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IntroductionPlacentas of term infants with birth asphyxia are reported to have more lesion such as maternal vascular malperfusion (MVM), fetal vascular malperfusion (FVM) and chorioamnionitis with fetal response (FIR) than those of term infants without birth asphyxia. We compared the placental pathology of asphyxiated newborns, including those who developed hypoxic-ischemic encephalopathy (HIE), with non-asphyxiated controls.MethodsWe conducted a retrospective case–control study of placentas from neonates with a gestational age ≥ 35 weeks, a birthweight ≥ 1,800 g, and no malformations. Cases were asphyxiated newborns (defined as those with an umbilical artery pH ≤ 7.0 or base excess ≤ −12 mMol, 10-minute Apgar score ≤ 5, or the need for resuscitation lasting >10 min) from a previous cohort, with (n=32) and without (n=173) diagnosis of HIE. Controls were non-asphyxiated newborns from low-risk l (n= 50) or high-risk (n= 68) pregnancies. Placentas were analyzed according to the Amsterdam Placental Workshop Group Consensus Statement 2014.ResultsCases had a higher prevalence of nulliparity, BMI>25, thick meconium, abnormal fetal heart monitoring, and acute intrapartum events than controls (p

Introduction: Acute respiratory distress syndrome (ARDS) is an acute form of diffuse lung injury characterized by (i) an intense inflammatory response, (ii) increased pulmonary vascular permeability, and (iii) the loss of respiratory pulmonary tissue. In this article we explore the therapeutic potential of hexarelin, a synthetic hexapeptide growth hormone secretagogue (GHS), in an experimental model of ARDS. Hexarelin has anti-inflammatory properties and demonstrates cardiovascular-protective activities including the inhibition of cardiomyocyte apoptosis and cardiac fibrosis, both of which may involve the angiotensin-converting enzyme (ACE) system. Methods: In our experimental model, ARDS was induced by the instillation of 100 mM HCl into the right bronchus; these mice were treated with hexarelin (320 μg/kg, ip) before (Pre) or after (Post) HCl challenge, or with vehicle. Respiratory system compliance, blood gas analysis, and differential cell counts in a selective bronchoalveolar lavage (BAL) were determined 6 or 24 hours after HCl instillation. In an extended study, mice were observed for a subsequent 14 days in order to assess lung fibrosis. Results: Hexarelin induced a significant improvement in lung compliance and a reduction of the number of total immune cells in BAL 24 hours after HCl instillation, accompanied with a lower recruitment of neutrophils compared with the vehicle group. At day 14, hexarelin-treated mice presented with less pulmonary collagen deposition compared with vehicle-treated controls. Conclusions: Our data suggest that hexarelin can inhibit the early phase of the inflammatory response in a murine model of HCl-induced ARDS, thereby blunting lung remodeling processes and fibrotic development.