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Context.--It has been recently suggested that dysregulation of developmental factors and disruption of cell turn-over could play a role in the pathogenesis of congenital cystic adenomatoid malformation of the lung (CCAM). The glial cell-derived neurotrophic factor (GDNF) is a growth factor involved in organogenesis, and the temporal pattern of GDNF expression suggests that this factor may play a role in lung development. Design.--We studied GDNF expression by immunohistochemistry in postnatally resected CCAM of the lung (n = 10), normal fetal lung (n = 5), and normal postnatal lung (n = 5). We also studied the association between GDNF expression and both cell proliferation and apoptosis. Results.--GDNF was expressed in both epithelial and endothelial compartments of normal fetal lung, whereas no expression was found in normal postnatal lung. In contrast, in CCAM tissue, there was strong GDNF immunostaining that was restricted to epithelial cells. The percentage of proliferating epithelial cells was higher in CCAM tissue than in normal postnatal lung (6.3% vs 1.7%, P < .005). Apoptotic bodies were found in the mesenchyme of both normal fetal lung and CCAM tissue, whereas virtually no apoptotic bodies were detected in normal postnatal lung. Conclusions.--Abnormal GDNF expression in CCAM suggests a dysregulation of the GDNF signaling pathway and argues in favor of a focal arrest in maturation during development. GDNF expression in lung tissue seems to be correlated with cell proliferation, suggesting that this factor could play a role in the growth of both fetal lung and CCAM., Congenital cystic adenomatoid malformation of the lung (CCAM) is an uncommon condition characterized by cysts of various sizes lined by bronchiolar- or alveolar-like epithelium. (1) The pathogenesis of CCAM remains [...]

Background Thrombus composition has the potential to affect acute ischemic stroke (AIS) treatment. Objective To evaluate in an in vitro test the correlation of clot composition, especially erythrocytes (red blood cells (RBGs)), with the variation of signal intensity ratio (SIR) obtained with MRI sequences used for AIS, and qualification of the susceptibility vessel sign effect using clot analogs. Materials and methods Nine ovine clots were fixed in a gelatin-manganese solution and studied by MRI (T2GE, T2-weighted gradient echo; SWI, susceptibility-weighted imaging; FLAIR, fluid attenuated inversion recovery). RBG concentration was estimated using regression models (5LR, single linear regression; MLR, multiple linear regression; RF, random Forest; and ANN, artificial neural networking), which combined the SIR-histology relationship of three MRI sequences. results Negative correlation was found between SIR and RBC concentration. T2GE SWI could not statistically distinguish clots with RBC content >54% and <23%. SLR was applied only to FLAIR images since T2GE and SWI demonstrated signal saturation. All four regression models showed a correlation between MRI and histology: SLR=0.981; MLR=0.986; RF=0.994, and ANN=0.971. One unknown clot was studied and agreement between SIR and histological analyses was found in all models. Conclusions We presented a method to quantify RBC concentration in clot analogs, combining SWI, T2GE, and FLAIR. This in vitro study has some limitations, so clot collection after thrombectomy with simultaneous imaging analysis is necessary to validate this model. [ABSTRACT FROM AUTHOR]