Prenatal Education in the Digital Age.

The millennial pregnant patient expects an innovative approach to prenatal care. Patients are reaching to peer support online communities or engaging in direct-to-consumer mobile applications during their pregnancy. Currently developed solutions show promise, however, the clinical impact and generalizability of these solutions remains unclear. Technology has the potential to decrease health care disparities, improve patient and provider satisfaction as well as clinical outcomes. In this article we discuss traditional models of prenatal education as well and suggest how obstetricians should consider utilizing technology as an approach to provide prenatal education to their patients.

Nuclear receptor corepressor and histone deacetylase 3 govern circadian metabolic physiology.

Rhythmic changes in histone acetylation at circadian clock genes suggest that temporal modulation of gene expression is regulated by chromatin modifications. Furthermore, recent studies demonstrate a critical relationship between circadian and metabolic physiology. The nuclear receptor corepressor 1 (Ncor1) functions as an activating subunit for the chromatin modifying enzyme histone deacetylase 3 (Hdac3). Lack of Ncor1 is incompatible with life, and hence it is unknown whether Ncor1, and particularly its regulation of Hdac3, is critical for adult mammalian physiology. Here we show that specific, genetic disruption of the Ncor1-Hdac3 interaction in mice causes aberrant regulation of clock genes and results in abnormal circadian behaviour. These mice are also leaner and more insulin-sensitive owing to increased energy expenditure. Unexpectedly, loss of a functional Ncor1-Hdac3 complex in vivo does not lead to sustained increases in known catabolic genes, but instead significantly alters the oscillatory patterns of several metabolic genes, demonstrating that circadian regulation of metabolism is critical for normal energy balance. These findings indicate that activation of Hdac3 by Ncor1 is a nodal point in the epigenetic regulation of circadian and metabolic physiology.

Assessing the impact of telehealth implementation on postpartum outcomes for Black birthing people.

BACKGROUND: The COVID-19 pandemic led to the rapid uptake of telemedicine services, which have been shown to be potentially cost-saving and of comparable quality to in-person care for certain populations. However, there are some concerns regarding the feasibility of implementation for marginalized populations, and the impact of widespread implementation of these services on health disparities has not been well studied. OBJECTIVE: This study aimed to assess the impact of telehealth implementation on postpartum care during the COVID-19 pandemic on racial disparities in visit attendance and completion of postpartum care goals. STUDY DESIGN: In this retrospective cohort study at a single tertiary care center, differences in outcomes between all Black and non-Black patients who had scheduled postpartum visits before and after telehealth implementation for postpartum care were compared. The primary outcome was postpartum visit attendance. The secondary outcomes included postpartum depression screening, contraception selection, breastfeeding status, completion of postpartum 2-hour glucose tolerance test, and cardiology follow-up for hypertensive disorders of pregnancy. In multivariable analysis, interaction terms were used to evaluate the differential impact of telehealth implementation by race. RESULTS: Of 1579 patients meeting the inclusion criteria (780 in the preimplementation group and 799 in the postimplementation group), 995 (63%) self-identified as Black. In the preimplementation period, Black patients were less likely to attend a postpartum visit than non-Black patients (63.9% in Black patients vs 88.7% in non-Black patients; adjusted odds ratio, 0.48; 95% confidence interval, 0.29-0.79). In the postimplementation period, there was no difference in postpartum visit attendance by race (79.1% in Black patients vs 88.6% in non-Black patients; adjusted odds ratio, 0.74; 95% confidence interval, 0.45-1.21). In addition, significant differences across races in postpartum depression screening during the preimplementation period became nonsignificant in the postimplementation period. Telehealth implementation for postpartum care significantly reduced racial disparities in postpartum visit attendance (interaction P=.005). CONCLUSION: Telehealth implementation for postpartum care during the COVID-19 pandemic was associated with decreased racial disparities in postpartum visit attendance.

Retinol saturase promotes adipogenesis and is downregulated in obesity.

Adipocyte differentiation is controlled by many transcription factors, but few known downstream targets of these factors are necessary for adipogenesis. Here we report that retinol saturase (RetSat), which is an enzyme implicated in the generation of dihydroretinoid metabolites, is induced during adipogenesis and is directly regulated by the transcription factor peroxisome proliferator activated receptor gamma (PPARgamma). Ablation of RetSat dramatically inhibited adipogenesis but, surprisingly, this block was not overcome by the putative product of RetSat enzymatic activity. On the other hand, ectopic RetSat with an intact, but not a mutated, FAD/NAD dinucleotide-binding motif increased endogenous PPARgamma transcriptional activity and promoted adipogenesis. Indeed, RetSat was not required for adipogenesis when cells were provided with exogenous PPARgamma ligands. In adipose tissue, RetSat is expressed in adipocytes but is unexpectedly downregulated in obesity, most likely owing to infiltration of macrophages that we demonstrate to repress RetSat expression. Thiazolidinedione treatment reversed low RetSat expression in adipose tissue of obese mice. Thus, RetSat plays an important role in the biology of adipocytes, where it favors normal differentiation, yet is reduced in the obese state. RetSat is thus a novel target for therapeutic intervention in metabolic disease.

IL-1 receptor blockade prevents fetal cortical brain injury but not preterm birth in a mouse model of inflammation-induced preterm birth and perinatal brain injury.

PROBLEM: Exposure to intrauterine inflammation, associated with preterm birth, has been linked to a devastating spectrum of neurobehavioral disorders. Mechanisms of this injury are unknown. Using a mouse model of intrauterine inflammation, we have observed a disruption of fetal neuronal morphology along with a marked elevation of interleukin (IL)-1ß in the fetal brain and placenta. In this study, we hypothesized that IL-1 plays a key role in perinatal brain injury. METHOD OF STUDY: Utilizing a mouse model of inflammation-induced preterm birth, we investigated the role of IL-1 in fetal cortical injury as well as preterm birth. In these studies, dams received systemic treatment with IL-1 receptor antagonist prior to administration of intrauterine inflammation. RESULTS: Systemic maternal antagonism of IL-1 improved fetal cortical neuronal injury associated with the exposure to intrauterine inflammation, without affecting the phenotype of preterm birth. IL-1 receptor antagonist blocked activation of neuronal nitric oxide synthase in perinatal cortex, a key enzyme implicated in neurotoxicity. CONCLUSION: Our data suggest that fetal cortical brain injury and preterm birth may occur by divergent mechanisms. Furthermore, our studies indicate maternal administration of IL-1 receptor antagonist (IL-1RA) blocked neuronal nitric oxide synthase activation observed in the brain cortex and, we speculate, that this alteration in activation leads to demonstrated decreased neurotoxicity.