Nutrients cause grassland biomass to outpace herbivory.

Human activities are transforming grassland biomass via changing climate, elemental nutrients, and herbivory. Theory predicts that food-limited herbivores will consume any additional biomass stimulated by nutrient inputs ('consumer-controlled'). Alternatively, nutrient supply is predicted to increase biomass where herbivores alter community composition or are limited by factors other than food ('resource-controlled'). Using an experiment replicated in 58 grasslands spanning six continents, we show that nutrient addition and vertebrate herbivore exclusion each caused sustained increases in aboveground live biomass over a decade, but consumer control was weak. However, at sites with high vertebrate grazing intensity or domestic livestock, herbivores consumed the additional fertilization-induced biomass, supporting the consumer-controlled prediction. Herbivores most effectively reduced the additional live biomass at sites with low precipitation or high ambient soil nitrogen. Overall, these experimental results suggest that grassland biomass will outstrip wild herbivore control as human activities increase elemental nutrient supply, with widespread consequences for grazing and fire risk.

TYPE TESTING OF LiF:Mg,Cu,P (TLD-100H) WHOLE-BODY DOSEMETERS FOR THE ASSESSMENT OF Hp(10) AND Hp(0.07).

In this work, the initial results of the type testing of the LiF:Mg,Cu,P (TLD-100H) whole-body personal dosemeters are presented. An assessment of reproducibility, linearity of the response, the residual signal as a function of the dose, energy and angular dependence of the response was performed. In general, the dosemeters show good reproducibility for different dose values and a linear behaviour for a range between 0.1 and 300 mSv. The detection limits obtained are lower than 50 µSv. The system presents a good energy and angular response for different radiation qualities.

Enhanced lipidic algae biomass production using gas transfer from a fermentative Rhodosporidium toruloides culture to an autotrophic Chlorella protothecoides culture.

In order to produce single-cell oil for biodiesel, a yeast and a microalga were, for the first time, grown in two separate reactors connected by their gas-phases, taking advantage of their complementary nutritional metabolisms, i.e., respiration and photosynthesis. The yeast Rhodosporidium toruloides was used for lipid production, originating a carbon dioxide-enriched outlet gas stream which in turn was used to stimulate the autotrophic growth of Chlorella protothecoides in a vertical-alveolar-panel (VAP) photobioreactor. The microalgal biomass productivity was 0.015 gL(-1)h(-1), and its lipid productivity attained 2.2 mgL(-1)h(-1) when aerated with the outlet gas stream from the yeast fermenter. These values represent an increase of 94% and 87%, respectively, as compared to a control culture aerated with air. The CO2 bio-fixed by the microalgal biomass reached an estimated value of 29 mgL(-1)h(-1) in the VAP receiving the gas stream from the fermenter, a value 1.9 times higher than that measured in the control VAP.

Sources of hepatic glycogen synthesis following a milk-containing breakfast meal in healthy subjects.

During feeding, dietary galactose is a potential source of hepatic glycogen synthesis; but its contribution has not been measured to date. In the presence of deuterated water ((2)H(2)O), uridine diphosphate (UDP)-glucose derived from galactose is not enriched, whereas the remainder derived from glucose-6-phosphate (G6P) is enriched in position 2 to the same level as body water, assuming complete G6P-fructose-6-phosphate (F6P) exchange. Hence, the difference between UDP-glucose position 2 and body water enrichments reflects the contribution of galactose to glycogen synthesis relative to all other sources. In study 1, G6P-F6P exchange in 6 healthy subjects was quantified by supplementing a milk-containing breakfast meal with 10 g of [U-(2)H(7)]glucose and quantifying the depletion of position 2 enrichment in urinary menthol glucuronide. In study 2, another 6 subjects ingested (2)H(2)O and acetaminophen followed by an identical breakfast meal with 10 g of [1-(13)C]glucose to resolve direct/indirect pathways and galactose contributions to glycogen synthesis. Metabolite enrichments were determined by (2)H and (13)C nuclear magnetic resonance. In study 1, G6P-F6P exchange approached completion; therefore, the difference between position 2 and body water enrichments in study 2 (0.20% ± 0.03% vs 0.27% ± 0.03%, P < .005) was attributed to galactose glycogenesis. Dietary galactose contributed 19% ± 3% to glycogen synthesis. Of the remainder, 58% ± 5% was derived from the direct pathway and 22% ± 4% via the indirect pathway. The contribution of galactose to hepatic glycogen synthesis was resolved from that of direct and indirect pathways using a combination of (2)H(2)O and [1-(13)C]glucose tracers.

Simple measurement of gluconeogenesis by direct 2H NMR analysis of menthol glucuronide enrichment from 2H2O.

The contribution of gluconeogenesis to fasting glucose production was determined by a simple measurement of urinary menthol glucuronide (MG) 2H enrichment from 2H2O. Following ingestion of 2H2O (0.5% body water) during an overnight fast and a pharmacological dose (400 mg) of a commercial peppermint oil preparation the next morning, 364 micromol MG was quantitatively recovered from a 2-h urine collection by ether extraction and a 125 micromol portion was directly analyzed by 2H NMR. The glucuronide 2H-signals were fully resolved and their relative intensities matched those of the monoacetone glucose derivative. The pharmacokinetics and yields of urinary MG after ingestion of 400 mg peppermint oil as either gelatin or enteric-coated capsules 1 h before breakfast were quantified in five healthy subjects. Gelatin capsules yielded 197 +/- 81 micromol of MG from the initial 2-h urine collection while enteric-coated capsules gave 238 +/- 84 micromol MG from the 2- to 4-h urine collection.

Toxicity of prolonged exposure to ethanol and gasoline autoengine exhaust gases.

A comparative chronic inhalation exposure study was performed to investigate the potential health effects of gasoline and ethanol engine exhaust fumes. Test atmospheres of gasoline and ethanol exhaust were given to Wistar rats and Balb C mice housed in inhalation chambers for a period of 5 weeks. Gas concentration and physical parameters were continually monitored during the exposure period. Several biological parameters were assessed after the exposure including pulmonary function, mutagenicity, and hematological, biochemical, and morphological examinations. The results demonstrated that the chronic toxicity of the gasoline-fueled engine is significantly higher than that of the ethanol engine.

Pulmonary function of rats exposed to ethanol and gasoline fumes.

This paper describes the effects of repeated exposure to gasoline and ethanol exhaust fumes on the pulmonary mechanics of rats assessed by whole-body plethysmography. Two groups of 12 male Wistar albino rats each were tested before and after exposure to diluted gasoline or ethanol exhaust gases for 5 weeks, 8 h per day and 5 days per week. An additional group of 12 rats were exposed to clean air under the same experimental conditions. The variations of the functional parameters observed in the three groups before and after exposure were compared. Peak Expiratory Flow and Forced Expiratory Mean Flows in the ranges 0-25%, 25-50% and 50-75% of Forced Vital Capacity were significantly reduced in animals exposed to gasoline exhaust fumes, whereas the group exposed to ethanol exhaust fumes did not differ from the control group. This respiratory impairment is probably due to the presence of SO2 and the quality of the hydrocarbons in gasoline exhaust gases.