ABSTRACT
Racial inequalities in breastfeeding have been a U.S. national concern, prompting health science research and public discourse. Social science research reveals structural causes, including racism in labor conditions, maternity care practices, and lactation support. Yet research shows that popular and health science discourses disproportionately focus on individual and community factors, blaming Black women and communities for unequal breastfeeding rates. This study examines how scientific reports are communicated to the public through a critical analysis of 104 U.S. news articles reporting research on racial disparities in breastfeeding. Findings show that articles acknowledge unequal treatment within maternity care but justify it by presenting Black patients as overburdening the maternity care systems they use due to low socioeconomic status, welfare dependency, poor family support, and poor health. Through these representations, articles co-construct racialized motherhood and maternity care systems in ways that hide manifestations of obstetric racism and combat social support for systemic change.
ABSTRACT
Background: Thyroid hormone (TH) action is mediated by three major thyroid hormone receptor (THR) isoforms α1, ß1, and ß2 (THRA1, THRB1, and THRB2). These THRs and a fourth major but non-TH binding isoform, THRA2, are encoded by two genes Thra and Thrb. Reliable antibodies against all THR isoforms are not available, and THR isoform protein levels in mammalian tissues are often inferred from messenger RNA (mRNA) levels. Methods: We generated knock-in mouse models expressing endogenously and identically 2X hemagglutenin epitope (HA)-tagged THRs (THRA1/2, THRB1, and THRB2), which could then be detected by commercially available anti-HA antibodies. Using nuclear enrichment, immunoprecipitation, and Western blotting, we determined relative THR protein expression in 16 mouse organs. Results: In all peripheral organs tested except the liver, the predominant THR isoform was THRA1. Surprisingly, in metabolically active organs such as fat and muscle, THRB1 protein levels were up to 10 times lower than that of THRA1, while their mRNA levels appeared similar. In contrast to peripheral organs, the central nervous system (CNS) had a unique pattern with relatively low levels of both THRB1 and THRA1, and high levels of THRA2 expression. As expected, THRB2 was highly expressed in the pituitary, but a previously unknown sex-specific difference in THRB2 expression was found (female mice having higher pituitary expression than male mice). Higher THRB2 expression appears to make the central axis more sensitive to TH as both serum thyrotropin and Tshb mRNA levels were lower in female mice. Conclusions: Direct comparison of THR protein abundance in different organs using endogenously tagged HA-THR mouse lines shows that expression of THR isoforms is regulated at transcriptional and posttranscriptional levels, and in organ-specific manner. The prevalence of THRA1 and low abundance of THRB1 in majority of peripheral tissues suggest that peripheral actions of these isoforms should be revisited. A unique pattern of high THRA2 in CNS warrants further exploration of this non-TH binding isoform in brain development. Finally, THRB2, in addition to cell-specific control, is also regulated in a sex-specific manner, which may change the hypothalamus-pituitary-thyroid axis set point and perhaps metabolism in males and females.
