We hypothesized that cord blood cystatin C (CysC) levels are elevated in neonates who have life-threatening pulmonary hypoplasia and oligohydramnios due to severe renal dysfunction.
Fstl1-deficient mice exhibit reduced airspaces, impaired alveolar epithelial cell differentiation, and insufficient production of surfactant proteins similar to PH in human CDH.
This report expands the phenotype of CRB2 mutations to include lung hypoplasia and uretero-pelvic renal anomalies, and confirms cardiac malformation as a feature.
Downstream therapeutic targeting of the Wnt5a-TMEM67-ROR2 axis might, therefore, reduce or prevent pulmonary hypoplasia in ciliopathies and other congenital conditions.
Our results suggest that oxidative damage may be play a important role in patients with N-SCLC, and that GSTM1 and GSTT1 null genotypes may predispose the cells of patients with N-SCLC to increased oxidative damage.
Our objective is to investigate the genetic polymorphisms of the glutathione S-transferase M1 and T1 genes (GSTM1 and GSTT1) and evaluate oxidative damage in patients with non-small lung cancer (N-SCLC).
Our results suggest that oxidative damage may be play a important role in patients with N-SCLC, and that GSTM1 and GSTT1 null genotypes may predispose the cells of patients with N-SCLC to increased oxidative damage.
We report a case of recurrent oligohydramnios in a mother with an ErbB4 mutation and speculate that the effects on the placenta through decreased vascularization contributed to oligohdyramnios and subsequent pulmonary hypoplasia in the newborn.
Chicken ovalbumin upstream promoter-transcription factor II (COUP-TFII) is a transcription factor in the steroid/thyroid hormone receptor superfamily, and targeted ablation of COUP-TFII causes CDH and associated lung hypoplasia in mice.
Small lung volumes were prospectively associated with an increased risk for poor cognitive function and dementia in non-carriers of the APOE epsilon4 gene.
It was shown that loss of NFIA results in hydrocephalus and agenesis of the corpus callosum and that NFIB deficiency leads to neurological defects and to severe lung hypoplasia, whereas Nfic knockout mice exhibit specific tooth defects.
Fetoscopic endoluminal tracheal occlusion performed in the sheep model to correct lung hypoplasia increased leptin expression, partially restored KGF expression, and fully restored neuregulin expression.
It was shown that loss of NFIA results in hydrocephalus and agenesis of the corpus callosum and that NFIB deficiency leads to neurological defects and to severe lung hypoplasia, whereas Nfic knockout mice exhibit specific tooth defects.
Overexpression of ghrelin in hypoplastic lungs and the effect of exogenous administration of ghrelin to nitrofen-treated dams strongly suggest a role for ghrelin in mechanisms involved in attenuation of fetal lung hypoplasia, most likely through a GHSR1a-independent pathway.