Mass Properties Comparison of Dismounted and Ground-Mounted Head-Supported Mass Configurations to Existing Performance and Acute Injury Risk Guidelines.

In order to limit the aviator's exposure to potentially unsafe helmet configurations, the U.S. Army Aeromedical Research Laboratory (USAARL) developed the USAARL Head-supported mass (HSM) Performance Curve and Acute Injury Risk Curve as guidelines for Army aviation HSM. These Curves remain the only established guidelines for Army HSM, but have limited applicability outside of the aviation environment. Helmet developers and program managers have requested guidelines be developed for the dismounted, ground-mounted, and airborne operating environments that consider currently fielded and proposed HSM configurations. The aim of this project was to measure mass properties (mass and center of mass offset) of currently fielded and proposed HSM configurations and compare them against the existing USAARL HSM Curve guidelines. Mass properties were collected for 71 unique dismounted and ground-mounted HSM configurations. None of the 71 HSM configurations met the Acute Injury Risk Curve recommendations, and only 11 of the 71 configurations met Performance Curve recommendations. While some helmets fell within acceptable limits, the addition of night vision goggles and protective masks pushed all configurations outside of the recommended guidelines. Future guidelines will need to be expanded to consider the operating environment, movement techniques, and primary mechanism of injury.

Increased trabecular bone and improved biomechanics in an osteocalcin-null rat model created by CRISPR/Cas9 technology.

Osteocalcin, also known as bone γ-carboxyglutamate protein (Bglap), is expressed by osteoblasts and is commonly used as a clinical marker of bone turnover. A mouse model of osteocalcin deficiency has implicated osteocalcin as a mediator of changes to the skeleton, endocrine system, reproductive organs and central nervous system. However, differences between mouse and human osteocalcin at both the genome and protein levels have challenged the validity of extrapolating findings from the osteocalcin-deficient mouse model to human disease. The rat osteocalcin (Bglap) gene locus shares greater synteny with that of humans. To further examine the role of osteocalcin in disease, we created a rat model with complete loss of osteocalcin using the CRISPR/Cas9 system. Rat osteocalcin was modified by injection of CRISPR/Cas9 mRNA into the pronuclei of fertilized single cell Sprague-Dawley embryos, and animals were bred to homozygosity and compound heterozygosity for the mutant alleles. Dual-energy X-ray absorptiometry (DXA), glucose tolerance testing (GTT), insulin tolerance testing (ITT), microcomputed tomography (µCT), and a three-point break biomechanical assay were performed on the excised femurs at 5 months of age. Complete loss of osteocalcin resulted in bones with significantly increased trabecular thickness, density and volume. Cortical bone volume and density were not increased in null animals. The bones had improved functional quality as evidenced by an increase in failure load during the biomechanical stress assay. Differences in glucose homeostasis were observed between groups, but there were no differences in body weight or composition. This rat model of complete loss of osteocalcin provides a platform for further understanding the role of osteocalcin in disease, and it is a novel model of increased bone formation with potential utility in osteoporosis and osteoarthritis research.

Differential effects of IGF-1 deficiency during the life span on structural and biomechanical properties in the tibia of aged mice.

Advanced aging is associated with the loss of structural and biomechanical properties in bones, which increases the risk for bone fracture. Aging is also associated with reductions in circulating levels of the anabolic signaling hormone, insulin-like growth factor (IGF)-1. While the role of IGF-1 in bone development has been well characterized, the impact of the age-related loss of IGF-1 on bone aging remains controversial. Here, we describe the effects of reducing IGF-1 at multiple time points in the mouse life span--early in postnatal development, early adulthood, or late adulthood on tibia bone aging in both male and female igf (f/f) mice. Bone structure was analyzed at 27 months of age using microCT. We find that age-related reductions in cortical bone fraction, cortical thickness, and tissue mineral density were more pronounced when IGF-1 was reduced early in life and not in late adulthood. Three-point bone bending assays revealed that IGF-1 deficiency early in life resulted in reduced maximum force, maximum bending moment, and bone stiffness in aged males and females. The effects of IGF-1 on bone aging are microenvironment specific, as early-life loss of IGF-1 resulted in decreased cortical bone structure and strength along the diaphysis while significantly increasing trabecular bone fraction and trabecular number at the proximal metaphysis. The increases in trabecular bone were limited to males, as early-life loss of IGF-1 did not alter bone fraction or number in females. Together, our data suggest that the age-related loss of IGF-1 influences tibia bone aging in a sex-specific, microenvironment-specific, and time-dependent manner.