Characteristics and Complication Rates of Mandibular Fractures Caused by Violent Mechanisms Versus Nonviolent Mechanisms.

Background: Mandibular fractures due to intentionally violent mechanisms represent a unique subset of facial fractures. The objective of our research is to identify how violence affects patterns of mandibular fractures and their outcomes. Methods: In this institutional review board-approved, retrospective study, we examined our institution's records for adult patients >18 years of age who presented with ≥ 1 mandibular fractures from January 2011 to January 2022. Violence was defined as trauma intended to hurt another or self. Demographics, fractures, mechanism, concomitant injuries, treatment, and complications were analyzed with Excel and SPSS statistical software. Results: A total of 692 patients were diagnosed with mandibular fractures, with 323 of these due to violence (47%). These patients of violence (POVs) had an average fracture per patient of 1.6 ± 0.7. The majority (88%) were male and African American (33%), and the average age was 34.3 ± 13.2 years. The most common violent mechanism was a punch (68%). The POVs presented with fewer concomitant injuries, were less likely to be admitted to the intensive care unit, and were more often surgically managed with open reduction than were patients of nonviolence (PONVs) (P < .01). POVs were more likely to have healing complications; though not statistically significant, this population was observed to be frequently lost to follow-up (P = .12). POVs notably had a much higher proportion of hardware exposure among complications than was seen in PONVs (23% vs 9%). Conclusions: Patients with violent fracture mechanisms may tend to be predisposed to more complications compared with patients who have nonviolent fracture mechanisms despite lesser severities due to social determinants of health. Characteristics of this patient subset may tend to cause difficulties in postoperative care and follow-up. Effective discharge instruction communication, patient outreach programs, and homelessness and drug abuse screening in this subset may help reduce healing complications.

Mouse models of patent ductus arteriosus (PDA) and their relevance for human PDA.

The ductus arteriosus (DA) is a unique fetal vascular shunt, which allows blood to bypass the developing lungs in utero. After birth, changes in complex signaling pathways lead to constriction and permanent closure of the DA. The persistent patency of the DA (PDA) is a common disorder in preterm infants, yet the underlying causes of PDA are not fully defined. Although limits on the availability of human DA tissues prevent comprehensive studies on the mechanisms of DA function, mouse models have been developed that reveal critical pathways in DA regulation. Over 20 different transgenic models of PDA in mice have been described, with implications for human DA biology. Similarly, we enumerate 224 human single-gene syndromes that are associated with PDA, including a small subset that consistently feature PDA as a prominent phenotype. Comparison and functional analyses of these genes provide insight into DA development and identify key regulatory pathways that may serve as potential therapeutic targets for the management of PDA.

Role of dopamine and selective dopamine receptor agonists on mouse ductus arteriosus tone and responsiveness.

BACKGROUND: Indomethacin treatment for patent ductus arteriosus (PDA) is associated with acute kidney injury (AKI). Fenoldopam, a dopamine (DA) DA1-like receptor agonist dilates the renal vasculature and may preserve renal function during indomethacin treatment. However, limited information exists on DA receptor-mediated signaling in the ductus and fenoldopam may prevent ductus closure given its vasodilatory nature. METHODS: DA receptor expression in CD-1 mouse vessels was analyzed by qPCR and immunohistochemistry. Concentration-response curves were established using pressure myography. Pretreatment with SCH23390 (DA1-like receptor antagonist), phentolamine (α -adrenergic receptor antagonist) or indomethacin addressed mechanisms for DA-induced changes. Fenoldopam's effects on postnatal ductus closure were evaluated in vivo. RESULTS: DA1 receptors were expressed equally in ductus and aorta. High-dose DA induced modest vasoconstriction under newborn O2 conditions. Phentolamine inhibited DA-induced constriction, while SCH23390 augmented constriction, consistent with a vasodilatory role for DA1 receptors. Despite this, fenoldopam had little effect on ductus tone nor indomethacin- or O2-induced constriction and did not impair postnatal closure in vivo. CONCLUSION(S): DA receptors are present in the ductus but have limited physiologic effects. DA-induced ductus vasoconstriction is mediated via α-adrenergic pathways. The absence of DA1-mediated impairment of ductus closure supports the study of potential role for fenoldopam during PDA treatment.