Digital morphogenesis

Digital morphogenesis is a type of generative art in which complex shape development, or morphogenesis, is enabled by computation. This concept is applicable in many areas of design, art, architecture, and modeling. The concept was originally developed in the field of biology, later in geology, geomorphology, and architecture. In architecture, it describes tools and methods for creating forms and adapting them to a known environment. Developments in digital morphogenesis have allowed construction and analysis of structures in more detail than could have been put into a blueprint or model by hand, with structure at all levels defined by iterative algorithms. As fabrication techniques advance, it is becoming possible to produce objects with fractal or other elaborate structures. Alan Turing Neri Oxman Rivka Oxman Birger Ragnvald Sevaldson Burry, Jane, et al. (2005). 'Dynamical Structural Modeling: A Collaborative Design Exploration', International Journal of Architectural Computing, 3, 1, pp. 27–42 Colabella, Enrica and Soddu, Celestino (1992). GENERATIVE ART & DESIGN Theory, Methodology and Projects. Environmental Design of MORPHOGENESIS, Genetic Codes of Artificial (English Version, Argenia Pub. 2020); Il Progetto Ambientale di Morfogenesi (italian version) (Bologna: Progetto Leonardo) De Landa, Manuel (1997). A Thousand Years of Nonlinear History (New York: Zone Books) Feuerstein, Günther (2002). Biomorphic Architecture: Human and Animal Forms in Architecture (Stuttgart; London: Axel Menges) Frazer, John H. (1995). An Evolutionary Architecture, Themes VII (London: Architectural Association) Hensel, Michael and Achim Menges (2008). 'Designing Morpho-Ecologies: Versatility and Vicissitude of Heterogeneous Space', Architectural Design, 78, 2, pp. 102–111 Hensel, Michael, Achim Menges, and Michael Weinstock, eds (2004). Emergence: Morphogenetic Design Strategies, Architectural Design (London: Wiley) Hensel, Michael and Achim Menges (2006). 'Material and Digital Design Synthesis', Architectural Design, 76, 2, pp.

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AR-401(y): Studio MA1 (Huang)

The studio examines the effects of artificial intelligence and automation on architecture and cities. We explore meaningful form generating processes by the use of algorithmic and parametric tools and

AR-402(y): Studio MA2 (Huang)

This studio explores the meaningful generation of architectures by the use of artificial intelligence/deep learning and parametric tools and introduces the notion of the digital vernacular in architec

The May-Hegglin anomaly gene MYH9 is a negative regulator of platelet biogenesis modulated by the Rho-ROCK pathway

Olaia Maria Naveiras Torres-Quiroga, Zhao Chen

The gene implicated in the May-Hegglin anomaly and related macrothrombocytopenias, MYH9, encodes myosin-IIA, a protein that enables morphogenesis in diverse cell types. Defective myosin-IIA complexes are presumed to perturb megakaryocyte (MK) differentiation or generation of proplatelets. We observed that Myh9(-/-) mouse embryonic stem (ES) cells differentiate into MKs that are fully capable of proplatelet formation (PPF). In contrast, elevation of myosin-IIA activity, by exogenous expression or by mimicking constitutive phosphorylation of its regulatory myosin light chain (MLC), significantly attenuates PPF. This effect occurs only in the presence of myosin-IIA and implies that myosin-IIA influences thrombopoiesis negatively. MLC phosphorylation in MKs is regulated by Rho-associated kinase (ROCK), and consistent with our model, ROCK inhibition enhances PPF. Conversely, expression of AV14, a constitutive form of the ROCK activator Rho, blocks PPF, and this effect is rescued by simultaneous expression of a dominant inhibitory MLC form. Hematopoietic transplantation studies in mice confirm that interference with the putative Rho-ROCK-myosin-IIA pathway selectively decreases the number of circulating platelets. Our studies unveil a key regulatory pathway for platelet biogenesis and hint at Sdf-1/CXCL12 as one possible extracellular mediator. The unexpected mechanism for Myh9-associated thrombocytopenia may lead to new molecular approaches to manipulate thrombopoiesis.

American Society of Hematology2007