Changes in Household Challenges and Subsequent Child Welfare Report.

INTRODUCTION: Preventing child maltreatment and reducing adverse childhood experiences is critical for improving adult health. To inform prevention efforts, it is necessary to move beyond static risk models and instead model the dynamic changes in household challenges during the prebirth and early childhood periods. This study examined the effect of changes in the number of household challenges from prebirth (12 months before birth of a child) to early childhood (3 years after birth) period on the risk of a child maltreatment report by age 3 years. METHODS: This retrospective cohort study linked data from the Alaska 2009-2011 Pregnancy Risk Assessment Monitoring System, its 3-year follow-up survey, and administrative records through 2019. Participants were 1,699 birthing parents. Latent class analyses identified prebirth and early childhood low- and high-challenge respondent groups on the basis of the level of reported household challenges. The authors then modeled the relationships between group transition membership and the risk of maltreatment using latent transition analysis. Analyses were conducted in 2021. RESULTS: Households transitioning from a high-challenge-prebirth status to a low-challenge-early-childhood status had a lower predicted risk for child services report than households remaining in the high-challenges group. Transitioning from low- to high-challenges status predicted the highest risk for child services report than that of all other groups. CONCLUSIONS: To reduce the risk of child maltreatment and subsequent adverse childhood experiences, healthcare providers should screen parents for the presence of household challenges during both pregnancy and early childhood and connect patients to resources targeted at reducing those challenges and providing continuous familial support.

Changes in skeletal muscle and tendon structure and function following genetic inactivation of myostatin in rats.

Myostatin is a negative regulator of skeletal muscle and tendon mass. Myostatin deficiency has been well studied in mice, but limited data are available on how myostatin regulates the structure and function of muscles and tendons of larger animals. We hypothesized that, in comparison to wild-type (MSTN(+/+) ) rats, rats in which zinc finger nucleases were used to genetically inactivate myostatin (MSTN(Δ/Δ) ) would exhibit an increase in muscle mass and total force production, a reduction in specific force, an accumulation of type II fibres and a decrease and stiffening of connective tissue. Overall, the muscle and tendon phenotype of myostatin-deficient rats was markedly different from that of myostatin-deficient mice, which have impaired contractility and pathological changes to fibres and their extracellular matrix. Extensor digitorum longus and soleus muscles of MSTN(Δ/Δ) rats demonstrated 20-33% increases in mass, 35-45% increases in fibre number, 20-57% increases in isometric force and no differences in specific force. The insulin-like growth factor-1 pathway was activated to a greater extent in MSTN(Δ/Δ) muscles, but no substantial differences in atrophy-related genes were observed. Tendons of MSTN(Δ/Δ) rats had a 20% reduction in peak strain, with no differences in mass, peak stress or stiffness. The general morphology and gene expression patterns were similar between tendons of both genotypes. This large rodent model of myostatin deficiency did not have the negative consequences to muscle fibres and extracellular matrix observed in mouse models, and suggests that the greatest impact of myostatin in the regulation of muscle mass may not be to induce atrophy directly, but rather to block hypertrophy signalling.