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Register a new userCorrelations between Chondroitin Sulfate Physicochemical Properties and its in-vitro Absorption and Anti-inflammatory Activity
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Here, we investigated the influence of physicochemical characteristics of chondroitin sulfate (CS) on its in vitro absorption and anti-inflammatory activity. We used eight different synthetic and natural CS samples with a range of molecular weights (7-35 kDa) and sulfation patterns. Our studies indicate that the absorption of CS is moderately correlated to percentage of chondroitin-6-sulfate while the anti-inflammatory activity may be weakly related to the molecular weight and the amount of total sulfation in the samples. Our in vitro studies could provide helpful screening tools for quick and effective evaluation of CS samples as a preliminary step towards in vivo studies.
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Through the last decade, cold atmospheric plasma (CAP) has emerged as an innovative therapeutic option for cancer treatment. Recently, we have set up a potentially safe atmospheric pressure plasma jet device that displays antitumoral properties in a preclinical model of cholangiocarcinoma (CCA), a rare and very aggressive cancer emerging from the biliary tree with few efficient treatments. In the present study, we aimed at deciphering the molecular mechanisms underlying the antitumor effects of CAP towards CCA both in an in vivo and in vitro context. In vivo, using subcutaneous xenografts into immunocompromised mice, CAP treatment of CCA induced DNA lesions and tumor cell apoptosis, as evaluated by 8-oxoguanine and cleaved caspase-3 immunohistochemistry, respectively. Analysis of the tumor microenvironment showed changes in markers related to macrophage polarization. In vitro, incubation of CCA cells with CAP-treated culture media (i.e. plasma-activated media, PAM) led to a dose response decrease in cell survival. At molecular level, CAP treatment induced double-strand DNA breaks, followed by an increased phosphorylation and activation of the cell cycle master regulators CHK1 and p53, leading to cell cycle arrest and cell death by apoptosis. In conclusion, CAP is a novel therapeutic option to consider for CCA in the future.
Thromboembolic complications remain a central issue in management of patients on mechanical circulatory support. Despite the best practices employed in design and manufacturing of modern ventricular assist devices, complexity and modular nature of these systems often introduces internal steps and crevices in the flow path which can serve as nidus for thrombus formation. Thrombotic potential is influenced by multiple factors including the characteristics of the flow and surface chemistry of the biomaterial. This study explored these elements in the setting of blood flow over a micro-crevice using a multi-constituent numerical model of thrombosis. The simulations reproduced the platelet deposition patterns observed experimentally and elucidated the role of flow, shear rate, and surface chemistry in shaping the deposition. The results offer insights for design and operation of blood-contacting devices.
Several biological tissues undergo changes in their geometry and in their bulk material properties by modelling and remodelling processes. Modelling synthesises tissue in some regions and removes tissue in others. Remodelling overwrites old tissue material properties with newly formed, immature tissue properties. As a result, tissues are made up of different patches, i.e., adjacent tissue regions of different ages and different material properties, within evolving boundaries. In this paper, generalised equations governing the spatio-temporal evolution of such tissues are developed within the continuum model. These equations take into account nonconservative, discontinuous surface mass balance due to creation and destruction of material at moving interfaces, and bulk balance due to tissue maturation. These equations make it possible to model patchy tissue states and their evolution without explicitly maintaining a record of when/where resorption and formation processes occurred. The time evolution of spatially averaged tissue properties is derived systematically by integration. These spatially-averaged equations cannot be written in closed form as they retain traces that tissue destruction is localised at tissue boundaries. The formalism developed in this paper is applied to bone tissues, which exhibit strong material heterogeneities due to their slow mineralisation and remodelling processes. Evolution equations are proposed in particular for osteocyte density and bone mineral density. Effective average equations for bone mineral density (BMD) and tissue mineral density (TMD) are derived using a mean-field approximation. The error made by this approximation when remodelling patchy tissue is investigated. The specific time signatures of BMD or TMD during remodelling events may provide a way to detect these events occurring at lower, unseen spatial resolutions from microCT scans.
The concept of internal anatomical asymmetry is familiar; usually in humans the heart is on the left and the liver is on the right, however how does the developing embryo know to produce this consistent laterality? Symmetry breaking initiates with left-right asymmetric cilia-driven fluid mechanics in a small fluid-filled structure called the ventral node in mice. However the question of what converts this flow into left-right asymmetric development remains unanswered. A leading hypotheses is that flow transports morphogen containing vesicles within the node, the absorption of which results in asymmetrical gene expression. To investigate how vesicle transport might result in the situs patterns observed in wildtype and mutant experiments, we extend the open source Stokes flow package, NEAREST, to consider the hydrodynamic and Brownian motion of particles in a mouse model with flow driven by one, two, and 112 beating cilia. Three models for morphogen-containing particle released are simulated to assess their compatibility with observed results in oligociliated and wildtype mouse embryos: uniformly random release, localised cilium stress induced release, and localised release from motile cilia themselves. Only the uniformly random release model appears consistent with the data, with neither localised-release model resulting in significant transport in the oligociliated embryo.
Biological invasion, whereby populations of motile and proliferative individuals lead to moving fronts that invade into vacant regions, are routinely studied using partial differential equation (PDE) models based upon the classical Fisher--KPP model. While the Fisher--KPP model and extensions have been successfully used to model a range of invasive phenomena, including ecological and cellular invasion, an often--overlooked limitation of the Fisher--KPP model is that it cannot be used to model biological recession where the spatial extent of the population decreases with time. In this work we study the textit{Fisher--Stefan} model, which is a generalisation of the Fisher--KPP model obtained by reformulating the Fisher--KPP model as a moving boundary problem. The nondimensional Fisher--Stefan model involves just one single parameter, $kappa$, which relates the shape of the density front at the moving boundary to the speed of the associated travelling wave, $c$. Using numerical simulation, phase plane and perturbation analysis, we construct approximate solutions of the Fisher--Stefan model for both slowly invading and slowly receding travelling waves, as well as for rapidly receding travelling waves. These approximations allow us to determine the relationship between $c$ and $kappa$ so that commonly--reported experimental estimates of $c$ can be used to provide estimates of the unknown parameter $kappa$. Interestingly, when we reinterpret the Fisher--KPP model as a moving boundary problem, many disregarded features of the classical Fisher--KPP phase plane take on a new interpretation since travelling waves solutions with $c < 2$ are not normally considered. This means that our analysis of the Fisher--Stefan model has both practical value and an inherent mathematical value.
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