Factors associated with mothers' hesitancy to receive a COVID-19 vaccine.

Vaccine hesitancy can impact maternal and child vaccination rates. We examined factors associated with mothers' hesitancy to receive a COVID-19 vaccine using data from an online survey conducted from mid-February to mid-March 2021. Among unvaccinated participants (N = 203), 28% reported that they would probably not or definitely not get a COVID-19 vaccine. Mothers with high school/GED/trade/technical education (38% hesitant, aOR = 4.0, 95% CI: 1.2-13.2), Associate's degree (43%, aOR = 6.8, 95% CI: 2.4-19.5), and Bachelor's degree (30%, aOR = 3.1, 95% CI: 1.1-8.4) were more likely to report vaccine hesitancy compared to mothers with a graduate degree (19%). Non-Hispanic Black mothers (40% hesitant, aOR = 2.8, 95% CI: 1.0-7.6) were more likely to be vaccine hesitant compared to non-Hispanic white mothers (19%). Mothers with low pandemic-related anxiety were more likely to report vaccine hesitancy than mothers with high pandemic-related anxiety (56% vs 23% hesitant; aOR = 4.8, 95% CI: 1.7-14.1). Research is needed to understand informational, emotional, and attitudinal factors contributing to COVID-19 vaccine hesitancy among mothers to develop and test effective public health messaging to increase vaccination rates.

TRF2-mediated stabilization of hREST4 is critical for the differentiation and maintenance of neural progenitors.

Telomere repeat binding factor 2 (TRF2) is a component of the shelterin complex that is known to bind and protect telomeric DNA, yet the detection of TRF2 in extra-telomeric regions of chromosomes suggests other roles for TRF2 besides telomere protection. Here, we demonstrate that TRF2 plays a critical role in antagonizing the repressive function of neuron-restrictive silencer factor, also known as repressor element-1 silencing transcription factor (REST), during the neural differentiation of human embryonic stem cells (hESCs) by enhancing the expression of a truncated REST splice isoform we term human REST4 (hREST4) due to its similarity to rodent REST4. We show that TRF2 is specifically upregulated during hESC neural differentiation concordantly with an increase in the expression of hREST4 and that both proteins are highly expressed in NPCs. Overexpression of TRF2 in hESCs increases hREST4 levels and induces their neural differentiation, whereas TRF2 knockdown in hESCs and NPCs reduces hREST4 expression, hindering their ability to differentiate to the neural lineage. Concurrently, we show that TRF2 directly interacts with the C-terminal of hREST4 through its TRF2 core binding motif [F/Y]xL, protecting hREST4 from ubiquitin-mediated proteasomal degradation and consequently furthering neural induction. Thus, the TRF2-mediated counterbalance between hREST4 and REST is vital for both the generation and maintenance of NPCs, suggesting an important role for TRF2 in both neurogenesis and function of the central nervous system.