Selective serotonin reuptake inhibitor antidepressant use in first trimester pregnancy and risk of specific congenital anomalies: a European register-based study.

Evidence of an association between early pregnancy exposure to selective serotonin reuptake inhibitors (SSRI) and congenital heart defects (CHD) has contributed to recommendations to weigh benefits and risks carefully. The objective of this study was to determine the specificity of association between first trimester exposure to SSRIs and specific CHD and other congenital anomalies (CA) associated with SSRI exposure in the literature (signals). A population-based case-malformed control study was conducted in 12 EUROCAT CA registries covering 2.1 million births 1995-2009 including livebirths, fetal deaths from 20 weeks gestation and terminations of pregnancy for fetal anomaly. Babies/fetuses with specific CHD (n = 12,876) and non-CHD signal CA (n = 13,024), were compared with malformed controls whose diagnosed CA have not been associated with SSRI in the literature (n = 17,083). SSRI exposure in first trimester pregnancy was associated with CHD overall (OR adjusted for registry 1.41, 95 % CI 1.07-1.86, fluoxetine adjOR 1.43 95 % CI 0.85-2.40, paroxetine adjOR 1.53, 95 % CI 0.91-2.58) and with severe CHD (adjOR 1.56, 95 % CI 1.02-2.39), particularly Tetralogy of Fallot (adjOR 3.16, 95 % CI 1.52-6.58) and Ebstein's anomaly (adjOR 8.23, 95 % CI 2.92-23.16). Significant associations with SSRI exposure were also found for ano-rectal atresia/stenosis (adjOR 2.46, 95 % CI 1.06-5.68), gastroschisis (adjOR 2.42, 95 % CI 1.10-5.29), renal dysplasia (adjOR 3.01, 95 % CI 1.61-5.61), and clubfoot (adjOR 2.41, 95 % CI 1.59-3.65). These data support a teratogenic effect of SSRIs specific to certain anomalies, but cannot exclude confounding by indication or associated factors.

Landslide detection and monitoring capability of boat-based mobile laser scanning along Dieppe coastal cliffs, Normandy

Integrated in a wide research assessing destabilizing and triggering factors to model cliff dynamic along the Dieppe's shoreline in High Normandy, this study aims at testing boat-based mobile LiDAR capabilities by scanning 3D point clouds of the unstable coastal cliffs. Two acquisition campaigns were performed in September 2012 and September 2013, scanning (1) a 30-km-long shoreline and (2) the same test cliffs in different environmental conditions and device settings. The potentials of collected data for 3D modelling, change detection and landslide monitoring were afterward assessed. By scanning during favourable meteorological and marine conditions and close to the coast, mobile LiDAR devices are able to quickly scan a long shoreline with median point spacing up to 10cm. The acquired data are then sufficiently detailed to map geomorphological features smaller than 0.5m2. Furthermore, our capability to detect rockfalls and erosion deposits (>m3) is confirmed, since using the classical approach of computing differences between sequential acquisitions reveals many cliff collapses between Pourville and Quiberville and only sparse changes between Dieppe and Belleville-sur-Mer. These different change rates result from different rockfall susceptibilities. Finally, we also confirmed the capability of the boat-based mobile LiDAR technique to monitor single large changes, characterizing the Dieppe landslide geometry with two main active scarps, retrogression up to 40m and about 100,000m3 of eroded materials.

Neuroprotection by selective neuronal deletion of Atg7 in neonatal brain injury.

Perinatal asphyxia induces neuronal cell death and brain injury, and is often associated with irreversible neurological deficits in children. There is an urgent need to elucidate the neuronal death mechanisms occurring after neonatal hypoxia-ischemia (HI). We here investigated the selective neuronal deletion of the Atg7 (autophagy related 7) gene on neuronal cell death and brain injury in a mouse model of severe neonatal hypoxia-ischemia. Neuronal deletion of Atg7 prevented HI-induced autophagy, resulted in 42% decrease of tissue loss compared to wild-type mice after the insult, and reduced cell death in multiple brain regions, including apoptosis, as shown by decreased caspase-dependent and -independent cell death. Moreover, we investigated the lentiform nucleus of human newborns who died after severe perinatal asphyxia and found increased neuronal autophagy after severe hypoxic-ischemic encephalopathy compared to control uninjured brains, as indicated by the numbers of MAP1LC3B/LC3B (microtubule-associated protein 1 light chain 3)-, LAMP1 (lysosomal-associated membrane protein 1)-, and CTSD (cathepsin D)-positive cells. These findings reveal that selective neuronal deletion of Atg7 is strongly protective against neuronal death and overall brain injury occurring after HI and suggest that inhibition of HI-enhanced autophagy should be considered as a potential therapeutic target for the treatment of human newborns developing severe hypoxic-ischemic encephalopathy.