Sonographic appearance of the cavum septum pellucidum et vergae in normal fetuses in the second and third trimesters of pregnancy.

BACKGROUND: To characterize the cavum septum pellucidum et vergae (CSPV) in normal fetuses in the second to third trimester. METHODS: The cavum septum pellucidum (CSP) and CSPV were investigated in 322 uncomplicated singleton pregnancies from 25 to 39 weeks' gestation. Visualization rate, width, and morphology of both CSP and cavum vergae (CV) were assessed by ultrasound and MRI. RESULTS: The CSP and CSPV visualization rates were 100% and 7.8% (25/322), respectively. The mean widths were 6.3 ± 1.2 mm (3.4-10 mm) and 6.7 ± 1.0 mm (5.1-9 mm), respectively, with no significant correlation between width and gestational age (r = -0.108, p > 0.05 and r = -0.182, p > 0.05, respectively). In CSPV fetuses, the CV to CSP ratio was 1.004 ± 0.018 (0.967-1.033). All CSPVs were rectangular in the transverse plane and extended posteriorly beyond the midpoint of the brain. CONCLUSIONS: Common features of CSPVs include (1) a rectangular morphology, (2) communication between the two cavities, (3) a CV width within the normal range for CSP, and (4) a CV-CSP ratio of 1. These findings may help distinguish normal from abnormal CSPV.

A single-point mutation in FGFR2 affects cell cycle and Tgfbeta signalling in osteoblasts.

Fgf and Tgfbeta are key regulators of bone development. It is not known, however, whether there is a relationship between defective Fgf signalling, resulting in a premature cranial suture fusion, and Tgfbeta signalling. We used mouse calvaria osteoblasts carrying a mutation (hFGFR2-C278F) associated with Crouzon and Pfeiffer syndromes to investigate effects of this mutation on cell growth and possible mechanisms underlying it. Mutated osteoblasts displayed reduced S-phase, increased apoptosis and increased differentiation. As Tgfbeta signalling appeared to be required in an autocrine/paracrine manner for osteoblast proliferation, we tested the hypothesis that reduced growth might be due, at least in part, to an altered balance between FGF and Tgfbeta signalling. Tgfbeta expression was indeed decreased in mutated osteoblasts, as compared to osteoblasts carrying the wild type hFGFR2. Treatment with Tgfbeta, however, neither increased proliferation in mutated osteoblasts, unlike in controls, nor rescued proliferation in control osteoblasts treated with an Erk1/2 inhibitor. Significantly, Erk2, that is important for proliferation, was reduced relatively to Erk1 in mutated cells. Altogether this study suggests that the hFGFR2-C278F mutation affects the osteoblast ability to respond to Tgfbeta stimulation via the Erk pathway and that the overall effect of the mutation is a loss of function.