20 research outputs found
A qualitative study of barriers and enablers to the establishment of robust clinical research data management systems in low and middle income countries
Exploring African lion (Panthera leo) behavioural phenotypes: individual differences and correlations between sociality, boldness and behaviour
Increasing our understanding of personality, at an individual and group level, is crucial to the pre-release assessment of social species within ex situ reintroduction programs. We conducted the first exploration into the personality of a captive-origin pride of African lions (Panthera leo), assessing behavioural variations and consistencies in daily activity, social and hunting behaviour, and boldness. Data were collected via direct observations, while a species-specific protocol for testing boldness, using playbacks, was developed. Differences in sex, age and session time for the activity budget were evaluated using Pearson correlations and repeated-measures ANOVA, while social interactions were analysed using social network analysis. Spearman’s correlations were conducted to assess for associations between boldness scores, activity and sociality. The two boldness tests provided a range of scores per lion, indicating that the test was effective. Correlations and variations in individual behaviour indicated that adults and sub-adults have specific roles within pride behaviour. Correlations between boldness and activity and social behaviours provided information on the role of individuals, allowing investigation into the behaviour of a dominant and a social keystone. Our study indicates that evaluating various aspects of behaviour in conjunction with boldness has the potential to assist the pre-release assessment of a pride within an ex situ reintroduction program.The final publication is available at Springer via http://dx.doi.org/10.1007/s10164-016-0473-
Investigating endogenous immune-mediated monocyte memory in rheumatoid arthritis
\ua9 2025 The Author(s). Objectives: Inflammation triggered by endogenous stimuli that signal cellular stress or tissue injury must be tightly controlled to balance robust protection from intrinsic danger while avoiding catastrophic destruction of healthy tissues. Here, we assess the contribution of innate memory to this balance. Methods: Memory evoked by the extracellular matrix protein tenascin-C, a damage-associated, toll-like receptor 4 (TLR4) agonist, was compared to that induced by the pathogenic TLR4 agonist lipopolysaccharide (LPS) by transcriptomic and epigenetic profiling of monocytes from healthy individuals or people with rheumatoid arthritis (RA), and tissue macrophages from the RA synovium. Results: Tenascin-C reprograms monocyte response to subsequent threats, inducing concomitantly suppressed and enhanced responses to rechallenge. Comparative analysis of tenascin-C and LPS revealed common and distinct gene expression signatures, effects controlled transcriptionally and associated with stimulus-specific epigenetic mediators. Altered responses following rechallenge after priming with tenascin-C were not limited to subsequent TLR4 activation but were evident in response to various pathogenic and endogenous stimuli detected by different receptors. In healthy monocytes primed with tenascin-C, rechallenge with stimuli found at high levels in the joints of people with RA resulted in trained responses that were not induced by LPS, including genes associated with chronic inflammation, tissue destruction, altered metabolism, and poor treatment response in RA. The expression of a large subset of these genes was elevated in monocytes from people with RA in the absence of any stimulation and in RA synovial macrophage populations associated with disease flare. Moreover, higher levels of permissive complexes within key epigenetic nodes and increased bivalent modification creating poised loci within endogenously trained genes were observed in RA cells. Conclusions: These data highlight how innate reprogramming during ‘sterile’ inflammatory diseases contributes to chronicity, uncovering pathways unique to endogenous immune triggers that could provide disease-specific points of intervention without engendering global immune suppression
