009-003), a parallel funding partnership between the Wellcome Trust and the Department of Health, and the Wellcome Trust Sanger Institute (grant number WT098051). We acknowledge support from the UK Department of Health via the NIHR comprehensive Biomedical Research Centre award to Guy's and St. Thomas' National Health Service (NHS) Foundation Trust in partnership with King's College London. This research was also supported by the NIHR Great Ormond Street Hospital Biomedical Research Centre. J.H.C. is in receipt of an NIHR Senior Investigator Award. The research team acknowledges the support of the NIHR through the Comprehensive Clinical Research Network. The views expressed are those of the author(s) and not necessarily those of the NHS, the NIHR, Department of Health, or Wellcome Trust. E.R.M. acknowledges support from NIHR Cambridge Biomedical Research Centre, an NIHR Senior Investigator Award, and the University of Cambridge has received salary support in respect of E.R.M. from the NHS in the East of England through the Clinical Academic Reserve. I.E.S. is supported by the National Health and Medical Research Council of Australia (Program Grant and Practitioner Fellowship)