1. |
- Buckley, Yvonne M., et al.
(författare)
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Causes and consequences of variation in plant population growth rate : a synthesis of matrix population models in a phylogenetic context
- 2010
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Ingår i: Ecology Letters. - : Wiley. - 1461-023X .- 1461-0248. ; 13:9, s. 1182-1197
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Forskningsöversikt (refereegranskat)abstract
- Explaining variation in population growth rates is fundamental to predicting population dynamics and population responses to environmental change. In this study, we used matrix population models, which link birth, growth and survival to population growth rate, to examine how and why population growth rates vary within and among 50 terrestrial plant species. Population growth rates were more similar within species than among species; with phylogeny having a minimal influence on among-species variation. Most population growth rates decreased over the observation period and were negatively autocorrelated between years; that is, higher than average population growth rates tended to be followed by lower than average population growth rates. Population growth rates varied more through time than space; this temporal variation was due mostly to variation in post-seedling survival and for a subset of species was partly explained by response to environmental factors, such as fire and herbivory. Stochastic population growth rates departed from mean matrix population growth rate for temporally autocorrelated environments. Our findings indicate that demographic data and models of closely related plant species cannot necessarily be used to make recommendations for conservation or control, and that post-seedling survival and the sequence of environmental conditions are critical for determining plant population growth rate.
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2. |
- Burns, Jean H., et al.
(författare)
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Empirical tests of life-history evolution theory using phylogenetic analysis of plant demography
- 2010
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Ingår i: Journal of Ecology. - : Wiley. - 0022-0477 .- 1365-2745. ; 98:2, s. 334-344
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Tidskriftsartikel (refereegranskat)abstract
- 1. A primary goal of evolutionary ecology is to understand factors selecting for the diversity of life histories. Life-history components, such as time-to-reproduction, adult survivorship and fecundity, might differ among species because of variation in direct and indirect benefits of these life histories in different environments or might have lower-than-expected variability because of phylogenetic constraints. Here, we present a phylogenetic examination of demography and life histories using a data base of 204 terrestrial plant species. 2. Overall, statistical models without phylogeny were preferred to models with phylogeny for vital rates and elasticities, suggesting that they lacked phylogenetic signal and are evolutionarily labile. However, the effect of phylogeny was significant in models including sensitivities, suggesting that sensitivities exhibit greater phylogenetic signal than vital rates or elasticities. 3. Species with a greater age at first reproduction had lower fecundity, consistent with a cost of delayed reproduction, but only in some habitats (e.g. grassland). We found no evidence for an indirect benefit of delayed reproduction via a decrease in variation in fecundity with age to first reproduction. 4. The greater sensitivity and lower variation in survival than in fecundity was consistent with buffering of more important vital rates, as others have also found. This suggests that studies of life-history evolution should include survival, rather than only fecundity, for the majority of species. 5. Synthesis. Demographic matrix models can provide informative tests of life-history theory because of their shared construction and outputs and their widespread use among plant ecologists. Our comparative analysis suggested that there is a cost of delayed reproduction and that more important vital rates exhibit lower variability. The absolute importance of vital rates to population growth rates (sensitivities) exhibited phylogenetic signal, suggesting that a thorough understanding of life-history evolution might require an understanding of the importance of vital rates, not just their means, and the role of phylogenetic history.
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3. |
- Jallow, Muminatou, et al.
(författare)
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Genome-wide and fine-resolution association analysis of malaria in West Africa.
- 2009
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Ingår i: Nature Genetics. - : Springer Science and Business Media LLC. - 1061-4036 .- 1546-1718. ; , s. 657-665
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Tidskriftsartikel (refereegranskat)abstract
- We report a genome-wide association (GWA) study of severe malaria in The Gambia. The initial GWA scan included 2,500 children genotyped on the Affymetrix 500K GeneChip, and a replication study included 3,400 children. We used this to examine the performance of GWA methods in Africa. We found considerable population stratification, and also that signals of association at known malaria resistance loci were greatly attenuated owing to weak linkage disequilibrium (LD). To investigate possible solutions to the problem of low LD, we focused on the HbS locus, sequencing this region of the genome in 62 Gambian individuals and then using these data to conduct multipoint imputation in the GWA samples. This increased the signal of association, from P = 4 x 10(-7) to P = 4 x 10(-14), with the peak of the signal located precisely at the HbS causal variant. Our findings provide proof of principle that fine-resolution multipoint imputation, based on population-specific sequencing data, can substantially boost authentic GWA signals and enable fine mapping of causal variants in African populations.
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4. |
- Langrish, Jeremy P., et al.
(författare)
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Controlled exposures to air pollutants and risk of cardiac arrhythmia
- 2014
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Ingår i: Journal of Environmental Health Perspectives. - : Environmental Health Perspectives. - 0091-6765 .- 1552-9924. ; 122:7, s. 747-753
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Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Epidemiological studies have reported associations between air pollution exposure and increases in cardiovascular morbidity and mortality. Exposure to air pollutants can influence cardiac autonomic tone and reduce heart rate variability, and may increase the risk of cardiac arrhythmias, particularly in susceptible patient groups. OBJECTIVES: We investigated the incidence of cardiac arrhythmias during and after controlled exposure to air pollutants in healthy volunteers and patients with coronary heart disease. METHODS: We analyzed data from 13 double-blind randomized crossover studies including 282 participants (140 healthy volunteers and 142 patients with stable coronary heart disease) from whom continuous electrocardiograms were available. The incidence of cardiac arrhythmias was recorded for each exposure and study population. RESULTS: There were no increases in any cardiac arrhythmia during or after exposure to dilute diesel exhaust, wood smoke, ozone, concentrated ambient particles, engineered carbon nanoparticles, or high ambient levels of air pollution in either healthy volunteers or patients with coronary heart disease. CONCLUSIONS: Acute controlled exposure to air pollutants did not increase the short-term risk of arrhythmia in participants. Research employing these techniques remains crucial in identifying the important pathophysiological pathways involved in the adverse effects of air pollution, and is vital to inform environmental and public health policy decisions.
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