Saudi Cultural Missions Theses & Dissertations
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Item Restricted Epigenetic Habitats : Mimesis and Living Architecture in Light of Catharine Malabou’s Meditation About Synaptic Chips(Univeristy College London, 2024) Alangari, Nujud; Vivaldi, Jordi4 Mimesis has been integrated with architecture for a long time—from ancient civilisations e.g. ancient Greece and the Renaissance to the modern and postmodern eras. These architectural eras tend to respond to Platonic or Kantian schemes, illustrating the evolution of architectural mimesis. For Plato, mimesis meant copying and reproducing nature through art; for Kant, however, it was more about harmonising beauty and function than copying from nature. Kant believed that art is a creation of genius which does not copy nature directly but rather reinvents nature’s rules into artistic expression. While rich in their interpretation of imitation, both concepts lack the dynamic meaning of mimesis when it comes to mimicking human intelligence. In this context, I would like to address the following question: Is the arrival of AI and robotics in architecture demanding a new epigenetic scheme for thinking about mimesis? I would like to address this question by considering Catherine Malabou’s interpretation of the concept of ‘synaptic chips’ that has been discussed in her work on epigenetic mimesis—an idea that transforms the entire picture of AI in architecture. The discussion of synaptic chips as presented by Malabou serves as a metaphorical basis for the evolution and adaptation of architectural design. Architectural designs may similarly evolve through the influence of connections that are synaptic-like; such structures respond to changes in their environments based on environmental stimuli. This approach—which is epigenetic—to mimesis suggests a shift more profound from just replicating forms to creating architectures that learn from their surroundings, thus adapting to them. This reveals a more complex interplay between form, function and environment than what is traditionally understood under Platonic or Kantian mimesis. Through this extension of mimesis by Malabou using neuroscience plus epigenetics, one can infer an avenue towards dynamic designs: designs that are more responsive and, in turn, enhance mimetic capabilities of AI systems within architecture—thereby also enhancing the architectural design’s adaptability and functionality.14 0Item Restricted EPIGENETIC AND TRANSCRIPTIONAL DYNAMIC IN PERIODONTAL DISEASE(University of North Carolina at Chapel Hill, 2017-03-19) Hefni, Eman; Barros, SilvanaObjectives: Several studies have shown the involvement of epigenetics with periodontal disease. Since functional dissociation of Paracellular permeability is expected during bacterial infection, we hypothesize that the methylation of host oral epithelial DNA represents an important element in the disruption of barrier function and pathogenesis of periodontal diseases. With this In vitro study, we aimed to assess whether there is altered epithelial permeability measuring trans epithelial resistance after Porphyromonas gingivalis (P. gingivalis), Campylobacter rectus (C. rectus) and Fusobacterium nucleatum (F. nucleatum) infection. Plakophilin2 (PKP2) methylation status and expression levels were also investigated. In addition, investigate the potential effects of DNA methyltransferase (DNMT) inhibitors on epithelial barrier function in response to infection with periodontal pathogen in human gingival epithelial cells. Methods: Primary human gingival epithelial cells (HGEPs) were stimulated with P. gingivalis, strain, C. rectus and F. nucleatum (MOI 50) either in the presence or absence of DNMT inhibitors (10 μM of RG108 or EGCG). CellTiter-Blue® Cell Viability Assay (Promega) was used to determine an optimum cell density and maximum inhibitor concentration at which cell viability is maintained. Transepithelial electrical resistance (TER) at various time points were performed using an EVOM® electrical resistance system. DNA methylation was quantified by PCR using EpiTect Methyl II PCR Primer Assays for PKP2. Immunofluorescence analysis was performed using PKP2 antibody and analysis performed using Zeiss710 confocal microscope. Results: Exposure of HGEPs to P. gingivalis resulted in decreased TER (P=<0.001) associated with increased cell permeability. Methylation assays showed increased methylation levels of the PKP2 in comparison to non-infected controls (P=<0.001) and an associated PKP2 down-regulation (P=<0.005). For infected cells treated with DNMT inhibitors, PKP2 mRNA expression was increased (P=<0.001) and TER values similar to non-infected cells. Comparatively, immunofluorescent staining of the PKP2 protein showed reduced protein expression in infected cells not treated with DNMT inhibitors. Conclusion: DNA methylation levels of PKP2 can affect epithelial barrier function potentially conferring increased susceptibility to infection. DNMT inhibitors can affect cell adhesion dissociation in response to infection minimizing the disturbance to the barrier function.12 0