The mechanism of human labour remains poorly understood, limiting our ability to manage complications of parturition such as preterm labour and induction of labour. In this study we have investigated the effect of labour on plasma metabolites immediately following delivery, comparing cord and maternal plasma taken from women who laboured spontaneously and delivered vaginally with women who were delivered via elective caesarean section and did not labour. Samples were analysed using ultra high-performance liquid chromatography-tandem mass spectrometry. Welch’s two-sample t-test was used to identify any significant differences. Of 826 metabolites measured, 26.9% (222/826) were significantly altered in maternal plasma and 21.1% (174/826) in cord plasma. Labour involves changes in many maternal organs and poses acute metabolic demands in the uterus and in the fetus and these are reflected in our results. While a proportion of these differences are likely to be secondary to the physiological demands of labour itself, these results present a comprehensive picture of the metabolome in the maternal and fetal circulations at the time of delivery and can be used to guide future studies. We discuss potential causal pathways for labour including endocannabinoids, ceramides, sphingolipids and steroids. Further work is necessary to confirm the specific pathways involved in the spontaneous onset of labour.

Objectives.  To determine whether laryngeal reflux (LPR) affects the population size and distribution of laryngeal mucosal flora in humans; and whether LPR alters the integrity of the laryngeal mucosa. Further, to specifically assess whether Helicobacter pylori (H. pylori) is present in the laryngeal mucosa and if LPR is associated with this. Methods.  Laryngeal mucosal biopsies were taken from patients diagnosed LPR‐positive or LPR‐negative, none of whom had laryngeal disease. Presence of bacteria and epithelial integrity were determined by: fluorescent in situ hybridisation using oligonucleotide probes specific to all Eubacteria and H. pylori; real‐time PCR specific for H. Pylori and all bacteria; and immunofluorecence using an antibody to occludin. Results.  Helicobacter pylori was discovered in all the biopsies tested – both in those taken from patients who did not have LPR and those that did – with no significant difference in its distribution between the two groups. Helicobacter pylori was found in both the epithelium and lamina propria of the laryngeal mucosa. Further, an increase in the number of total Eubacteria present in the laryngeal mucosa was found to be significantly associated with LPR (LPR mean 58.2 se 19.0 bacteria/field of view, non‐LPR mean 17.3 se 4.7; P = 0.02). Conclusions.  The association between LPR and an increase in total Eubacteria in the laryngeal mucosa presents a possible aetiology for pathological symptoms associated with LPR. The fact that H. pylori was present in all of the laryngeal mucosal biopsies has significant implications for upper airway research.