Muscle activity and human motion are useful parameters to map the diagnosis, treatment, and rehabilitation of neurological and movement disorders. In laboratory and clinical environments, electromyography and motion capture systems enable the collection of accurate, high-resolution data on human movement and corresponding muscle activity. However, controlled surroundings limit both the length of time and the breadth of activities that can be measured. Features of movement, critical to understanding patient progress, can change during the course of a day and daily activities may not correlate to the limited motions examined in a laboratory. We introduce a system to measure motion and muscle activity simultaneously over the course of a day in an uncontrolled environment with minimal preparation time and ease of implementation that enables daily usage. Our system combines a bespoke inertial measurement unit (IMU) and mechanomyography sensor, which measures the mechanical signal of muscular activity. The IMU can collect data continuously, and transmit wirelessly, for up to 10 h. We describe the hardware design and validation, and outline the data analysis (including data processing and activity classification algorithms) for the sensing system. Furthermore, we present two pilot studies to demonstrate utility of the system, including activity identification in six able-bodied subjects with an accuracy of 98%, and monitoring motion/muscle changes in a subject with cerebral palsy and of a single leg amputee over extended periods ($\sim$5 h). We believe these results provide a foundation for mapping human muscle activity and corresponding motion changes over time, providing a basis for a range of novel rehabilitation therapies.

Purpose of the Review: Bone adapts structure and material properties in response to its mechanical environment, a process called mechanoadpatation. For the past 50 years, finite element modeling has been used to investigate the relationships between bone geometry, material properties, and mechanical loading conditions. This review examines how we use finite element modeling in the context of bone mechanoadpatation.Recent Findings: Finite element models estimate complex mechanical stimuli at the tissue and cellular levels, help explain experimental results, and inform the design of loading protocols and prosthetics.Summary: FE modeling is a powerful tool to study bone adaptation as it complements experimental approaches. Before using FE models, researchers should determine whether simulation results will provide complementary information to experimental or clinical observations and should establish the level of complexity required. As imaging technics and computational capacity continue increasing, we expect FE models to help in designing treatments of bone pathologies that take advantage of mechanoadaptation of bone.

Molecular alteration in type I collagen, i.e., substituting the α2 chain with α1 chain in tropocollagen molecule, can cause osteogenesis imperfecta (OI), a brittle bone disease, which can be represented by a mouse model (oim/oim). In this work, we use dual-frequency Atomic Force Microscopy (AFM) and incorporated with molecular modeling to quantify the ultrastructure and stiffness of the individual native collagen fibers from wildtype (+/+) and oim/oim diseased mice humeri. Our work presents direct experimental evidences that the +/+ fibers have highly organized and compact ultrastructure and corresponding ordered stiffness distribution. In contrast, oim/oim fibers have ordered but loosely packed ultrastructure with uncorrelated stiffness distribution, as well as local defects. The molecular model also demonstrates the structural and molecular packing differences between +/+ and oim/oim collagens. The molecular mutation significantly altered sub-fibril structure and mechanical property of collagen fibers. This study can give the new insight for the mechanisms and treatment of the brittle bone disease.

Purpose of the Study: The incidence of tendon injuries increases dramatically with age, which presents a major clinical burden. While previous studies have sought to identify age-related changes in extracellular matrix structure and function, few have been able to explain fully why aged tissues are more prone to degeneration and injury. In addition, recent studies have also demonstrated that age-related processes in humans may be sex-dependent, which could be responsible for muddled conclusions in changes with age. In this study, we investigate short-term responses through an ex vivo explant culture model of stress deprivation that specifically questions how age and sex differentially affect the ability of tendons to respond to altered mechanical stimulus. Materials and Methods: We subjected murine flexor explants from young (4 months of age) and aged (22–24 months of age) male and female mice to stress-deprived culture conditions for up to 1 week and investigated changes in viability, cell metabolism and proliferation, matrix biosynthesis and composition, gene expression, and inflammatory responses throughout the culture period. Results and Conclusions: We found that aging did have a significant influence on the response to stress deprivation, demonstrating that aged explants have a less robust response overall with reduced metabolic activity, viability, proliferation, and biosynthesis. However, age-related changes appeared to be sex-dependent. Together, this work demonstrates that the aging process and the subsequent effect of age on the ability of tendons to respond to stress-deprivation are inherently different based on sex, where male explants favor increased activity, apoptosis, and matrix remodeling while female explants favor reduced activity and tissue preservation.