Heritability of the pharyngeal airway volume and dimensions as assessed from siblings with overt malocclusions.

OBJECTIVE: To quantify the relative contributions of genetic and environmental factors to airway volume and dimensions in orthodontic patients. MATERIALS AND METHODS: One hundred and twenty-five siblings from 57 families were selected. Cone beam computed tomography scans were taken as part of the orthodontic records and the Dolphin3D © imaging software was used to determine airway volume and dimensions. SOLAR program was implemented to calculate heritability. RESULTS: The heritability of the airway volume was negligible but increased significantly from 5% to 72% (95% confidence interval was 27% to 100%) when anterior-posterior (AP) dimension was controlled in the calculating model. CONCLUSION: The capacity to maintain, rather than having proper AP dimension of the airway, seems to be the most critical mark of a proper airway volume.

C. elegans lifespan extension by osmotic stress requires FUdR, base excision repair, FOXO, and sirtuins.

Moderate stress can increase lifespan by hormesis, a beneficial low-level induction of stress response pathways. 5'-fluorodeoxyuridine (FUdR) is commonly used to sterilize Caenorhabditis elegans in aging experiments. However, FUdR alters lifespan in some genotypes and induces resistance to thermal and proteotoxic stress. We report that hypertonic stress in combination with FUdR treatment or inhibition of the FUdR target thymidylate synthase, TYMS-1, extends C. elegans lifespan by up to 30%. By contrast, in the absence of FUdR, hypertonic stress decreases lifespan. Adaptation to hypertonic stress requires diminished Notch signaling and loss of Notch co-ligands leads to lifespan extension only in combination with FUdR. Either FUdR treatment or TYMS-1 loss induced resistance to acute hypertonic stress, anoxia, and thermal stress. FUdR treatment increased expression of DAF-16 FOXO and the osmolyte biosynthesis enzyme GPDH-1. FUdR-induced hypertonic stress resistance was partially dependent on sirtuins and base excision repair (BER) pathways, while FUdR-induced lifespan extension under hypertonic stress conditions requires DAF-16, BER, and sirtuin function. Combined, these results demonstrate that FUdR, through inhibition of TYMS-1, activates stress response pathways in somatic tissues to confer hormetic resistance to acute and chronic stress. C. elegans lifespan studies using FUdR may need re-interpretation in light of this work.