The Prevalence of Stress Fractures and the Associated LEAF-Q Responses, Self-Reported Exercise Volume and Dietary Behaviors in Female Recreational Runners.

Previous research suggests a high prevalence of low energy availability (LEA) and stress fractures (SF) among competitive female endurance athletes. However, much less is known about these issues among recreational female runners. This study aimed to assess the prevalence and number of self-reported SF and risk of LEA among noncompetitive, recreationally active female runners, aged 18 - 25 years. Additionally, it compared characteristics between females with a history of multiple SF vs. one or no SF, and between those 'at risk' vs. 'not at risk' of LEA. Female recreational runners (n=485) completed an online survey that included the Low Energy Availability in Females Questionnaire (LEAF-Q) and the Disordered Eating Screening Assessment (DESA-6). Thirty-three percent of participants reported ≥ 2 SF. Eighty-two percent of the ≥ 2 SF group were classified as 'at risk' of LEA (LEAF-Q score ≥ 8). In addition, ≥ 2 SF was associated with higher total LEAF-Q score, self-reported intentional food restriction for weight loss, and self-reported current eating disorder while weekly exercise duration was inversely associated with ≥ 2 SF. In conclusion, one-third of participants had multiple SF with a majority (82%) of this group classified as 'at risk' of LEA. Screening tools such as the LEAF-Q and DESA-6 are useful tools to identify characteristics associated with multiple SF in this demographic, especially questions regarding food restriction and the presence of a current or previous eating disorder.

Neurodegeneration in a novel invertebrate model system: Failed microtubule-mediated cell adhesion and unraveling of macroglia.

Neurodegenerative diseases are among the main causes of death in the United States, leading to irreversible disintegration of neurons. Despite intense international research efforts, cellular mechanisms that initiate neurodegeneration remain elusive, thus inhibiting the development of effective preventative and early onset medical treatment. To identify underlying cellular mechanisms that initiate neuron degeneration, it is critical to identify histological and cellular hallmarks that can be linked to underlying biochemical processes. Due to the poor tissue preservation of degenerating mammalian brain tissue, our knowledge regarding histopathological hallmarks of early to late degenerative stages is only fragmentary. Here, we introduce a novel model organism to study histological hallmarks of neurodegeneration, the spider Cupiennius salei. We utilized toluidine blue-stained 0.9-µm serial semithin and 50-nm ultrathin sections of young and old spider nervous tissue. Our findings suggest that the initial stages of neurodegeneration in spiders may be triggered by (1) dissociation of neuron- and glia-derived microtubules, and (2) the weakening of microtubule-associated desmosomal junctions that lead to the unraveling of neuron-insulating macroglia, compromising the structural integrity of affected neurons. The involvement of macroglia in the disposal of neuronal debris described here-although different in the proposed transport mechanisms-shows resemblance to the mammalian glymphatic system. We propose that this model system is highly suitable to investigate invertebrate neurodegenerative processes from early onset to scar formation and that this knowledge may be useful for the study of neurodegeneration in mammalian tissue.