40 research outputs found
Mismatch between obesogenic intrauterine environment and low-fat postnatal diet may confer offspring metabolic advantage
Objective: Mismatch between a depleted intrauterine environment and a substrate-rich postnatal environment confers an increased risk of offspring obesity and metabolic syndrome. Maternal diet-induced obesity (MATOB) is associated with the same outcomes. These experiments tested the hypothesis that a mismatch between a nutrient-rich intrauterine environment and a low-fat postnatal environment would ameliorate offspring metabolic morbidity
Mismatch between obesogenic intrauterine environment and low-fat postnatal diet may confer an offspring metabolic advantage
SARS-CoV-2 mRNA vaccination elicits robust antibody responses in children
Publisher Copyright: Copyright © 2022 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works. Distributed under a Creative Commons Attribution License 4.0 (CC BY)Although children have been largely spared from coronavirus disease 2019 (COVID-19), the emergence of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) variants of concern (VOCs) with increased transmissibility, combined with fluctuating mask mandates and school reopenings, has led to increased infections and disease among children. Thus, there is an urgent need to roll out COVID-19 vaccines to children of all ages. However, whether children respond equivalently to adults to mRNA vaccines and whether dosing will elicit optimal immunity remain unclear. Here, we aimed to deeply profile the vaccine-induced humoral immune response in 6- to 11-year-old children receiving either a pediatric (50 μg) or adult (100 μg) dose of the mRNA-1273 vaccine and to compare these responses to vaccinated adults, infected children, and children who experienced multisystem inflammatory syndrome in children (MIS-C). Children elicited an IgG-dominant vaccine-induced immune response, surpassing adults at a matched 100-μg dose but more variable immunity at a 50-μg dose. Irrespective of titer, children generated antibodies with enhanced Fc receptor binding capacity. Moreover, like adults, children generated cross-VOC humoral immunity, marked by a decline of omicron-specific receptor binding domain, but robustly preserved omicron spike protein binding. Fc receptor binding capabilities were also preserved in a dose-dependent manner. These data indicate that both the 50- and 100-μg doses of mRNA vaccination in children elicit robust cross-VOC antibody responses and that 100-μg doses in children result in highly preserved omicron-specific functional humoral immunity.publishersversionPeer reviewe
Second-trimester loss and subsequent pregnancy outcomes: What is the real risk?
Objective:
This study was performed to determine whether second-trimester pregnancy loss was associated with an increased risk for spontaneous preterm birth or recurrent second-trimester loss in a subsequent pregnancy.
Study Design
A retrospective cohort study was conducted. Patients with a second-trimester pregnancy loss (n =3D 38), a spontaneous preterm birth (n =3D 76), and a full term delivery (n =3D 76) were identified from 2002 to 2005 (index pregnancy). Computerized medical records were used to obtain demographic and obstetrical histories.
Results:
Frequencies of subsequent second-trimester loss were 27%, 3%, and 1% in the second-trimester loss, spontaneous preterm birth, and full-term delivery cohorts, respectively. Frequencies of subsequent spontaneous preterm birth were 33%, 39.5%, and 9% in the same 3 cohorts. Patients with a prior second-trimester loss were 10.8 times more likely to have recurrent second-trimester loss or spontaneous preterm birth, compared with those with prior full-term delivery (confidence interval 3.6 to 32.1, P < .0001).
Conclusion:
Patients with a prior second-trimester loss are at significantly increased risk for spontaneous preterm birth and recurrent second-trimester loss in their next pregnanc
Perinatal exposure to maternal obesity: Lasting cardiometabolic impact on offspring
Evidence from epidemiological, clinical, and animal model studies clearly demonstrates that prenatal and lactational maternal obesity and high-fat diet consumption are associated with cardiometabolic morbidity in offspring. Fetal and offspring sex may be an important effect modifier. Adverse offspring cardiometabolic outcomes observed in the setting of maternal obesity include an increased risk for obesity, features of metabolic syndrome (hypertension, hyperglycemia and insulin resistance, hyperlipidemia, increased adiposity), and non-alcoholic fatty liver disease. This review article synthesizes human and animal data linking maternal obesity and high-fat diet consumption in pregnancy and lactation to adverse cardiometabolic outcomes in offspring. We review key mechanisms underlying skeletal muscle, adipose tissue, pancreatic, liver, and central brain reward programming in obesity-exposed offspring, and how such malprogramming contributes to offspring cardiometabolic morbidity
Fetal brain and placental programming in maternal obesity: A review of human and animal model studies
Both human epidemiologic and animal model studies demonstrate that prenatal and lactational exposure to maternal obesity and high-fat diet are associated with adverse neurodevelopmental outcomes in offspring. Neurodevelopmental outcomes described in offspring of obese women include cognitive impairment, autism spectrum disorder (ASD), attention deficit hyperactivity disorder, anxiety and depression, disordered eating, and propensity for reward-driven behavior, among others. This review synthesizes human and animal data linking maternal obesity and high-fat diet consumption to abnormal fetal brain development, and neurodevelopmental and psychiatric morbidity in offspring. It highlights key mechanisms by which maternal obesity and maternal diet impact fetal and offspring development, and sex differences in offspring programming. In addition, we review placental effects of maternal obesity, and the role the placenta might play as an indicator vs mediator of fetal programming