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Individual Metabolism (individual + metabolism)
Selected AbstractsAllometric scaling of maximum population density: a common rule for marine phytoplankton and terrestrial plantsECOLOGY LETTERS, Issue 5 2002Andrea Belgrano A primary goal of macroecology is to identify principles that apply across varied ecosystems and taxonomic groups. Here we show that the allometric relationship observed between maximum abundance and body size for terrestrial plants can be extended to predict maximum population densities of marine phytoplankton. These results imply that the abundance of primary producers is similarly constrained in terrestrial and marine systems by rates of energy supply as dictated by a common allometric scaling law. They also highlight the existence of general mechanisms linking rates of individual metabolism to emergent properties of ecosystems. [source] Allometry, growth and population regulation of the desert shrub Larrea tridentataFUNCTIONAL ECOLOGY, Issue 2 2008A. P. Allen Summary 1Quantifying the effects of individual- and population-level processes on plant-community structure is of fundamental importance for understanding how biota contribute to the flux, storage and turnover of matter and energy in ecosystems. 2Here we synthesize plant-allometry theory with empirical data to evaluate the roles of individual metabolism and competition in structuring populations of the creosote Larrea tridentata, a dominant shrub in deserts of southwestern North America. 3At the individual level, creosote data support theoretical predictions with regard to the size dependence of total leaf mass, short-term growth rates of leaves and long-term growth rates of entire plants. Data also support the prediction that root,shoot biomass allocation is independent of plant size. 4At the population level, size,abundance relationships within creosote stands deviate strongly from patterns observed for steady-state closed-canopy forests due to episodic recruitment events. This finding highlights that carbon storage and turnover in water-limited ecosystems can be inherently less predictable than in mesic environments due to pronounced environmental forcing on demographic variables. 5Nevertheless, broad-scale comparative analyses across ecosystems indicate that the relationship of total abundance to average size for creosote populations adhere to the thinning rule observed and predicted by allometry theory. This finding indicates that primary production in water-limited ecosystems can be independent of standing biomass due to competition among plants for resources. 6Our synthesis of theory with empirical data quantifies the primary roles of individual-level metabolism and competition in controlling the dynamics of matter and energy in water-limited ecosystems. [source] Linking the global carbon cycle to individual metabolismFUNCTIONAL ECOLOGY, Issue 2 2005A. P. ALLEN Summary 1We present a model that yields ecosystem-level predictions of the flux, storage and turnover of carbon in three important pools (autotrophs, decomposers, labile soil C) based on the constraints of body size and temperature on individual metabolic rate. 2The model predicts a 10 000-fold increase in C turnover rates moving from tree- to phytoplankton-dominated ecosystems due to the size dependence of photosynthetic rates. 3The model predicts a 16-fold increase in rates controlled by respiration (e.g. decomposition, turnover of labile soil C and microbial biomass) over the temperature range 0,30 °C due to the temperature dependence of ATP synthesis in respiratory complexes. 4The model predicts only a fourfold increase in rates controlled by photosynthesis (e.g. net primary production, litter fall, fine root turnover) over the temperature range 0,30 °C due to the temperature dependence of Rubisco carboxylation in chloroplasts. 5The difference between the temperature dependence of respiration and photosynthesis yields quantitative predictions for distinct phenomena that include acclimation of plant respiration, geographic gradients in labile C storage, and differences between the short- and long-term temperature dependence of whole-ecosystem CO2 flux. 6These four sets of model predictions were tested using global compilations of data on C flux, storage and turnover in ecosystems. 7Results support the hypothesis that the combined effects of body size and temperature on individual metabolic rate impose important constraints on the global C cycle. The model thus provides a synthetic, mechanistic framework for linking global biogeochemical cycles to cellular-, individual- and community-level processes. [source] The application of carbon isotope ratio mass spectrometry to doping controlJOURNAL OF MASS SPECTROMETRY (INCORP BIOLOGICAL MASS SPECTROMETRY), Issue 7 2008Adam T. Cawley Abstract The administration of synthetic steroid copies is one of the most important issues facing sports. Doping control laboratories accredited by the World Anti-Doping Agency (WADA) require methods of analysis that allow endogenous steroids to be distinguished from their synthetic analogs in urine. The ability to measure isotope distribution at natural abundance with high accuracy and precision has increased the application of Gas Chromatography,Combustion,Isotope Ratio Mass Spectrometry (GC,C,IRMS) to doping control in recent years. GC,C,IRMS is capable of measuring the carbon isotope ratio (,13C) of urinary steroids and confirm their synthetic origin based on the abnormal 13C content. This tutorial describes some of the complexities encountered by obtaining valid ,13C measurements from GC,C,IRMS and the need for careful interpretation of all relevant information concerning an individual's metabolism in order to make an informed decision with respect to a doping violation. Copyright © 2008 John Wiley & Sons, Ltd. [source] Is Prenatal Glucocorticoid Administration Another Origin Of Adult Disease?CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 11 2001John P Newnham SUMMARY 1. The intra-uterine environment is now believed to play a major role in the origin of many adult diseases. Illnesses in which there is significant ,programming' before the time of birth include hypertension, diabetes, coronary heart disease and stroke. Acting on a genetic predisposition, intra-uterine triggers appear to programme the individual's metabolism and endocrine milieu and, after birth, these risk factors are then either amplified or minimized by environmental influences. The triggers operative during fetal life that have been studied most extensively are undernutrition and glucocorticoid exposure. 2. Over the past decade, a series of studies in sheep have focused on the perinatal and life-long consequences of glucocorticoid exposure in mid- to late-pregnancy. These studies in the sheep model have shown that maternal injections with glucocorticoids, in a manner similar to clinical treatment for women at risk of preterm birth, enhance fetal lung maturation, but were also associated with developmental and other functional alterations that are of concern. With weekly doses to the mother, there is restricted fetal growth, delayed myelination of the central nervous system, altered blood pressure soon after birth and increased insulin response to glucose challenge in early adulthood. If the glucocorticoids are given to the fetus by ultrasound-guided intramuscular injection, rather than to the mother, the effects on lung maturation are similar, but growth is spared and blood pressure after birth is unaltered. Increased insulin response to glucose challenge occurs in early adulthood with glucocorticoid by either route and is independent of growth restriction. 3. The findings in experimental animals are supported by studies of children in the Western Australian Preterm Infant Follow-up Study. Multivariate analyses have shown that increasing the number of glucocorticoid exposures, for the purpose of enhancing lung maturation prior to preterm birth, is associated with reduced birthweight and behavioural disorders at 3 years of age. 4. The results of these animal and clinical studies provide further support for a role of prenatal glucocorticoid exposure in triggering predisposition to adult disease. Further exploration of these models is expected to uncover the mechanisms and lead to effective strategies that may underpin clinical interventions. [source] | ||||||||||