Anomalous cell sorting behavior in mixed monolayers discloses hidden system complexities

In tissue development, wound healing and aberrant cancer progression cell–cell interactions drive mixing and segregation of cellular composites. However, the exact nature of these interactions is unsettled. Here we study the dynamics of packed, heterogeneous cellular systems using wound closure experiments. In contrast to previous cell sorting experiments, we find non-universal sorting behavior. For example, monolayer tissue composites with two distinct cell types that show low and high neighbor exchange rates (i.e., MCF-10A & MDA-MB-231) produce segregated domains of each cell type, contrary to conventional expectation that the construct should stay jammed in its initial configuration. On the other hand, tissue compounds where both cell types exhibit high neighbor exchange rates (i.e., MDA-MB-231 & MDA-MB-436) produce highly mixed arrangements despite their differences in intercellular adhesion strength. The anomalies allude to a complex multi-parameter space underlying these sorting dynamics, which remains elusive in simpler systems and theories merely focusing on bulk properties. Using cell tracking data, velocity profiles, neighborhood volatility, and computational modeling, we classify asymmetric interfacial dynamics. We indicate certain understudied facets, such as the effects of cell death & division, mechanical hindrance, active nematic behavior, and laminar & turbulent flow as their potential drivers. Our findings suggest that further analysis and an update of theoretical models, to capture the diverse range of active boundary dynamics which potentially influence self-organization, is warranted

Variability and host density independence in inductions-based estimates of environmental lysogeny.

Temperate bacterial viruses (phages) may enter a symbiosis with their host cell, forming a unit called a lysogen. Infection and viral replication are disassociated in lysogens until an induction event such as DNA damage occurs, triggering viral-mediated lysis. The lysogen-lytic viral reproduction switch is central to viral ecology, with diverse ecosystem impacts. It has been argued that lysogeny is favoured in phages at low host densities. This paradigm is based on the fraction of chemically inducible cells (FCIC) lysogeny proxy determined using DNA-damaging mitomycin C inductions. Contrary to the established paradigm, a survey of 39 inductions publications found FCIC to be highly variable and pervasively insensitive to bacterial host density at global, within-environment and within-study levels. Attempts to determine the source(s) of variability highlighted the inherent complications in using the FCIC proxy in mixed communities, including dissociation between rates of lysogeny and FCIC values. Ultimately, FCIC studies do not provide robust measures of lysogeny or consistent evidence of either positive or negative host density dependence to the lytic-lysogenic switch. Other metrics are therefore needed to understand the drivers of the lytic-lysogenic decision in viral communities and to test models of the host density-dependent viral lytic-lysogenic switch

CEIP-IMD El Valle : PFG septiembre, 2017, Tribunal 15.20

El tema a desarrollar en el presente proyecto es la creación de un centro de educación infantil y primaria en el Casco Histórico de Sevilla. Un centro de educación infantil y primaria es mucho más que un colegio, es un lugar para la enseñanza, la convivencia, los valores y el crecimiento, donde su diseño debe estar enfocado a ser un espacio abierto, dinámico y acogedor.Universidad de Sevilla. Arquitect

A Random Sequential Adsorption Model for Protein Adsorption to Surfaces Functionalized with Poly(ethylene oxide)

A random sequential adsorption model for the adsorption of proteins to surfaces functionalized with poly(ethylene oxide)/poly(ethylene glycol) at a range of molecular weights and grafting densities is presented. An excellent fit of the model predictions to experimental results suggests that the random arrangement of polymer chains leading to polymer‐free “bald” spots is a critical factor in primary protein adsorption

Quantifying and understanding protein adsorption to non-fouling surfaces

Surfaces grafted with poly(ethylene oxide) (PEO) are known to resist protein adsorption. Research efforts in this field have focused on both developing surfaces with better resistance to protein adsorption and understanding the origin of resistance of PEO grafted surfaces to protein adsorption. In the first part of this contribution, we describe a novel quantification technique for extremely low protein coverage on surfaces. This technique utilizes measurement of the landing rate of microtubule filaments on kinesin proteins adsorbed on a surface to determine the kinesin density. The detection limit of our technique is 100 times lower than that of standard characterization methods and is employed to test the performance of novel and established coatings with outstanding resistance to protein adsorption. In the second part, a random sequential adsorption (RSA) model is presented for protein adsorption to PEO coated surfaces. The model suggests that PEO chains act as almost perfect steric barriers to protein adsorption. Furthermore, it can be used to predict the performance of a variety of systems towards resisting protein adsorption and can help in the design of better non-fouling surface coatings

Two-Stage Capture Employing Active Transport Enables Sensitive and Fast Biosensors

Nanoscale sensors enable the detection of analytes with improved signal-to-noise ratio but suffer from mass transport limitations. Molecular shuttles, assembled from, e.g., antibody-functionalized microtubules and kinesin motor proteins, can selectively capture analytes from solution and deliver the analytes to a sensor patch. This two-stage process can accelerate mass transport to nanoscale biosensors and facilitate the rapid detection of analytes. Here, the possible increase of the signal-to-noise ratio is calculated, and the optimal layout of a system which integrates active transport is determined

Modeling the Mechanics of Cancer: Effect of Changes in Cellular and Extra-Cellular Mechanical Properties

Malignant transformation, though primarily driven by genetic mutations in cells, is also accompanied by specific changes in cellular and extra-cellular mechanical properties such as stiffness and adhesivity. As the transformed cells grow into tumors, they interact with their surroundings via physical contacts and the application of forces. These forces can lead to changes in the mechanical regulation of cell fate based on the mechanical properties of the cells and their surrounding environment. A comprehensive understanding of cancer progression requires the study of how specific changes in mechanical properties influences collective cell behavior during tumor growth and metastasis. Here we review some key results from computational models describing the effect of changes in cellular and extra-cellular mechanical properties and identify mechanistic pathways for cancer progression that can be targeted for the prediction, treatment and prevention of cancer