An inverse problem approach to identify the internal force of a mechanosensation process in a cardiac myocyte

Mechanosensation and mechanotransduction are fundamental processes in understanding the link between physical stimuli and biological responses which currently still remain not well understood. The precise molecular mechanism involved in stress and strain detection in cells is unclear. Sarcomeres are the contractile machines of a cardiac myocyte and two main sarcomeric components that are directly involved in the sensation and transmission of mechanical stimuli are titin and filaments (thin and thick). Titin is known as the largest protein in biology with a mass of up to 4.2 MDa. Its flexible region (I-band region) may function as a length sensor (ε=l/l0) while its Z-disc domain may be involved in the sensation of tension and stress (σView the MathML source). Filaments act as contractile machineries by converting biochemical signals into mechanical work which in response cells either shorten or relax. Based on these considerations and a qualitative understanding of the maladaptation contribution to the development of heart failure, an inverse problem approach is taken to evaluate the contractile force in a mathematical model that describes mechanosensation in normal heart cells. Different functional forms to describe the contractile force are presented and for each of them we study the computational efficiency and accuracy of two numerical techniques

Physiological processes of inflammation and edema initiated by sustained mechanical loading in subcutaneous tissues : a scoping review

Deep tissue injuries are pressure ulcers which initiate in the subcutaneous tissues and extend through a bottom-up pathway. Once deep tissue injuries are visual at skin level, serious irreversible tissue damage has already occurred. In pressure ulcer development, inflammation and edema are coupled physiological processes associated with tissue damage arising due to sustained mechanical loading. This study aimed to provide an in-depth overview of the physiological processes of inflammation and edema initiated by sustained mechanical loading in subcutaneous tissues, in the context of pressure ulceration. A scoping review was performed according to the framework by Arksey and O'Malley. The databases MEDLINE, EMBASE, Web of Science, and Scopus, and the reference lists of included studies were searched for in vivo (animal, human), and in vitro studies matching the study objectives (from inception to 28 May 2018). No restrictions for inclusion were applied for study design, setting, participants, and year of publication. A total of 12 studies were included, varying in study design, sample characteristics, amount and duration of mechanical loads that were applied, follow-up time, and assessment methods. Neutrophil infiltration and edema occur in the subcutaneous tissues nearly immediately after the application of load on soft tissues. The amount of neutrophils and edema increase in the first days after the mechanical insult and decrease once healing has been initiated and no supplementary mechanical load was applied. One study indicated that edema may extend up to the level of the dermo-epidermal junction. Further research should focus on how deep tissue inflammation and edema are reflected into unique tissue changes at skin level, and how abnormal inflammatory responses manifest (e.g. when the nervous system is not functioning normally)