Short- and long-term alterations of hematopoietic cell lineages in rats with congenital iron deficiency.

Data support that fetal iron delivery is prioritized to hemoglobin in erythrocytes (RBC). Iron deficiency (ID) during pregnancy can cause congenital ID, i.e.

Influence of Biological Sex and Congenital Iron Deficiency on Neonatal Cytokine Responses.

Background/objectives: Stimulated cord blood mononuclear cell (CBMC) cytokine responses were previously shown to predict the risk of childhood atopic disease. Iron deficiency (ID) at birth may also program atopic disease. Males are at a higher risk of pediatric atopic disease, but it is not known whether congenital ID impacts CBMC immune responses differentially by sex.

Prognostic Performance of Hematological and Serum Iron and Metabolite Indices for Detection of Early Iron Deficiency Induced Metabolic Brain Dysfunction in Infant Rhesus Monkeys.

Background: The current pediatric practice of monitoring for infantile iron deficiency (ID) via hemoglobin (Hgb) screening at one y of age does not identify preanemic ID nor protect against later neurocognitive deficits.

Objectives: To identify biomarkers of iron-related metabolic alterations in the serum and brain and determine the sensitivity of conventional iron and heme indices for predicting risk of brain metabolic dysfunction using a nonhuman primate model of infantile ID.

Methods: Simultaneous serum iron and RBC indices, and serum and cerebrospinal fluid (CSF) metabolomic profiles were determined in 20 rhesus infants, comparing iron sufficient (IS; N = 10) and ID (N = 10) infants at 2 and 4 mo of age.

The Impact of a Scholarly Concentration Program on Medical Student Research in Pediatrics.

Introduction: To promote scientific inquiry, medical schools encourage medical students to participate in scholarly concentration programs (SCP). Manuscript publishing, a proxy of productivity, enhances medical student understanding of scientific inquiry. To evaluate an elective medical SCP offered between the first two years of medical school, the pediatrician authors' primary aim was to study the publishing productivity of the program participants in the University of Wisconsin (UW) School of Medicine and Public Health Department of Pediatrics compared to other departments.

Reticulocyte Hemoglobin Equivalent has Comparable Predictive Accuracy as Conventional Serum Iron Indices for Predicting Iron Deficiency and Anemia in a Nonhuman Primate model of Infantile Iron Deficiency.

Background: Infantile iron deficiency (ID) causes anemia and compromises neurodevelopment. Current screening relies on hemoglobin (Hgb) determination at 1 year of age, which lacks sensitivity and specificity for timely detection of infantile ID. Low reticulocyte Hgb equivalent (RET-He) indicates ID, but its predictive accuracy relative to conventional serum iron indices is unknown.

Tandem mass tag proteomic and untargeted metabolomic profiling reveals altered serum and CSF biochemical datasets in iron deficient monkeys.

The effects of early-life iron deficiency anemia (IDA) extend past the blood and include both short- and long-term adverse effects on many tissues including the brain. Prior to IDA, iron deficiency (ID) can cause similar tissue effects, but a sensitive biomarker of iron-dependent brain health is lacking. To determine serum and CSF biomarkers of ID-induced metabolic dysfunction we performed proteomic and metabolomic analysis of serum and CSF at 4- and 6- months from a nonhuman primate model of infantile IDA.

Multiomic profiling of iron-deficient infant monkeys reveals alterations in neurologically important biochemicals in serum and cerebrospinal fluid before the onset of anemia.

The effects of iron deficiency (ID) during infancy extend beyond the hematologic compartment and include short- and long-term adverse effects on many tissues including the brain. However, sensitive biomarkers of iron-dependent brain health are lacking in humans. To determine whether serum and cerebrospinal fluid (CSF) biomarkers of ID-induced metabolic dysfunction are concordant in the pre/early anemic stage of ID before anemia in a nonhuman primate model of infantile iron deficiency anemia (IDA).

Impact and interactions between risk factors on the iron status of at-risk neonates.

Objective: Examine interactions between perinatal risk factors for congenital iron deficiency (ID) using two cohorts.

Study Design: Iron status in a composite 767-member cord blood cohort and a NICU cohort of 257 infants < 33 weeks of gestation or small for gestational age (SGA). Risks for ID were examined.

Serum Ferritin Threshold for Iron Deficiency Screening in One-Year-Old Children.

The American Academy of Pediatrics recommends universal hemoglobin screening for iron deficiency anemia using hemoglobin <110 g/L at the 1-year-old well child visit. Our retrospective study suggests the need for combined hemoglobin and serum ferritin iron deficiency screening and raising the diagnostic serum ferritin threshold to 24-25 μg/L.

Thyroid Hormone Function in Small for Gestational Age Term Newborns.

Objective: To test the hypothesis that term-born small for gestational age (SGA) neonates have elevated thyroid-stimulating hormone (TSH) concentrations and an increased incidence of congenital hypothyroidism compared with non-SGA term neonates.

Study Design: This retrospective cohort study included all term neonates screened in Wisconsin in 2015 and 2016. The cohort was divided based on SGA status, defined as birth weight <10th percentile as calculated from the World Health Organization's sex-specific growth charts for age 0-2 years.

Cord blood DNA methylation modifications in infants are associated with white matter microstructure in the context of prenatal maternal depression and anxiety.

Maternal and environmental factors influence brain networks and architecture via both physiological pathways and epigenetic modifications. In particular, prenatal maternal depression and anxiety symptoms appear to impact infant white matter (WM) microstructure, leading us to investigate whether epigenetic modifications (i.e.

Correcting iron deficiency anemia with iron dextran alters the serum metabolomic profile of the infant Rhesus Monkey.

Background: The effects of infantile iron deficiency anemia (IDA) extend beyond hematological indices and include short- and long-term adverse effects on multiple cells and tissues. IDA is associated with an abnormal serum metabolomic profile, characterized by altered hepatic metabolism, lowered NAD flux, increased nucleoside levels, and a reduction in circulating dopamine levels.

Objectives: The objective of this study was to determine whether the serum metabolomic profile is normalized after rapid correction of IDA using iron dextran injections.

Infantile Iron Deficiency Affects Brain Development in Monkeys Even After Treatment of Anemia.

A high percent of oxidative energy metabolism is needed to support brain growth during infancy. Unhealthy diets and limited nutrition, as well as other environmental insults, can compromise these essential developmental processes. In particular, iron deficiency anemia (IDA) has been found to undermine both normal brain growth and neurobehavioral development.

A Practical Screening Tool to Predict Early Childhood Obesity Risk: Examining a Birth Cohort.

Children obese at the age of 5 years are at greater risk of lifelong obesity. Because certain risks of obesity can be identified in early infancy, a tool for obesity risk prediction in early life would be clinically useful. We investigated predictors of obesity risk in a novel, prospectively collected healthy birth cohort recruited for demographic risks to develop iron deficiency at 1 year, a cohort leveraged because risk factors for iron deficiency and obesity overlap.

Iron Nutrition, Erythrocytes, and Erythropoietin in the NICU: Erythropoietic and Neuroprotective Effects.

Prematurity, maternal diabetes, maternal smoking, being medically underserved, and small size for gestational age are common characteristics of neonates in the NICU and can predispose them to develop congenital iron deficiency. Iron is critical for organ development. In the fetus and newborn, iron is prioritized for red blood cell production, sometimes at the expense of other tissues, including the brain.

Maternal iron nutriture modulates placental development in a rat model of fetal alcohol spectrum disorder.

Prenatal alcohol exposure (PAE) causes developmental abnormalities known as fetal alcohol spectrum disorder (FASD). Maternal iron status modulates the severity of these defects in the offspring. Because the placenta is central in supporting fetal development, we investigated whether maternal iron status similarly modulates alcohol's effects in the placenta.

Early-Life Iron Deficiency and Its Natural Resolution Are Associated with Altered Serum Metabolomic Profiles in Infant Rhesus Monkeys.

Background: Iron deficiency is the most common nutrient deficiency in human infants aged 6 to 24 mo, and negatively affects many cellular metabolic processes, including energy production, electron transport, and oxidative degradation of toxins. There can be persistent influences on long-term metabolic health beyond its acute effects.

Objectives: The objective was to determine how iron deficiency in infancy alters the serum metabolomic profile and to test whether these effects persist after the resolution of iron deficiency in a nonhuman primate model of spontaneous iron deficiency.

Cord Blood-Derived Exosomal CNTN2 and BDNF: Potential Molecular Markers for Brain Health of Neonates at Risk for Iron Deficiency.

Maternal iron deficiency anemia, obesity, and diabetes are prevalent during pregnancy. All are associated with neonatal brain iron deficiency (ID) and neurodevelopmental impairment. Exosomes are extracellular vesicles involved in cell-cell communication.

Alcohol's Dysregulation of Maternal-Fetal IL-6 and p-STAT3 Is a Function of Maternal Iron Status.

Background: Prenatal alcohol exposure (PAE) causes long-term growth and neurodevelopmental deficits that are worsened by maternal iron deficiency (ID). In our preclinical rat model, PAE causes fetal anemia, brain ID, and elevated hepatic iron via increased maternal and fetal hepcidin synthesis. These changes are normalized by a prenatal iron-fortified (IF) diet.

Cord Blood Erythropoietin and Hepcidin Reflect Lower Newborn Iron Stores due to Maternal Obesity during Pregnancy.

Objective: Obesity during pregnancy impedes fetal iron endowment. In adults, both iron depletion and hypoxia stimulate erythropoietin (Epo) production, while hepcidin, the primary iron regulator, is inhibited by Epo and stimulated by obesity. To understand this relationship in fetuses, we investigated obesity, inflammation, and fetal iron status on fetal Epo and hepcidin levels.

Maternal Perceived Stress during Pregnancy Increases Risk for Low Neonatal Iron at Delivery and Depletion of Storage Iron at One Year.

Objective: To investigate the impact of maternal stress during pregnancy on newborn iron and stage 1 iron deficiency at 1 year of age.

Study Design: In total, 245 mothers and their newborn infants (52% male; 72% white) were recruited at the Meriter Hospital Birthing Center on the basis of known risk factors for iron deficiency. Umbilical cord blood hemoglobin and zinc protoporphyrin/heme (ZnPP/H) were determined to evaluate erythrocyte iron and plasma ferritin was determined to reflect storage iron.

Antibiotic Stewardship in the Neonatal Intensive Care Unit: Effects of an Automatic 48-Hour Antibiotic Stop Order on Antibiotic Use.

Background: Meeting antibiotic stewardship goals in the neonatal intensive care unit (NICU) is challenging because of the unique nature of newborns and the lack of specificity of clinical signs of sepsis. Antibiotics are commonly continued for 48 hours pending culture results and clinical status. The goal of this study was to examine if the implementation of a 48-hour automatic stop (autostop) order during NICU admissions would decrease antibiotic use at UnityPoint Health-Meriter.