In the United States, public funding restrictions prohibit the use of federal funding for abortion services. In this paper, we consider the ef- fects of these initial federal funding restrictions through the Hyde Amend- ment. We find that the federal prohibition of abortion funding raises fer- tility by two percent for young adult women in counties with high Med- icaid eligibility. The Hyde Amendment also disproportionately impacts non-white women, those more likely to be receiving Medicaid. After the Hyde Amendment, relative to white women, there is an increase in non- white hospitalizations for abortion complications, a temporary increase in nonwhite maternal mortality, and a worsening of non-white economic out- comes. Overall, federal abortion funding restrictions appear to widen health and economic racial disparities.

Celiac disease (CeD) is a multifaceted intestinal disorder with autoimmune characteristics, triggered by T cell recognition of gluten peptides presented in the context of HLA-DQ8, leading to inflammation. While the role of regulatory T cells (Tregs) in immune modulation is well-established, the specific contributions of thymic Tregs (tTregs) versus peripheral Tregs (pTregs) in mucosal tolerance remain uncertain. This study aims to elucidate the role of pTregs in gluten-induced inflammation using a novel mouse model. HLA-DQ8/Ab knockout (Ab ko) mice were bred with CNS-deficient (CNS -/-) mice, which lack the capacity to generate pTregs. Both HLA-DQ8/Ab ko and HLA-DQ8/Ab ko/CNS -/- mice were immunized with PT-Gliadin, and CD4+ T cells were sorted and transferred into HLA-DQ8/Ab ko/TCRαKO recipient mice. These recipients were fed a gluten-free or gluten-enriched diet for 12 weeks before euthanasia. Inflammation and immune cell profiles in small intestinal tissues and intraepithelial lymphocytes (IELs) were assessed. CNS -/- mice on a gluten-enriched diet exhibited significant weight loss and increased fecal lipocalin levels, indicative of inflammation. Analysis revealed a reduction in CD4+ T cells and Tregs and an increase in CD8+ T cells in intestinal tissues and IELs. However, activation markers of lymphocytes did not significantly differ between the groups. This adoptive transfer model provides a robust platform for investigating the role of pTregs in gluten tolerance and Celiac disease inflammation. It highlights the impact of pTreg deficiency on intestinal immune homeostasis and offers a valuable tool for future therapeutic studies.

Background: Thoracic aortic aneurysm and dissection (TAAD) is a life-threatening vascular disease that remains challenging to manage and treat due to the lack of approved and effective pharmacotherapies. Growing reports show the therapeutic effects of ketone supplementation in several cardiovascular diseases. However, whether ketone supplementation can attenuate TAAD development is unknown. Methods: 3 weeks old C57BL/6J mice were given in drinking water either β-aminopropionitrile fumarate (BAPN) alone to induce TAAD or BAPN with ketone ester, a form of ketone supplementation. The BODIPY 581/591 C11 dye was used to assess lipid peroxidation in the cultured cells in vitro. Immunohistochemistry of the aorta was employed to detect ferroptotic markers. Mechanisms underlying ferroptotic regulation were studied using western blotting and qPCR. Results: Ketone ester supplementation lowered the incidence of TAAD and increased the survival rate in mice in vivo. Intriguingly, β-hydroxybutyrate (βHB), the most abundant form of ketone bodies, suppressed RSL-3 (Ras-selective lethal 3)-induced lipid peroxidation in human aortic smooth muscle cells (hASMCs). Furthermore, βHB elevated the protein levels of key ferroptosis regulators, including GPX4 (glutathione peroxidase 4) and SLC7A11 (solute carrier family 7 member 11) in hASMCs in vitro. Conclusions: This preliminary study uncovered an important and previously unrecognized role of ketone ester in ameliorating the pathogenesis of TAAD, which may be through GPX4 induction and subsequent ferroptosis inhibition in smooth muscle cells. Keywords: β-hydroxybutyrate; ferroptosis; thoracic aortic aneurysm; aortic dissection; aortic smooth muscle cells