To develop quantitative methods for the clinical interpretation of the ballistocardiogram (BCG). A closed-loop mathematical model of the cardiovascular system is proposed to theoretically simulate the mechanisms generating the BCG signal, which is then compared with the signal acquired via accelerometry on a suspended bed. Simulated arterial pressure waveforms and ventricular functions are in good qualitative and quantitative agreement with those reported in the clinical literature. Simulated BCG signals exhibit the typical I, J, K, L, M, and N peaks and show good qualitative and quantitative agreement with experimental measurements. Simulated BCG signals associated with reduced contractility and increased stiffness of the left ventricle exhibit different changes that are characteristic of the specific pathological condition. The proposed closed-loop model captures the predominant features of BCG signals and can predict pathological changes on the basis of fundamental mechanisms in cardiovascular physiology. This paper provides a quantitative framework for the clinical interpretation of BCG signals and the optimization of BCG sensing devices. The present paper considers an average human body and can potentially be extended to include variability among individuals.

In this article we propose a novel mathematical description of biomass growth that combines poroelastic theory of mixtures and cellular population models. The formulation, potentially applicable to general mechanobiological processes, is here used to study the engineered cultivation in bioreactors of articular chondrocytes, a process of Regenerative Medicine characterized by a complex interaction among spatial scales (from nanometers to centimeters), temporal scales (from seconds to weeks) and biophysical phenomena (fluid-controlled nutrient transport, delivery and consumption; mechanical deformation of a multiphase porous medium). The principal contribution of this research is the inclusion of the concept of cellular “force isotropy” as one of the main factors influencing cellular activity. In this description, the induced cytoskeletal tensional states trigger signalling transduction cascades regulating functional cell behavior. This mechanims is modeled by a parameter which estimates the influence of local force isotropy by the norm of the deviatoric part of the total stress tensor. According to the value of the estimator, isotropic mechanical conditions are assumed to be the promoting factor of extracellular matrix production whereas anisotropic conditions are assumed to promote cell proliferation. The resulting mathematical formulation is a coupled system of nonlinear partial differential equations comprising: conservation laws for mass and linear momentum of the growing biomass; advection–diffusion–reaction laws for nutrient (oxygen) transport, delivery and consumption; and kinetic laws for cellular population dynamics. To develop a reliable computational tool for the simulation of the engineered tissue growth process the nonlinear differential problem is numerically solved by: (1) temporal semidiscretization; (2) linearization via a fixed-point map; and (3) finite element spatial approximation. The biophysical accuracy of the mechanobiological model is assessed in the analysis of a simplified 1D geometrical setting. Simulation results show that: (1) isotropic/anisotropic conditions are strongly influenced by both maximum cell specific growth rate and mechanical boundary conditions enforced at the interface between the biomass construct and the interstitial fluid; (2) experimentally measured features of cultivated articular chondrocytes, such as the early proliferation phase and the delayed extracellular matrix production, are well described by the computed spatial and temporal evolutions of cellular populations.

The main goal of this work is to clarify and quantify, by means of mathematical analysis, the role of structural viscoelasticity in the biomechanical response of deformable porous media with incompressible constituents to sudden changes in external applied loads. Models of deformable porous media with incompressible constituents are often utilized to describe the behavior of biological tissues, such as cartilages, bones and engineered tissue scaffolds, where viscoelastic properties may change with age, disease or by design. Here, for the first time, we show that the fluid velocity within the medium could increase tremendously, even up to infinity, should the external applied load experience sudden changes in time and the structural viscoelasticity be too small. In particular, we consider a one-dimensional poro-visco-elastic model for which we derive explicit solutions in the cases where the external applied load is characterized by a step pulse or a trapezoidal pulse in time. By means of dimensional analysis, we identify some dimensionless parameters that can aid the design of structural properties and/or experimental conditions as to ensure that the fluid velocity within the medium remains bounded below a certain given threshold, thereby preventing potential tissue damage. The application to confined compression tests for biological tissues is discussed in detail. Interestingly, the loss of viscoelastic tissue properties has been associated with various disease conditions, such as atherosclerosis, Alzheimer’s disease and glaucoma. Thus, the findings of this work may be relevant to many applications in biology and medicine.