Preterm infant body composition, working memory, and temperament.

Altered body composition in preterm infants is associated with risks to cognitive development, but the effect specific to prefrontal cortex (PFC) development is unknown. We were interested in the impact of fat mass (FM) and fat free mass (FFM) gains out to 4 months corrected gestational age (CGA) on PFC development, as indexed by working memory and temperament. This is a prospective observational pilot study recruiting 100 preterm (<33 weeks gestation), appropriate for gestational age, and very low birth weight infants, of which 49 infants met inclusion criteria. Body composition was measured using air displacement plethysmography at hospital discharge and 4 months CGA. Questionnaire based temperament assessments were completed at 12 and 24 months CGA and a working memory assessment was completed at 24 months CGA. Associations between developmental tests and body composition obtained at term and 4 months were analyzed. Increased FM at discharge was associated with increased fear and decreased soothability at 12 months. Increased FM at 4 months was associated with increased activity level, increased distress from limitations at 12 months and decreased attentional shifting, decreased frustration, and decreased inhibitory control at 24 months. Increased FFM at 4 months was associated with increased activity level at 12 months and increased impulsivity and decreased low intensity pleasure at 24 months. In this exploratory pilot study, increased FM out to 4 months and increased FFM after discharge are associated with negative markers of infant temperament. Infant temperament may be sensitive to body composition status at least to 4 months CGA.

Pediatric sleep and pain: etiologies, consequences, and clinical considerations.

STUDY OBJECTIVES: To examine current evidence of the relationship between sleep and pain from the neonatal period through adolescence. This review serves as a critical review of the literature and of the needs for future research on pediatric sleep and pain. METHODS: The PubMed online database was queried from January 1, 1960, to March 1, 2020, producing 149 articles applicable to pain and sleep in the pediatric population. Of those, 97 articles were cited in this review with the key articles including over 3800 participants. RESULTS: The pediatric literature supports the relationship between poor sleep (both sleep efficiency and nighttime awakenings) and subsequent risk for pain, especially among children with chronic disease. The reverse effect of pain on sleep is not yet well delineated. The key moderating factors explored in the literature are pharmacologic and nonpharmacologic therapies, psychologic health, and the etiology of pain. There is evidence that both altered sleep and pain early in life impact neurodevelopment, as seen by changes in sleep structure in clinical studies and alterations in brain development in animal models. CONCLUSIONS: The complicated relationship between sleep and pain is critically important during pediatric development when alterations to a normal sleep structure can have a lifelong impact. It is becoming clear that sleep deprivation and poor sleep quality exacerbate pain. Further research is needed into the complex alterations of sleep in chronic pain conditions as well as treatments to improve sleep in pediatric care. CITATION: Morris EE, Howell MJ, Pickup E, Iber C, Wang SG. Pediatric sleep and pain: etiologies, consequences, and clinical considerations. J Clin Sleep Med. 2022;18(9):2281-2289.

Randomized Trial of Early Enhanced Parenteral Nutrition and Later Neurodevelopment in Preterm Infants.

Retrospective studies indicate that the parenteral provision of calories, proteins, and lipids in the first week of life is associated with improved later neurodevelopment. We aimed to determine whether infants randomized to an enhanced parenteral nutrition protocol had improved developmental outcomes at 4, 12, or 24 months corrected age (CA). In total, 90 preterm infants (<32 weeks gestational age and <1500 g) were randomized to receive enhanced parenteral nutrition (PN) or standard PN during the first week of life. The enhanced group received a higher glucose infusion rate and intralipids. Neurodevelopmental outcomes included pattern-reversal visually evoked potentials (VEP) at 4 months CA (n = 33) and the Bayley Scales of Infant Development (BSID) at 12 (n = 46) and 24 (n = 29) months CA. P100 latency was longer in the intervention group, indicating slower processing speed (145 vs. 178 ms, p = 0.01). This association did not hold in multivariable analysis adjusting for potentially confounding variables. BSID scores were not associated with enhanced PN. Higher enteral energy and protein intake regardless of randomization group were associated with faster processing speed at 4 months CA (p ≤ 0.02 for both). Enhanced early PN was not associated with improved neurodevelopment; however, first-week enteral caloric and protein intake were associated with improved speed of processing.

A GA microsatellite in the Fli1 promoter modulates gene expression and is associated with systemic lupus erythematosus patients without nephritis.

INTRODUCTION: The transcription factor Fli1 is implicated in the pathogenesis of systemic lupus erythematosus (SLE). Recently, a GA(n) polymorphic microsatellite was characterized in the mouse Fli1 promoter that modulates promoter activity and is truncated in two lupus mouse models compared to non-autoimmune prone mice. In this work, we characterize a homologous GA(n) microsatellite in the human Fli1 promoter. The purpose of this study is to determine the effect of the microsatellite length on Fli1 promoter activity in vitro and to determine if the length of the GA(n) microsatellite is associated with SLE and/or specific disease characteristics. METHODS: Constructs with variable lengths of the GA(n) microsatellite in the Fli1 promoter were generated and analyzed in promoter/reporter (P/R) assays in a human T cell line. Using three SLE patient cohorts and matched controls, microsatellite length was measured and association with the presence of disease and the occurrence of specific disease manifestations was assessed. RESULTS: P/R assays demonstrated that the presence of a shorter microsatellite resulted in higher Fli1 promoter activity. A significant association was observed in the lupus cohort SLE in Gullah Health (SLEIGH) between the GA(26) base pair allele and absence of nephritis. CONCLUSIONS: This study demonstrates that a GA(n) microsatellite in the human Fli1 promoter is highly polymorphic. The length of the microsatellite is inversely correlated to Fli1 promoter activity in a human T cell line. Although no association between microsatellite length and lupus was observed, an association between a specific microsatellite length and patients without nephritis in the SLEIGH cohort was observed.