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This paper describes the chemical conditions that should favour the biodegradation of organic pollutants. Thermodynamic considerations help to define the reaction that can occur under defined chemical conditions. The BTEX (benzene, toluene, ethylbenzene, and xylene) degradation is focused on benzene, as it is the most toxic oil component and also because it has the slowest degradation rate under most field conditions. Several studies on benzene degradation allow the understanding of the basic degradation mechanisms and their importance in field conditions. The use of models is needed to interpret field data when transport, retardation, and degradation occur. A detailed comparison of two existing models shows that the limits imposed by oxygen transport must be simulated precisely to reach correct plumes shapes and dimensions, and that first-order kinetic approaches may be misleading. This analysis led us to develop a technique to measure directly biodegradation in the field. The technique to recirculate water at the borehole scale and the CO2 analysis are depicted. First results of biodegradation show that this technique is able to easily detect the degradation of 1 mg/l of hydrocarbons and that, in oxic media, a fast degradation rate of mixed fuel is observed.

Aquatic scientists generally recognize that controlled experiments are required to establish cause-effect relationships (e.g., Havens and Aumen, 2000), and understanding ecological processes is key to accurately predicting complex ecosystem responses. However, resource managers may have at their disposal only a limited amount of observational data when faced with management decisions. Hence, there may be a tendency to use simple empirical models for decision making. An example of eutrophication management in lakes illustrates a pitfall of this approach when used independently of other scientific information.

Environmental economics deals with the optimal allocation of production factors and correcting market failure in protecting the environment. Market failure occurs because of externalities, common property resources, and public goods. Environmental policy instruments include direct regulation, taxes/subsidies, tradable permits, deposit systems, voluntary agreements, and persuasion.Environmental policies usually focus on one pollutant or environmental issue but may have substantial impacts on other emissions and environmental problems. Neglecting these impacts will result in suboptimal policies. We present an integrated optimisation model for determining cost-effective strategies to simultaneously reduce emissions of several pollutants from several sources, allowing for interrelations between sources and abatement options. Our integrated approach in regard to acidifying compounds and greenhouse gases will be able to provide cost-effective policy options that will result in lower overall abatement costs.This paper shows that efficient emission reduction can be calculated, but we argue that, for transboundary air pollution and climate change, it is difficult to implement the socially optimal solution because strong incentives exist for “free-riding”. In order to implement efficient policies, international environmental agree-ments like the Gothenburg or the Kyoto Protocol are necessary to establish stable coalitions. The stability of these agreements depends on the distribution of costs and benefits over countries and on the redistribution of the gains of cooperation.

The concept of cascading trophic interactions predicts that an increase in piscivore biomass in lakes will result in decreased planktivorous fish biomass, increased herbivorous zooplankton biomass, and decreased phytoplankton biomass. Though often accepted as a paradigm in the ecological literature and adopted by lake managers as a basis for lake management strategies, the trophic cascading interactions hypothesis has not received the unequivocal support (in the form of rigorous experimental testing) that might be expected of a paradigm. Here we review field experiments and surveys, testing the hypothesis that effects of increasing piscivore biomass will cascade down through the food web yielding a decline in phytoplankton biomass. We found 39 studies in the scientific literature examining piscivore effects on phytoplankton biomass. Of the studies, 22 were confounded by supplemental manipulations (e.g., simultaneous reduction of nutrients or removal of planktivores) and could not be used to assess piscivore effects. Of the 17 nonconfounded studies, most did not find piscivore effects on phytoplankton biomass and therefore did not support the trophic cascading interactions hypothesis. However, the trophic cascading interactions hypothesis also predicts that lake systems containing piscivores will have lower phytoplankton biomass for any given phosphorus concentration. Based on regression analyses of chlorophyll�total phosphorus relationships in the 17 nonconfounded piscivore studies, this aspect of the trophic cascading interactions hypothesis was supported. The slope of the chlorophyll vs. total phosphorus regression was lower in lakes with planktivores and piscivores compared with lakes containing only planktivores but no piscivores. We hypothesize that this slope can be used as an indicator of “functional piscivory” and that communities with extremes of functional piscivory (zero and very high) represent classical 3- and 4-trophic level food webs.

It is shown that the delay time of a chalcogenide glass threshold switch is not significantly affected by strong illumination, sufficient to increase the conductance by an order of magnitude. This means that the initiation of threshold switching is not due to free carriers within the bulk material. Noise measurements in the pre-threshold region demonstrate the existence of noise, in excess of thermal noise, increasing sharply towards the threshold point. The results suggest impact ionization by carriers originating at the electrodes as the best available hypothesis for the nature of the threshold condition.

The neuropathy target esterase is a membrane-bound enzyme linked to organophosphate-induced distal neuropathy. Here we report a tentative mechanism of its solubilization from chicken embryo brains by using phospholipase A2. The enzyme was released from brain membranes after degradation of their structural phospholipids initiated by phospholipase A2. L-α-lysophosphatidylcholine, tested as a representative product of phospholipid hydrolysis, was identified as a new efficient detergent for solubilization of the neuropathy target esterase.

The objective of this article was to determine the current practice on amikacin dosing and monitoring in spinal cord injury patients from spinal cord physicians and experts. Physicians from spinal units and clinical pharmacologists were asked to provide protocol for dosing and monitoring of amikacin therapy in spinal cord injury patients. In a spinal unit in Poland, amikacin is administered usually 0.5 g twice daily. A once-daily regimen of amikacin is never used and amikacin concentrations are not determined. In Belgium, Southport (U.K.), Spain, and the VA McGuire Medical Center (Richmond, Virginia), amikacin is given once daily. Whereas peak and trough concentrations are determined in Belgium, only trough concentration is measured in Southport. In both these spinal units, modification of the dose is not routinely done with a nomogram. In Spain and the VA McGuire Medical Center, monitoring of serum amikacin concentration is not done unless a patient has renal impairment. In contrast, the dose/interval of amikacin is adjusted according to pharmacokinetic parameters at the Edward Hines VA Hospital (Hines, Illinois), where amikacin is administered q24h or q48h, depending on creatinine clearance. Spinal cord physicians from Denmark, Germany, and the Kessler Institute for Rehabilitation (West Orange, New Jersey) state that they do not use amikacin in spinal injury patients. An expert from Canada does not recommend determining serum concentrations of amikacin, but emphasizes the value of monitoring ototoxicity and nephrotoxicity. Experts from New Zealand recommend amikacin in conventional twice- or thrice-daily dosing because of the theoretical increased risk of neuromuscular blockade and apnea with larger daily doses in spinal cord injury patients. On the contrary, experts from Greece, Israel, and the U.S. recommend once-daily dosing and determining amikacin pharmacokinetic parameters for each patient. As there is considerable variation in clinical practice across spinal units and experts differ on ideal dosing and monitoring of amikacin therapy in spinal cord injury patients, there is an urgent need to develop best-practice guidelines.