4 resultados para Phenotype

em Cambridge University Engineering Department Publications Database


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This paper tackles the novel challenging problem of 3D object phenotype recognition from a single 2D silhouette. To bridge the large pose (articulation or deformation) and camera viewpoint changes between the gallery images and query image, we propose a novel probabilistic inference algorithm based on 3D shape priors. Our approach combines both generative and discriminative learning. We use latent probabilistic generative models to capture 3D shape and pose variations from a set of 3D mesh models. Based on these 3D shape priors, we generate a large number of projections for different phenotype classes, poses, and camera viewpoints, and implement Random Forests to efficiently solve the shape and pose inference problems. By model selection in terms of the silhouette coherency between the query and the projections of 3D shapes synthesized using the galleries, we achieve the phenotype recognition result as well as a fast approximate 3D reconstruction of the query. To verify the efficacy of the proposed approach, we present new datasets which contain over 500 images of various human and shark phenotypes and motions. The experimental results clearly show the benefits of using the 3D priors in the proposed method over previous 2D-based methods. © 2011 IEEE.

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Physical forces generated by cells drive morphologic changes during development and can feedback to regulate cellular phenotypes. Because these phenomena typically occur within a 3-dimensional (3D) matrix in vivo, we used microelectromechanical systems (MEMS) technology to generate arrays of microtissues consisting of cells encapsulated within 3D micropatterned matrices. Microcantilevers were used to simultaneously constrain the remodeling of a collagen gel and to report forces generated during this process. By concurrently measuring forces and observing matrix remodeling at cellular length scales, we report an initial correlation and later decoupling between cellular contractile forces and changes in tissue morphology. Independently varying the mechanical stiffness of the cantilevers and collagen matrix revealed that cellular forces increased with boundary or matrix rigidity whereas levels of cytoskeletal and extracellular matrix (ECM) proteins correlated with levels of mechanical stress. By mapping these relationships between cellular and matrix mechanics, cellular forces, and protein expression onto a bio-chemo-mechanical model of microtissue contractility, we demonstrate how intratissue gradients of mechanical stress can emerge from collective cellular contractility and finally, how such gradients can be used to engineer protein composition and organization within a 3D tissue. Together, these findings highlight a complex and dynamic relationship between cellular forces, ECM remodeling, and cellular phenotype and describe a system to study and apply this relationship within engineered 3D microtissues.

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The interaction between Salmonella enterica and the host immune system is complex. The outcome of an infection is the result of a balance between the in vivo environment where the bacteria survive and grow and the regulation of fitness genes at a level sufficient for the bacteria to retain their characteristic rate of growth in a given host. Using bacteriological counts from tissue homogenates and fluorescence microscopy to determine the spread, localization, and distribution of S. enterica in the tissues, we show that, during a systemic infection, S. enterica adapts to the in vivo environment. The adaptation becomes a measurable phenotype when bacteria that have resided in a donor animal are introduced into a recipient naïve animal. This adaptation does not confer increased resistance to early host killing mechanisms but can be detected as an enhancement in the bacterial net growth rate later in the infection. The enhanced growth rate is lost upon a single passage in vitro, and it is therefore transient and not due to selection of mutants. The adapted bacteria on average reach higher intracellular numbers in individual infected cells and therefore have patterns of organ spread different from those of nonadapted bacteria. These experiments help in developing an understanding of the influence of passage in a host on the fitness and virulence of S. enterica.