A mixed-methods study to test a tailored coaching program for health researchers to manage stress and achieve work-life balance.

Dissemination and implementation (D&I) researchers serve critical scientific, practical, and personal roles in translating science to public health benefit. However, they face multifaceted barriers that may erode their capacity to plan, lead, and evaluate implementation. Individualized coaching focused on human flourishing is an unexplored approach to fully actualize D&I researchers' capacity to bridge the research-practice gap. The purpose of this exploratory pilot study was to investigate a tailored coaching program to support human flourishing among D&I researchers. A pragmatic, mixed-methods approach guided by the RE-AIM (Reach, Effectiveness, Adoption, Implementation, Maintenance) Framework was used to evaluate an individualized, nine session coaching program called FUEL (Focus, Unplug, Exercise, Love). Reach and Implementation were assessed through descriptive statistics and rapid qualitative analysis of surveys and coaching logs. Effectiveness and Maintenance were assessed through descriptive statistics and iterative content analysis of participant surveys, as well as iterative content analysis of proxy (e.g., colleague) semi-structured interviews. Reach results indicated that demand for coaching exceeded study enrollment capacity (n = 16 participants). Implementation results showed that the coach spent 12.96 ± 2.82 hr per participant over 3 months. Effectiveness and Maintenance results indicated that FUEL was well-received and provided participants with myriad psychological and professional benefits. Preliminary evidence suggests that the FUEL coaching program is a promising and feasible approach to enhance flourishing among D&I researchers. Future research is needed to evaluate Adoption and scalability. This pilot study may inform future D&I capacity-building initiatives that address researchers' holistic situatedness within the implementation process.

Magnesium sulfate differentially modulates fetal membrane inflammation in a time-dependent manner.

PROBLEM: Chorioamnionitis and infection-associated inflammation are major causes of preterm birth. Magnesium sulfate (MgSO4 ) is widely used in obstetrics as a tocolytic; however, its mechanism of action is unclear. This study sought to investigate how MgSO4 modulates infection-associated inflammation in fetal membranes (FMs), and whether the response was time dependent. METHOD OF STUDY: Human FM explants were treated with or without bacterial lipopolysaccharide (LPS); with or without MgSO4 added either: 1 hour before LPS; at the same time as LPS; 1 hour post-LPS; or 2 hours post-LPS. Explants were also treated with or without viral dsRNA and LPS, alone or in combination; and MgSO4 added 1 hour post-LPS After 24 hours, supernatants were measured for cytokines/chemokines; and tissue lysates measured for caspase-1 activity. RESULTS: Lipopolysaccharide-induced FM inflammation by upregulating the secretion of a number of inflammatory cytokines/chemokines. Magnesium sulfate administered 1-hour post-LPS inhibited FM secretion of IL-1ß, IL-6, G-CSF, RANTES, and TNFα. Magnesium sulfate administered 2 hours post-LPS augmented FM secretion of these factors as well as IL-8, IFNγ, VEGF, GROα and IP-10. Magnesium sulfate delivered 1- hour post-LPS inhibited LPS-induced caspase-1 activity, and inhibited the augmented IL-1ß response triggered by combination viral dsRNA and LPS. CONCLUSION: Magnesium sulfate differentially modulates LPS-induced FM inflammation in a time-dependent manner, in part through its modulation of caspase-1 activity. Thus, the timing of MgSO4 administration may be critical in optimizing its anti-inflammatory effects in the clinical setting. MgSO4 might also be useful at preventing FM inflammation triggered by a polymicrobial viral-bacterial infection.

Insulin resistance and metabolic syndrome in the pediatric population.

The metabolic syndrome is a constellation of specific anthropometric, physiological, and biochemical abnormalities predisposing affected individuals to the development of diabetes and cardiovascular disease. The syndrome is well described in the adult literature. However, its description in the pediatric literature is more limited. Due in large part to the normal physiological changes that occur in children and adolescents with respect to growth and puberty, investigators have also struggled to establish a standard definition of the syndrome in the pediatric age group, hindering coordinated research efforts. However, whatever definition of the syndrome is used, the prevalence of the metabolic syndrome in the pediatric age group has increased worldwide. Insulin resistance is the principal metabolic abnormality that is common to the development of the metabolic syndrome in both children and adults. This review summarizes current research regarding the pathophysiology of insulin resistance and how this may contribute to specific abnormalities seen in children and adolescents with the metabolic syndrome. Specifically, insulin resistance in pediatric patients is correlated with cardiovascular risk factors such as elevated blood pressure, dyslipidemia, and type 2 diabetes mellitus, all of which are significant risk factors for adult disease. In addition, current treatment and prevention strategies, including lifestyle modifications, pharmacologic agents, and certain surgical therapies, are highlighted. The need for collaborative changes at the family, school, city, state, and national levels to address the growing prevalence of the metabolic syndrome in the pediatric age group is also reviewed.

Floating-Harbor syndrome and intramedullary spinal cord ganglioglioma: case report and observations from the literature.

We report on a 5-year-old male with expressive language delay, developmental delay, short stature, and facial anomalies consistent with Floating-Harbor syndrome (FHS). In addition, he developed an intramedullary ganglioglioma. This is the first reported case of a tumor associated with FHS, and may represent an as yet undefined genetic link between spinal cord tumors and FHS, adding this syndrome to the growing list of disorders with a predisposition for tumor development.