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Physical and cognitive performances change across lifespan. Studying cohorts of individuals in specific age ranges and athletic abilities remains essential in assessing the underlying physiological mechanisms that result in such a drop in performance. This decline is now viewed as a unique phenotypic biomarker and a hallmark of the aging process. The rates of decline are well documented for sets of traits such as running or swimming but only a limited number of studies have examined the developmental and senescent phases together. Moreover, the few attempts to do so are merely descriptive and do not include any meaningful biological features. Here we propose an averaged and deterministic model, based on cell population dynamics, replicative senescence and functionality loss. It describes the age-related change of performance in 17 time-series phenotypic traits, including human physical and cognitive skills, mouse lemur strength, greyhound and thoroughbred speed, and mouse activity. We demonstrate that the estimated age of peak performance occurs in the early part of life (20.5% ± 6.6% of the estimated lifespan) thus emphasizing the asymmetrical nature of the relationship. This model is an initial attempt to relate performance dynamics to cellular dynamics and will lead to more sophisticated models in the future. [ABSTRACT FROM AUTHOR]

Despite improved surveillance capacities and WHO recommendations for subdistrict analysis, routine epidemic surveillance of acute bacterial meningitis in the African meningitis belt remains largely limited to the district level. We evaluated the appropriateness and performance of analyses at higher spatial resolution. We used suspected meningitis surveillance data at health centre (HC) resolution from Burkina Faso from 14 health districts spanning years 2004–2014 and analysed them using spatio-temporal statistics and generative models. An operational analysis compared epidemic signals at district and HC-level using weekly incidence thresholds. Eighty-four percent (N = 98/116) of epidemic clusters spanned only one HC-week. Spatial propagation of epidemic clusters was mostly limited to 10–30 km. During the 2004–2009 (with serogroup A meningitis) and 2010–2014 (after serogroup A elimination) period, using weekly HC-level incidence thresholds of 100 and 50 per 100,000 respectively, we found a gain in epidemic detection and timeliness in 9 (41% of total) and 10 (67%), respectively, district years with at least one HC signal. Individual meningitis epidemics expanded little in space, suggesting that a health centre level analysis is most appropriate for epidemic surveillance. Epidemic surveillance could gain in precision and timeliness by higher spatial resolution. The optimal threshold should be defined depending on the current background incidence of bacterial meningitis. [ABSTRACT FROM AUTHOR]