Separating the effects of ethnicity and socio-economic status on sleep practices of 6- to 7-month-old infants

Infant sleep undergoes significant re-organization throughout the first 12 months of life, with sleep quality having significant consequences for infant learning and cognitive development. While there has been great interest in the neural basis and developmental trajectories of infant sleep in general, relatively little is known about individual differences in infant sleep and the socio-economic and cultural sources of that variability. We investigated this using questionnaire sleep data in a large, unique multi-ethnic sample of 6-7 month-olds (n=174), with families from South Asian ethnic groups in the UK (Indian, Pakistani and Bangladeshi) being especially well represented. Consistent with previous data from less variable samples, no effects of SES on sleep latency or nocturnal sleep duration emerged. However, perinatal risk factors and ethnic differences did predict daytime sleep, sleep fragmentation and sleep-onset time. While these results should be interpreted with caution due to several limitations, they likely demonstrate that even when socio-economic status and ethnicity are much less confounded than in previous studies, they have a surprisingly limited impact on individual differences in sleep patterns in young infants.

Comparison of virulence genes found in draft genomes of F. necrophorum

Fusobacterium necrophorum is a causative agent of persistent sore throat syndrome, tonsillar abscesses and Lemierre’s syndrome (LS) in humans. LS is characterised by thrombophlebitis of the jugular vein and bacteraemia. It is a Gram-negative, anaerobic bacterium which to date has no available reference genome. Draft genomes suggest it to be a single circular chromosome of approximately 2.2Mb. A reference strain of each of the two F. necrophorum subspecies and a clinical isolate from a LS patient were sequenced on a Roche 454 GS-FLX+. Sequence data was assembled using Roche GS Assembler and the resulting contigs annotated using xBASE, Pfam and BLAST. The annotation data was mined for gene products associated with virulence revealing a leukotoxin, haemolysin, filamentous haemagglutinnin, adhesin, hemin receptor, phage genes, CRISPR-associated proteins, ecotin and a putative type V secretion system. Data will be presented on comparative genomics of the three strains, with a focus on putative virulence genes. Tools such as Artemis Comparison Tool and ClustalO were used for sequence alignments and PhyML was used to generate phylogenetic trees. Conserved motifs associated with virulence were also located. Understanding variations at the genomic level may help to explain the increased virulence of some F. necrophorum strains.

Acute hypoxia reduces plasma myostatin independent of hypoxic dose

Background: Muscle atrophy is seen ~ 25 % of patients with cardiopulmonary disorders, such as chronic obstructive pulmonary disorder and chronic heart failure. Multiple hypotheses exist for this loss, including inactivity, inflammation, malnutrition and hypoxia. Healthy individuals exposed to chronic hypobaric hypoxia also show wasting, suggesting hypoxia alone is sufficient to induce atrophy. Myostatin regulates muscle mass and may underlie hypoxic-induced atrophy. Our previous work suggests a decrease in plasma myostatin and increase in muscle myostatin following 10 hours of exposure to 12 % O2. Aims: To establish the effect of hypoxic dose on plasma myostatin concentration. Concentration of plasma myostatin following two doses of normobaric hypoxia (10.7 % and 12.3 % O2) in a randomised, single-blinded crossover design (n = 8 lowlanders, n = 1 Sherpa), with plasma collected pre (0 hours), post (2 hours) and 2 hours following (4 hours) exposure. Results: An effect of time was noted, plasma myostatin decreased at 4 hours but not 2 hours relative to 0 hours (p = 0.01; 0 hours = 3.26 [0.408] ng.mL-1, 2 hours = 3.33, [0.426] ng.mL-1, 4 hours = 2.92, [0.342] ng.mL-1). No difference in plasma myostatin response was seen between hypoxic conditions (10.7 % vs. 12.3 % O2). Myostatin reduction in the Sherpa case study was similar to the lowlander cohort. Conclusions: Decreased myostatin peptide expression suggests hypoxia in isolation is sufficient to challenge muscle homeostasis, independent of confounding factors seen in chronic cardiopulmonary disorders, in a manner consistent with our previous work. Decreased myostatin peptide may represent flux towards peripheral muscle, or a reduction to protect muscle mass. Chronic adaption to hypoxia does not appear to protect against this response, however larger cohorts are needed to confirm this. Future work will examine tissue changes in parallel with systemic effects.