19 research outputs found

    Platform business models : incumbent adaptation perspectives subsequent to discontinuous changes

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    This thesis explored the impact of platforms on South African Banking, Telecom and Media industries, studying how the industry competes or collaborates with the phenomenon. Thus far, research focuses on non-existential threats, which allowed for long-term adaptation and scant evidence about incumbent adaptation under discontinuous changes. This research looked at two key questions: (a) how discontinuous changes impact incumbents; and (b) how incumbents adapt their exploration and exploitation balance subsequent to discontinuous changes. A qualitative methodology was applied to answer these research questions. Semi-structured interviews were conducted with leaders and senior management involved in the organisational sense-making process to understand the phenomenon. Interview findings were analysed using thematic analysis to generate insights and meanings from the adaptation experiences. This study contributes to the literature by combing incumbent adaptation, discontinuous changes, and organisational design aspects based on in-depth interviews. There are four main findings: one, platforms were perceived as a threat, affirming past research; two, leadership assumes 3–5 years for full-scale adaptation before entirely disrupted, supporting past research in the domain; three, contrary to the literature, which expects increased exploration during discontinuous changes, Incumbents balancing their exploration and exploitation initiatives is a significant revelation; four, the transformation journey was mostly led by Top Management Teams (TMT), who preferred to run these initiatives as a separate organisation. However, these Incumbents are yet to achieve the much-talked-about network effects and the scale compared to digital-first ventures; whether their approach yields result or not, no Oracle can tell.Mini Dissertation (MPhil)--University of Pretoria, 2020.Gordon Institute of Business Science (GIBS)MPhilUnrestricte

    DRF 3188 a novel semi-synthetic analog of andrographolide: cellular response to MCF 7 breast cancer cells

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    Abstract Background We determined the effect of andrographolide and one of its novel semi-synthetic analog, DRF 3188, on the cell cycle of MCF 7 breast cancer cells. Methods The effect of the compounds on cell cycle was determined using FACS and western blot analysis of cell cycle proteins. Hollow fibre assay was used to determine if the compounds had the same effect on the cell cycle in vitro and in vivo. Results Our results from the in vitro and in vivo experiments show that both the compounds block the cell cycle at the G0-G1 phase through the induction of the cell cycle inhibitor, p27, and the concomitant decrease in the levels of Cdk4. Conclusion The results show that the novel semi-synthetic analog, DRF3188, and andrographolide bring about the anti cancer activity by a similar mechanism.</p

    DRF 3188 a novel semi-synthetic analog of andrographolide: cellular response to MCF 7 breast cancer cells-0

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    <p><b>Copyright information:</b></p><p>Taken from "DRF 3188 a novel semi-synthetic analog of andrographolide: cellular response to MCF 7 breast cancer cells"</p><p>BMC Cancer 2004;4():26-26.</p><p>Published online 18 Jun 2004</p><p>PMCID:PMC441383.</p><p>Copyright © 2004 Satyanarayana et al; licensee BioMed Central Ltd. This is an Open Access article: verbatim copying and redistribution of this article are permitted in all media for any purpose, provided this notice is preserved along with the article's original URL.</p

    Western blot analysis of cells treated with Andrographolide (25 μM) or DRF 3188 (5 μM) for 24 hours

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    <p><b>Copyright information:</b></p><p>Taken from "DRF 3188 a novel semi-synthetic analog of andrographolide: cellular response to MCF 7 breast cancer cells"</p><p>BMC Cancer 2004;4():26-26.</p><p>Published online 18 Jun 2004</p><p>PMCID:PMC441383.</p><p>Copyright © 2004 Satyanarayana et al; licensee BioMed Central Ltd. This is an Open Access article: verbatim copying and redistribution of this article are permitted in all media for any purpose, provided this notice is preserved along with the article's original URL.</p> An induction of the cell cycle inhibitor p27 and reduction in the levels of Cdk4 is observed. No change is observed in the levels of Cyclin D1, Cdk1 or Cyclin B1 in DRF 3188 treated cells. A similar effect is seen in the andrographolide treated cells, but a slight decrease in the level of Cdk 1 is observed. Lovastatin treated cells show decreased levels of Cdk1 and cyclin B1. Actin is used as the internal loading control. Densitometric analysis of the western blot with p27 antibody. An induction of p27 is seen in MCF7 cells treated with 25 uM Lovastatin (4.5 fold), 25 uM Andrographolide (3 fold) and 5 uM DRF3188 (2 fold). C) Densitometric analysis of the western blot with Cdk4 antibody. A decrease in the levels of Cdk4 is seen when MCF7 cells are treated with 25 uM Lovastatin (0.4 fold), 25 uM Andrographolide (0.8 fold) and 5 uM DRF3188 (0.4 fold)

    Synthesis and biological evaluation of new 3-substituted coumarin derivatives as selective inhibitors of human carbonic anhydrase IX and XII

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    AbstractThe Carbonic anhydrase isoforms IX and XII play a significant role in regulating the intracellular and extracellular pH in hypoxic tumours abetting the metastasis of solid tumours. Selective and potent inhibitors targeting carbonic anhydrase IX and XII reduce the activity of these isoforms in hypoxic tumours, representing an antitumor and antimetastatic mechanism. Coumarin-based derivatives are selective inhibitors of CA isoforms IX and XII. In this study, we report the design and synthesis of new 3-substituted coumarin derivatives with different functional moieties and their inhibitory activity against various carbonic anhydrase isoforms. We found that the tertiary sulphonamide derivative 6c showed selective inhibition against CA IX with IC50 of 4.1 µM. Similarly, the carbothioamides 7c, 7b and oxime ether derivative 20a exhibited good inhibition against CA IX and CA XII. Additionally, the binding mode was predicted and validated using molecular docking and dynamic simulations
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