Disproportionate impact of abortion restriction: Implications for emergency department clinicians.

Individuals experiencing intimate partner violence (IPV) and/or human trafficking (HT) are at increased risk of severe health consequences as a result of legislation criminalizing and/or restricting abortion, which is expected to increase as a result of the Supreme Court decision Dobbs v. Jackson. These risks are further stratified by race, socioeconomics, and other marginalizing demographic attributes. IPV and HT introduce barriers to maintaining physical and mental health, due to control of access to transportation and funds by the abuser, fear of retribution for seeking healthcare, and other barriers. Individuals experiencing IPV or HT often lack reproductive autonomy, as a result of facing reproductive coercion at the hands of their abusers. Following the Dobbs decision, these vulnerable patient populations will face further limitations on their reproductive autonomy and increased obstacles to obtaining an abortion if they medically need or desire one. This will likely result in more patients presenting to the emergency department due to complications from unsafe or unsupervised self-managed abortions, as well as patients being reluctant to report having obtained an unlawful abortion due to fear of legal consequences. This is particularly relevant to individuals experiencing IPV and HT, as they may be more likely to use these methods for obtaining an abortion due to numerous barriers. Emergency medicine clinicians are vital in providing care to these patients, as they frequently present to emergency departments. A multi-pronged approach to better support these patients is essential, involving an increased index of suspicion for IPV, HT or the complications of unsupervised abortion, improved organizational structures, specialized training for staff, improved screening methods, reflection on implicit bias, and recommendations for mindful documentation and legal considerations.

A SOX17-PDGFB signaling axis regulates aortic root development.

Developmental etiologies causing complex congenital aortic root abnormalities are unknown. Here we show that deletion of Sox17 in aortic root endothelium in mice causes underdeveloped aortic root leading to a bicuspid aortic valve due to the absence of non-coronary leaflet and mispositioned left coronary ostium. The respective defects are associated with reduced proliferation of non-coronary leaflet mesenchyme and aortic root smooth muscle derived from the second heart field cardiomyocytes. Mechanistically, SOX17 occupies a Pdgfb transcriptional enhancer to promote its transcription and Sox17 deletion inhibits the endothelial Pdgfb transcription and PDGFB growth signaling to the non-coronary leaflet mesenchyme. Restoration of PDGFB in aortic root endothelium rescues the non-coronary leaflet and left coronary ostium defects in Sox17 nulls. These data support a SOX17-PDGFB axis underlying aortic root development that is critical for aortic valve and coronary ostium patterning, thereby informing a potential shared disease mechanism for concurrent anomalous aortic valve and coronary arteries.