Phylogeny and metabolic scaling in mammals

The scaling of metabolic rates to body size is widely considered to be of great biological and ecological importance, and much attention has been devoted to determining its theoretical and empirical value. Most debate centers on whether the underlying power law describing metabolic rates is 2/3 (as predicted by scaling of surface area/volume relationships) or 3/4 ("Kleiber's law"). Although recent evidence suggests that empirically derived exponents vary among clades with radically different metabolic strategies, such as ectotherms and endotherms, models, such as the metabolic theory of ecology, depend on the assumption that there is at least a predominant, if not universal, metabolic scaling exponent. Most analyses claimed to support the predictions of general models, however, failed to control for phylogeny. We used phylogenetic generalized least-squares models to estimate allometric slopes for both basal metabolic rate (BMR) and field metabolic rate (FMR) in mammals. Metabolic rate scaling conformed to no single theoretical prediction, but varied significantly among phylogenetic lineages. In some lineages we found a 3/4 exponent, in others a 2/3 exponent, and in yet others exponents differed significantly from both theoretical values. Analysis of the phylogenetic signal in the data indicated that the assumptions of neither species-level analysis nor independent contrasts were met. Analyses that assumed no phylogenetic signal in the data (species-level analysis) or a strong phylogenetic signal (independent contrasts), therefore, returned estimates of allometric slopes that were erroneous in 30% and 50% of cases, respectively. Hence, quantitative estimation of the phylogenetic signal is essential for determining scaling exponents. The lack of evidence for a predominant scaling exponent in these analyses suggests that general models of metabolic scaling, and macro-ecological theories that depend on them, have little explanatory power.

The evolutionary ecology of resistance to parasitoids by Drosophila

Parasitoids are the most important natural enemies of many insect species. Larvae of many Drosophila species can defend themselves against attack by parasitoids through a cellular immune response called encapsulation. The paper reviews recent studies of the evolutionary biology and ecological genetics of resistance in Drosophila, concentrating on D. melanogaster. The physiological basis of encapsulation, and the genes known to interfere with resistance are briefly summarized. Evidence for within- and between-population genetic variation in resistance from isofemale line, artificial selection and classical genetic studies are reviewed. There is now firm evidence that resistance is costly to Drosophila, and the nature of this cost is discussed, and the possibility that it may involve a reduction in metabolic rate considered. Comparative data on encapsulation and metabolic rates across seven Drosophila species provides support for this hypothesis. Finally, the possible population and community ecological consequences of evolution in the levels of host resistance are examined.

Searching for the perfect surface area normalizing term - a comparison of BET surface area-, geometric surface area- and mass-normalized dissolution rates of anorthite and biotite

Dissolution rates were calculated for a range of grain sizes of anorthite and biotite dissolved under far from equilibrium conditions at pH 3, T = 20 degrees C. Dissolution rates were normalized to initial and final BET surface area, geometric surface area, mass and (for biotite only) geometric edge surface area. Constant (within error) dissolution rates were only obtained by normalizing to initial BET surface area for biotite. The normalizing term that gave the smallest variation about the mean for anorthite was initial BET surface area. In field studies, only current (final) surface area is measurable. In this study, final geometric surface area gave the smallest variation for anorthite dissolution rates and final geometric edge surface area for biotite dissolution rates. (c) 2005 Published by Elsevier B.V.

Effects of manure and fertilizer on grain yield, soil carbon and phosphorus in a 13-year field trial in semi-arid Kenya

Long-term indicators of soil fertility were assessed by measuring grain yield, soil organic carbon (SOC) and soil Olsen phosphorous for a P-deficient soil. In one set of treatments, goat manure was applied annually for 13 years at 0, 5 and 10 t ha(-1), and intercrops of sorghum/cowpea, millet/green gram and maize/pigeonpea were grown. Yield depended on rainfall and trends with time were not identifiable. Manure caused an upward trend in SOC, but 10 t ha(-1) manure did not give significantly more SOC than 5 t ha(-1). Only 10 t ha(-1) manure increased Olsen P. Measurements of both SOC and Olsen P are recommended. In another set of treatments, manure was applied for four years; the residual effect lasted another seven to eight years when assessed by yield, SOC and Olsen P Treatment with mineral fertilizers provided the same rates of N and P as 5 t hat manure and yields from manure and fertilizer were similar. Fertilizer increased Olsen P but not SOC. Management systems with occasional manure application and intermediate fertilizer applications should be assessed. Inputs and offtakes of C, N and P were measured for three years. Approximately 16, 25 and 11% of C, N and P respectively were stabilized into soil organic matter from 5 t ha(-1) a(-1) manure. The majority of organic P was fixed as soil inorganic P.

Effect of manure application on crop yield and soil chemical properties in a long-term field trial of semi-arid Kenya

The sustainability of cereal/legume intercropping was assessed by monitoring trends in grain yield, soil organic C (SOC) and soil extractable P (Olsen method) measured over 13 years at a long-term field trial on a P-deficient soil in semi-arid Kenya. Goat manure was applied annually for 13 years at 0, 5 and 10 t ha(-1) and trends in grain yield were not identifiable because of season-to-season variations. SOC and Olsen P increased for the first seven years of manure application and then remained constant. The residual effect of manure applied for four years only lasted another seven to eight years when assessed by yield, SOC and Olsen P. Mineral fertilizers provided the same annual rates of N and P as in 5 t ha(-1) manure and initially ,gave the same yield as manure, declining after nine years to about 80%. Therefore, manure applications could be made intermittently and nutrient requirements topped-up with fertilizers. Grain yields for sorghum with continuous manure were described well by correlations with rainfall and manure input only, if data were excluded for seasons with over 500 mm rainfall. A comprehensive simulation model should correctly describe crop losses caused by excess water.

Evaluating the risk of non-point source pollution from biosolids: integrated modelling of nutrient losses at field and catchment scales

A semi-distributed model, INCA, has been developed to determine the fate and distribution of nutrients in terrestrial and aquatic systems. The model simulates nitrogen and phosphorus processes in soils, groundwaters and river systems and can be applied in a semi-distributed manner at a range of scales. In this study, the model has been applied at field to sub-catchment to whole catchment scale to evaluate the behaviour of biosolid-derived losses of P in agricultural systems. It is shown that process-based models such as INCA, applied at a wide range of scales, reproduce field and catchment behaviour satisfactorily. The INCA model can also be used to generate generic information for risk assessment. By adjusting three key variables: biosolid application rates, the hydrological connectivity of the catchment and the initial P-status of the soils within the model, a matrix of P loss rates can be generated to evaluate the behaviour of the model and, hence, of the catchment system. The results, which indicate the sensitivity of the catchment to flow paths, to application rates and to initial soil conditions, have been incorporated into a Nutrient Export Risk Matrix (NERM).

Conservation of open solar magnetic flux and the floor in the heliospheric magnetic field

The near-Earth heliospheric magnetic field intensity, |B|, exhibits a strong solar cycle variation, but returns to the same ``floor'' value each solar minimum. The current minimum, however, has seen |B| drop below previous minima, bringing in to question the existence of a floor, or at the very least requiring a re-assessment of its value. In this study we assume heliospheric flux consists of a constant open flux component and a time-varying contribution from CMEs. In this scenario, the true floor is |B| with zero CME contribution. Using observed CME rates over the solar cycle, we estimate the ``no-CME'' |B| floor at ~4.0 +/- 0.3 nT, lower than previous floor estimates and below |B| observed this solar minimum. We speculate that the drop in |B| observed this minimum may be due to a persistently lower CME rate than the previous minimum, though there are large uncertainties in the supporting observational data.

Reconciling the electron counterstreaming and dropout occurrence rates with the heliospheric flux budget

Counterstreaming electrons (CSEs) are treated as signatures of closed magnetic flux, i.e., loops connected to the Sun at both ends. However, CSEs at 1 AU likely fade as the apex of a closed loop passes beyond some distance R, owing to scattering of the sunward beam along its continually increasing path length. The remaining antisunward beam at 1 AU would then give a false signature of open flux. Subsequent opening of a loop at the Sun by interchange reconnection with an open field line would produce an electron dropout (ED) at 1 AU, as if two open field lines were reconnecting to completely disconnect from the Sun. Thus EDs can be signatures of interchange reconnection as well as the commonly attributed disconnection. We incorporate CSE fadeout into a model that matches time-varying closed flux from interplanetary coronal mass ejections (ICMEs) to the solar cycle variation in heliospheric flux. Using the observed occurrence rate of CSEs at solar maximum, the model estimates R ∼ 8–10 AU. Hence we demonstrate that EDs should be much rarer than CSEs at 1 AU, as EDs can only be detected when the juncture points of reconnected field lines lie sunward of the detector, whereas CSEs continue to be detected in the legs of all loops that have expanded beyond the detector, out to R. We also demonstrate that if closed flux added to the heliosphere by ICMEs is instead balanced by disconnection elsewhere, then ED occurrence at 1 AU would still be rare, contrary to earlier expectations.

The impact of two arable field margin management schemes on litter decomposition

A primary objective of agri-environment schemes is the conservation of biodiversity; in addition to increasing the value of farmland for wildlife, these schemes also aim to restore natural ecosystem functioning. The management of scheme options can influence their value for delivering ecosystem services by modifying the composition of floral and faunal communities. This study examines the impact of an agri-environment scheme prescription on ecosystem functioning by testing the hypothesis that vegetation management influences decomposition rates in grassy arable field margins. The effects of two vegetation management practices in arable field margins - cutting and soil disturbance (scarification) - on litter decomposition were compared using a litterbag experimental approach in early April 2006. Bags had either small mesh designed to restrict access to soil macrofauna, or large mesh that would allow macrofauna to enter. Bags were positioned on the soil surface or inserted into the soil in cut and scarified margins, retrieved after 44, 103 and 250 days and the amount of litter mass remaining was calculated. Litter loss from the litterbags with large mesh was greater than from the small mesh bags, providing evidence that soil macrofauna accelerate rates of litter decomposition. In the large mesh bags, the proportion of litter remaining in bags above and belowground in the cut plots was similar, while in the scarified plots, there was significantly more litter left in the aboveground bags than in the belowground bags. This loss of balance between decomposition rates above and belowground in scarified margins may have implications for the development and maintenance of grassy arable field margins by influencing nutrient availability for plant communities. (C) 2008 Elsevier B.V. All rights reserved.

Economic analysis of integrated weed management in field bean (Phaseolus vulgaris L.)

Field experiments were conducted in field bean in the north-eastern part of the Republic of Croatia to compare weed control and crop response under different management practices within the critical period of field bean production. The practices consisted in broadcast application of labelled rate of preemergence herbicide (PRE) and postemergence herbicide application: (POST) broadcast, band application over the rows, and band application combined with mechanical cultivation using of different herbicide doses recommended by the manufacturer (2x, 1x, 1/2x, 1/4x, 1/8x). In 1999, weed control with PRE application of pendimethalin was superior to POST bentazone application due to late emergence of weeds and lack of residual herbicide control. In 2000 bentazone combined with cycloxydim controlled weeds in field bean better than PRE herbicide application. Based on the results of this research, single PRE or POST application of herbicide did not control a broad spectrum of weeds and did not provide the commercially acceptable full season control. Reduced rates of herbicide are not advisable tinder high weed pressure.

Why high seed densities within buried mesh bags may overestimate depletion rates of soil seed banks

1. Estimates of seed bank depletion rates are essential for modelling and management of plant populations. The seed bag burial method is often used to measure seed mortality in the soil. However, the density of seeds within seed bags is higher than densities in natural seed banks, which may elevate levels of pathogens and influence seed mortality. The aim of this study was to quantify the effects of fungi and seed density within buried mesh bags on the mortality of seeds. Striga hermonthica was chosen as the study species because it has been widely studied but different methods for measuring seed mortality in the soil have yielded contradictory estimates. 2. Seed bags were buried in soil and exhumed at regular time intervals to monitor mortality of the seeds in three field experiments during two rainy seasons. The effect of fungal activity on seed mortality was evaluated in a fungi exclusion experiment. Differences in seed-to-seed interaction were obtained by using two and four densities within the seed bags in consecutive years. Densities were created by mixing 1000 seeds with 0, 10, 100 or 1000 g of coarse sand. 3. The mortality rate was significantly lower when fungi were excluded, indicating the possible role of pathogenic fungi. 4. Decreasing the density of seeds in bags significantly reduced seed mortality, most probably because of decreased seed-to-seed contamination by pathogenic fungi. 5. Synthesis and applications. Models of plant populations in general and annual weeds in particular often use values from the literature for seed bank depletion rates. These depletion rates have often been estimated by the seed bag burial method, yet seed density within seed bags may be unrealistically high. Consequently, estimates of seed mortality rates may be too high because of an overestimation of the effects of soil or seed-borne pathogens. Species that have been classified from such studies as having short-lived seed banks may need to be re-assessed using realistic densities either within seed bags or otherwise. Similarly, models of seed bank dynamics based on such overestimated depletion rates may lead to incorrect conclusions regarding the seed banks and, perhaps, the management of weeds and rare species.

Metabolic syndrome: what is it and what are the implications?

Obesity and overweight are linked with a cluster of metabolic and vascular disorders that have been termed the metabolic syndrome. Although there is not yet a universally-accepted set of diagnostic criteria, most expert groups agree that the syndrome is characterised by impaired insulin sensitivity and hyperglycaemia, dyslipidaemia (elevated blood triacyglycerols with depressed HDL-cholesterol), abdominal obesity and hypertension. Based on existing published criteria estimates suggest that the syndrome affects a substantial percentage of the middle-aged and elderly populations of most European countries (10-20%) and confers increased risk of type 2 diabetes (2-8(.)8-fold) and CVD (1(.)5-6-fold), as well as having a marked effect on morbidity. Although the pathophysiology is incompletely understood, insulin resistance and abdominal obesity are central to subsequent abnormalities in circulating glucose and lipoproteins, and vascular function that lead to type 2 diabetes, atherosclerosis and CVD. The link between metabolic syndrome, type 2 diabetes and CVD, as well as inability to reverse the present rising rates of obesity, will lead to economically-unsustainable costs of health care in the next 10-20 years. Preventative strategies for metabolic syndrome are required to slow rates of progression and to reduce dependence on costly medical management. A notable development is recent evidence that shows that diet and exercise are more effective than drug treatment in preventing the development of type-2 diabetes in high-risk individuals. The LIPGENE project will investigate dietary fat quality as a strategy for the prevention of metabolic syndrome and identify food chain approaches that can support consumer attempts to alter their dietary patterns.

ACC2 gene polymorphisms, metabolic syndrome, and gene-nutrient interactions with dietary fat.

Acetyl-CoA carboxylase β (ACC2) plays a key role in fatty acid synthesis and oxidation pathways. Disturbance of these pathways is associated with impaired insulin responsiveness and metabolic syndrome (MetS). Gene-nutrient interactions may affect MetS risk. This study determined the relationship between ACC2 polymorphisms (rs2075263, rs2268387, rs2284685, rs2284689, rs2300453, rs3742023, rs3742026, rs4766587, and rs6606697) and MetS risk, and whether dietary fatty acids modulate this in the LIPGENE-SU.VI.MAX study of MetS cases and matched controls (n = 1754). Minor A allele carriers of rs4766587 had increased MetS risk (OR 1.29 [CI 1.08, 1.58], P = 0.0064) compared with the GG homozygotes, which may in part be explained by their increased body mass index (BMI), abdominal obesity, and impaired insulin sensitivity (P < 0.05). MetS risk was modulated by dietary fat intake (P = 0.04 for gene-nutrient interaction), where risk conferred by the A allele was exacerbated among individuals with a high-fat intake (>35% energy) (OR 1.62 [CI 1.05, 2.50], P = 0.027), particularly a high intake (>5.5% energy) of n-6 polyunsaturated fat (PUFA) (OR 1.82 [CI 1.14, 2.94], P = 0.01; P = 0.05 for gene-nutrient interaction). Saturated and monounsaturated fat intake did not modulate MetS risk. Importantly, we replicated some of these findings in an independent cohort. In conclusion, the ACC2 rs4766587 polymorphism influences MetS risk, which was modulated by dietary fat, suggesting novel gene-nutrient interactions.

Leptin receptor polymorphisms interact with polyunsaturated fatty acids to augment risk of insulin resistance and metabolic syndrome in adults.

The leptin receptor (LEPR) is associated with insulin resistance, a key feature of metabolic syndrome (MetS). Gene-fatty acid interactions may affect MetS risk. The objective was to investigate the relationship among LEPR polymorphisms, insulin resistance, and MetS risk and whether plasma fatty acids, a biomarker of dietary fatty acids, modulate this. LEPR polymorphisms (rs10493380, rs1137100, rs1137101, rs12067936, rs1805096, rs2025805, rs3790419, rs3790433, rs6673324, and rs8179183), biochemical measurements, and plasma fatty acid profiles were determined in the LIPGENE-SU.VI.MAX study of MetS cases and matched controls (n = 1754). LEPR rs3790433 GG homozygotes had increased MetS risk compared with the minor A allele carriers [odds ratio (OR) = 1.65; 95% CI: 1.05–2.57; P = 0.028], which may be accounted for by their increased risk of elevated insulin concentrations (OR 2.40; 95% CI: 1.28–4.50; P = 0.006) and insulin resistance (OR = 2.15; 95% CI: 1.18–3.90; P = 0.012). Low (less than median) plasma (n-3) and high (n-6) PUFA status exacerbated the genetic risk conferred by GG homozygosity to hyperinsulinemia (OR 2.92–2.94) and insulin resistance (OR 3.40–3.47). Interestingly, these associations were abolished against a high (n-3) or low (n-6) PUFA background. Importantly, we replicated some of these findings in an independent cohort. Homozygosity for the LEPR rs3790433 G allele was associated with insulin resistance, which may predispose to increased MetS risk. Novel gene-nutrient interactions between LEPR rs3790433 and PUFA suggest that these genetic influences were more evident in individuals with low plasma (n-3) or high plasma (n-6) PUFA.

Gene-nutrient interactions with dietary fat modulate the association between genetic variation of the ACSL1 gene and metabolic syndrome

Long-chain acyl CoA synthetase 1 (ACSL1) plays an important role in fatty acid metabolism and triacylglycerol (TAG) synthesis. Disturbance of these pathways may result in dyslipidemia and insulin resistance, hallmarks of the metabolic syndrome (MetS). Dietary fat is a key environmental factor that may interact with genetic determinants of lipid metabolism to affect MetS risk. We investigated the relationship between ACSL1 polymorphisms (rs4862417, rs6552828, rs13120078, rs9997745, and rs12503643) and MetS risk and determined potential interactions with dietary fat in the LIPGENE-SU.VI.MAX study of MetS cases and matched controls (n = 1,754). GG homozygotes for rs9997745 had increased MetS risk {odds ratio (OR) 1.90 [confidence interval (CI) 1.15, 3.13]; P = 0.01}, displayed elevated fasting glucose (P = 0.001) and insulin concentrations (P = 0.002) and increased insulin resistance (P = 0.03) relative to the A allele carriers. MetS risk was modulated by dietary fat, whereby the risk conferred by GG homozygosity was abolished among individuals consuming either a low-fat (<35% energy) or a high-PUFA diet (>5.5% energy). In conclusion, ACSL1 rs9997745 influences MetS risk, most likely via disturbances in fatty acid metabolism, which was modulated by dietary fat consumption, particularly PUFA intake, suggesting novel gene-nutrient interactions.