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Laboratory mice are routinely used in craniofacial research based on the relatively close genetic relationship and conservation of developmental pathways between humans and mice. Since genetic perturbations and disease states may have localized effects, data from individual cranial bones are valuable for the interpretation of experimental assays. We employ high-resolution microcomputed tomography to characterize cranial bones of C57BL/6J mice at embryonic day (E) 15.5 and E17.5, day of birth (P0), and postnatal day 7 (P7) and provide estimates of individual bone volume and tissue mineral density (TMD).Average volume and TMD values are reported for individual bones. Significant differences in volume and TMD during embryonic ages likely reflect early mineralization of cranial neural crest-derived and intramembranously forming bones. Although bones of the face and vault had higher TMD values during embryonic ages, bones of the braincase floor had significantly higher TMD values by P7.These ontogenetic data on cranial bone volume and TMD serve as a reference standard for future studies using mice bred on a C57BL/6J genetic background. Our findings also highlight the importance of differentiating "control" data from mice that are presented as "unaffected" littermates, particularly when carrying a single copy of a cre-recombinase gene.

The Postnatal Growth and Retinopathy of Prematurity (G-ROP) Study showed that the addition of postnatal weight gain to birth weight and gestational age detects similar numbers of infants with ROP, but requires examination of fewer infants. To determine the incremental cost-effectiveness of screening with G-ROP compared with conventional screening. We built a microsimulation model of a 1-year US birth cohort

ObjectiveTo characterise the association between sepsis and postnatal weight growth when accounting for the degree of growth restriction present at birth.DesignRetrospective matched cohort study using data from the Postnatal Growth and Retinopathy of Prematurity study. Participants were born with birth weights of ResultsOf 4785 eligible infants, 813 (17%) developed sepsis and 693 (85%) were matched 1:1 to controls. Sepsis was associated with a greater decline in weight z-score (mean difference −0.09, 95% CI −0.14 to −0.03). Postnatal weight growth failure (decline in weight z- score>1) was present in 237 (34%) infants with sepsis and 179 (26%) controls (adjusted OR 1.49, 95% CI 1.12 to 1.97). Longitudinal growth trajectories showed similar initial changes in weight z-scores between infants with and without sepsis. By 3 weeks after sepsis onset, there was a greater decline in weight z-scores relative to birth values in those with sepsis than without sepsis (delta z-score −0.89 vs −0.77; mean difference −0.12, 95% CI −0.18 to −0.05). This significant difference persisted until 36 weeks or discharge.ConclusionInfants with sepsis had similar early weight growth trajectories as infants without sepsis but developed significant deficits in weight that were not apparent until several weeks after the onset of sepsis.

Deviation in pulmonary surfactant structure–function activity can impair airway patency and lead to respiratory disorders. This novel study aims to evaluate the influence cigarette/e-cigarette vapour has on model surfactant films located within a simulated pulmonary environment using a lung biosimulator. Chromatographic analysis confirmed that nicotine levels were consistent with the sampling regimen employed. On exposure to smoke vapour, Langmuir isotherms exhibited condensed character and a significant reduction in maximum surface pressure was noted in all cases. Langmuir isocycles, reflective of the human breathing cycle, demonstrated condensed character on smoke vapour delivery. A reduction in themaximumsurface pressure was clear only in the case of cigarette vapour application. The components of cigarette vapour can cause oxidative damage to pulmonary surfactant and impair recycling. Neutral nicotine molecules can weaken the structure of the monolayer and cause destabilisation. A protective effect was evident in the case of repeated surfactant compression – relaxation cycles (i.e. the ability to reduce the surface tension term was impaired less), demonstrating a likely innate biological defensive mechanism of the lung. E-cigarette vapour appeared to have a reduced impact on surfactant performance, which may hold value in harm reduction over the longer term.