Flexible bronchoscopy is useful and safe in retrieving airway foreign bodies in children. With skilled personnel and perfect equipments, flexible bronchoscopy could be considered as the first choice for the removal of airway foreign body.

BackgroundLow birth weight is strongly correlated with an increased risk of adult diseases. Additionally, low birth weight might be a risk factor for asthma later in life.MethodsA systematic literature search of the PubMed database from 1966 to November 2013 was conducted. The criteria for inclusion of papers were as follows: case–control or cohort studies; the odds ratio (OR) or risk ratio (RR) estimates with the corresponding 95% confidence intervals (CIs) were presented, or there were sufficient data for calculation; and studies were published in English up to October 2013. Random-effect and fixed-effect meta-analyses, meta-regression, and cumulative meta-analysis were conducted.ResultsThirteen cohort studies and 1,105,703 subjects were included. The overall pooled RRs (95% CIs) of asthma risk for low birth weight were 1.162 (fixed-effects model, 95% CI, 1.128–1.197) and 1.152 (random-effects model, 95% CI, 1.082–1.222). In stratified analyses, the effect of low birth weight on childhood asthma was strong, particularly in studies conducted in Europe, those with a small sample size, and those published recently. A meta-regression analysis did not find significant determinants.ConclusionsThis meta-analysis shows that low birth weight significantly increases the risk of childhood asthma.

Embryonic lung development requires reciprocal endodermal-mesodermal interactions; mediated by various signaling proteins. Wnt/β-catenin is a signaling protein that exhibits the pivotal role in lung development, injury and repair while aberrant expression of Wnt/β-catenin signaling leads to asthmatic airway remodeling: characterized by hyperplasia and hypertrophy of airway smooth muscle cells, alveolar and vascular damage goblet cells metaplasia, and deposition of extracellular matrix; resulting in decreased lung compliance and increased airway resistance. The substantial evidence suggests that Wnt/β-catenin signaling links embryonic lung development and asthmatic airway remodeling. Here, we summarized the recent advances related to the mechanistic role of Wnt/β-catenin signaling in lung development, consequences of aberrant expression or deletion of Wnt/β-catenin signaling in expansion and progression of asthmatic airway remodeling, and linking early-impaired pulmonary development and airway remodeling later in life. Finally, we emphasized all possible recent potential therapeutic significance and future prospectives, that are adaptable for therapeutic intervention to treat asthmatic airway remodeling.

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Cholesterol modification of Hedgehog (Hh) ligands is fundamental for the activity of Hh signaling, and cholesterol biosynthesis is also required for intracellular Hh signaling transduction. Here, we investigated the roles and underlying mechanism of Hh signaling in metabolism of cholesterol. The main components of the Hh pathway are abundantly expressed in both human cytotrophoblasts and trophoblast-like cells. Activation of Hh signaling induces the conversion of cholesterol to progesterone (P4) and estradiol (E2) through up-regulating the expression of steroidogenic enzymes including P450 cholesterol side chain cleavage enzyme (P450scc), 3β-hydroxysteroid dehydrogenase type 1 (3β-HSD1), and aromatase. Moreover, inhibition of Hh signaling attenuates not only Hh-induced expression of steroidogenic enzymes but also the conversion of cholesterol to P4 and E2. Whereas Gli3 is required for Hh-induced P450scc expression, Gli2 mediates the induction of 3β-HSD1 and aromatase. Finally, in ovariectomized nude mice, systemic inhibition of Hh signaling by cyclopamine suppresses circulating P4 and E2 levels derived from a trophoblast-like choricarcinoma xenograft, and attenuates uterine response to P4 and E2. Together these results uncover a hitherto uncharacterized role of Hh signaling in metabolism of cholesterol.