Modeling the Effects of Macrophytes on Hydrodynamics

A computer model was created as a scientific and management tool for understanding the effects of macrophytes on hydrodynamics and water quality. A model was required that could simulate macrophytes in a complex water body and could be coupled to a multicompartment water quality model of phytoplankton, dissolved oxygen, nutrients, pH, and organic matter. This would permit the investigation of water resource issues where macrophyte growth, phytoplankton growth, nutrient loadings, and flood control were all contributing factors. The model was added as a compartment to the U.S. Army Corps of Engineers two-dimensional, laterally averaged, dynamic water quality model, CE-QUAL-W2 (Corps of Engineers, water quality, width averaged, two dimensional) and applied to the Columbia Slough, Ore. Features of the macrophyte model include the capability to simulate multiple submerged macrophyte species; transport of nutrient fluxes between plant biomass and the water column and/or sediments; growth limitation due to nutrient, light and temperature; simulation of the spatial distribution of macrophytes vertically and horizontally; the modeling of light attenuation in the water column caused by macrophyte concentration; and the modeling of open channel flow with channel friction due to macrophytes. The macrophyte model was tested through mass balances and sensitivity analyses. The modeling of channel friction was evaluated by comparing predicted water levels with data from tests conducted in a laboratory flume. Use of the model in the Columbia Slough showed reasonable predictive capability regarding estimated biomass and water level dynamics.     

Development and Application of a Phosphorus Model for a Shallow Oxbow Lake

A three-dimensional numerical model was developed for simulating the phosphorus concentration in shallow lakes. In this model, the computational domain was divided into two parts: the water column and the bed sediment layer. The processes of mineralization, settling, adsorption, desorption, bed release (diffusion), growth, and death of phytoplankton were taken into account, and the concentration of organic phosphorus, phosphate, and related water quality constituents was simulated. The concentrations of adsorbed (particulate) and dissolved phosphate due to adsorption-desorption were calculated using two formulas derived based on the Langmuir equation. The release rate of phosphorus from the bed sediment layer was calculated by considering the effects of the concentration gradient across the water-sediment interface, pH, temperature, dissolved oxygen concentration, and flow conditions. The adsorption and desorption of phosphate from sediment particles, as well as its release from bed sediment, were verified using laboratory experimental data. The model was calibrated and applied to Deep Hollow Lake in the Mississippi alluvial plain. The simulated trends and magnitudes of phosphorus concentration were compared with field observations. The simulation results show that there are strong interactions between sediment-related processes and phosphorus concentration.     

Neurotoxicity of ammonia and glutamate: molecular mechanisms and prevention

Ammonia is a main factor in the pathogenesis of hepatic encephalopathy. We found that acute ammonia toxicity is mediated by activation of NMDA receptors. Chronic moderate hyperammonemia prevents acute ammonia toxicity in rats. Chronic exposure of cultured neurons to 1 mM ammonia leads to impaired response of the NMDA receptor to activation by its agonists (due to decreased protein kinase C-mediated phosphorylation) and prevents glutamate (Glu) neurotoxicity. Compounds that prevent ammonia toxicity in mice (e.g. carnitine) also prevent Glu toxicity in cultured neurons. These compounds did not prevent activation of NMDA receptor or the rise of Ca2+. They interfered with subsequent steps in the toxic process. The protective effect of carnitine is mediated by activation of metabotropic Glu receptors. Agonists of mGluRs, especially of mGluR5, prevent Glu toxicity. Agonists of muscarinic receptors also prevent Glu toxicity and there seems to be an interplay between muscarinic and metabotropic Glu receptors in the protective effect. We have tried to identify intracellular events involved in the process of neuronal death. It is known that the rise of Ca2+ is an essential step. Glu leads to depletion of ATP; some compounds (e.g. carnitine) prevent Glu-induced neuronal death without preventing ATP depletion: additional events are required for neuronal death. Glu induces activation of Na+/K+-ATPase, which could be involved in the toxic process. Inhibitors of protein kinase C, calcineurin or nitric oxide synthase prevent Glu toxicity. Our results indicate that Glu toxicity can be prevented at different steps or by activating receptors coupled to the transduction pathways interfering with the toxic process. Agents acting on these steps could prevent excitotoxicity in vivo in animals.     

Nitrification Modeling in Pilot-Scale Chloraminated Drinking Water Distribution Systems

A suspended growth nitrification model was developed to describe nitrification dynamics in terms of chloramine, ammonia, nitrite, nitrate, and nitrifying bacteria concentrations in pilot-scale chloraminated drinking water systems. The model provided a semimechanistic base to study the regrowth and persistence of nitrifiers in chloraminated distribution systems. Results showed that the developed suspended growth model, without a biofilm nitrification component, was able to simulate and predict nitrification episodes in the pilot-scale systems. In the restricted low nutrient drinking water environment, growth kinetic parameters for nitrifiers were estimated to be significantly lower than ranges reported in the literature. The maximum specific growth rate and ammonia half-saturation constant for ammonia oxidizing bacteria were estimated to be 0.46?day?1and 0.023?mg NH3–N/L, respectively. In addition, an estimated reaction rate of 70±32?L/(mg?HPC?day) between chloramines and soluble microbial products suggests that heterotrophic growth can be a significant contributor to chloramine decay in some chloraminated distribution systems.     

Eutrophication Model for the Patuxent Estuary: Advances in Predictive Capabilities

A robust eutrophication and sediment diagenesis model has been developed for the Patuxent Estuary to study the impact of different nutrient loadings on phytoplankton biomass and dissolved oxygen (DO) levels. The modeling approach was to begin with an existing water quality model (CE-QUAL-W2) for the Patuxent Estuary (hereafter referred to as the Estuary). First, formulations for the water column kinetics were completely replaced with routines based on the WASP/EUTRO5 water quality model. Then, a sediment diagenesis component was added to simulate the accumulation and mineralization of organic matter in the sediment, the generation of sediment oxygen demand, and the flux of phosphate and ammonia from the sediment. Loadings from the tributaries for nutrients and flow were based on a combination of watershed modeling and sampling by scientists at the Smithsonian Environmental Research Center. The new model was able to reproduce the ambient water quality data from 1997 to 1999 by adequately simulating the high concentrations of phytoplankton and low DO levels in the Estuary. The model was then used to evaluate the response to various hypothetical nutrient loading scenarios. Model results show that phytoplankton growth in the upper Estuary is much more sensitive to nutrient loading from tributaries than in the lower estuary. Further, model results indicate that DO concentrations in the lower Estuary are largely influenced by levels of nutrients and organic carbon at the mouth of the Estuary.     

Absorption and metabolism of nivalenol in pigs

Effects of chronic concentrations of linuron (0, 0.5, 5, 15, 50, and 150 micrograms/L) were studied in indoor, macrophyte dominated, freshwater microcosms. The concentrations were kept at a constant level for 4 weeks. This paper is the first in a series of two and summarizes the course of the linuron concentrations in time and its effects on macrophytes, periphyton, and phytoplankton. These endpoints were studied from 3 weeks before the start of the treatment until 11 weeks after the start. The degradation of linuron in the water was lower at higher treatment levels, probably due to a decrease in pH. Linuron treatment resulted in a decrease in biomass of the macrophyte Elodea nuttallii and a clear decrease in abundance of the algae Cocconeis, Chroomonas, and Phormidium foveolarum. It was found that Cocconeis first decreased in biovolume and after 2 weeks also in abundance. The alga Chlamydomonas increased in abundance at the two highest doses, resulting in higher chlorophyll-a levels. The NOECs of 0.5 micrograms/L for the inhibition of the growth and photosynthesis of Elodea nuttallii, the abundance of Cocconeis and Chroomonas, and the oxygen and pH levels were the lowest recorded in the microcosms. The safety factors adopted by the EU in the Uniform Principles appeared to ensure adequate protection for the ecosystem in the case of chronic exposure to linuron.     

Modeling Zebra Mussel Impacts on Water Quality of Seneca River, New York

The concentrations of dissolved oxygen and chlorophyll have declined in the Seneca River, New York since 1991 as a result of zebra mussel respiration and filtering. Recently measured data were used to approximate flux rates of zebra mussel respiration, filtering, and phosphorus and ammonia mobilization. A model is developed that for the first time links dissolved oxygen, phytoplankton growth, and zebra mussel respiration and filtering. Good agreement is attained between the model calculations and longitudinal profiles of both dissolved oxygen and chlorophyll measured at low flow during 1997–1999. Flux rates derived from these analyses are consistent with results from other studies when normalized on the basis of zebra mussel number and tissue dry weight. Kinetic formulations for the zebra mussels are developed that describe respiration and filtering rates as a function of density, size distribution, and dissolved oxygen concentration. Several plausible test scenarios are examined using the model that indicate that both zebra mussel numbers and size distributions have a profound effect on the water quality of the Seneca River and therefore have important management and planning ramifications.     

Histopathological changes in rabbit uterus carcinoma after transcatheter arterial embolization using cisplatin

Axenic mass cultivation of Acanthamoeba castellanii in laboratory fermentors (141) yielded after 20 days approximately 3 g cells (wet weight). After a short lag phase amoebal cell numbers increased exponentially to a maximum of 3.5 x 10(5) cells per ml until cell death occurred after 20 days. Optical density and protein concentrations revealed identical patterns. During amoebal growth only 12-19% of the initially added glucose (100 mM) as sole carbon source was used. Large amounts of ammonia (1 g in 10.51 culture volume) were excreted into the medium which subsequently raised the pH from 6.6 to 7.7, and from 6.6 to 6.8 in 2 and 20 mM buffered media, respectively. Growth inhibition and cell death could not be explained by a depletion of glucose or oxygen limitations during growth. The production of ammonia had a growth inhibitory effect, however, the sudden termination of the exponential growth phase and cell death could not be explained by the toxic influence of ammonia only.     

Coupled Effects of Small-Scale Turbulence and Phytoplankton Biomass in a Small Stratified Lake

Recent laboratory studies demonstrated that small-scale fluid motion mediates phytoplankton physiological responses. We have investigated to what extent the laboratory studies are consistent with field measurements in a small stratified lake. We propose the rate of energy dissipation and corresponding Kolmogorov velocity are important scaling variables that describe the enhanced algal growth and the uptake of nutrients in a moving fluid under laboratory and field conditions. The ratio of nutrient flux to an alga in a moving fluid versus the nutrient flux in a stagnant fluid (Sherwood number) is quantified by the ratio of advective nutrient transport to molecular diffusion of a nutrient (Péclet number, PeK). The advective transport of nutrients is described by the layer-averaged Kolmogorov velocity (K). An enhanced algal growth due to fluid motion is proposed over the Péclet number range 6.7>PeK>1.3, with the maximal growth at PeK = 2.9. Field measurements recorded by a microstructure profiler demonstrated encouraging agreement between laboratory and field findings. The current mechanistic models of phytoplankton population dynamics could consider the proposed Péclet number with redefined characteristic velocity scale (K) in the formulation of subgrid scale closure fluxes on nutrient uptake and growth rate. Furthermore, the laboratory and field results presented in this study are intended to motivate researchers to question the validity of standard laboratory biotoxicity protocols and to modify existing procedures in the examination of effluent toxicity in the environment by including the fluid motion.     

Superoxide production and antioxidant enzymes in ammonia intoxication in rats

Injection of large doses of ammonium salts lead to the rapid death of animals. However, the molecular mechanisms involved in ammonia toxicity remain to be clarified. We have tested the effect of injecting 7 mmol/kg of ammonium acetate on the production of superoxide and on the activities of some antioxidant enzymes in rat liver, brain, erythrocytes and plasma. Glutathione peroxidase, superoxide dismutase and catalase activities were decreased in liver and brain (both in cytosolic and mitochondrial fractions) and also in blood red cells, while glutathione reductase activity remained unchanged. Superoxide production in submitochondrial particles from liver and brain was increased by more than 100% in both tissues. Both diminished activity of antioxidant enzymes and increased superoxide radical production could lead to oxidative stress and cell damage, which could be involved in the mechanism of acute ammonia toxicity.     

Wave Damping in Reed: Field Measurements and Mathematical Modeling

Wave damping in vegetation in shallow lakes reduces resuspension and thereby improves the light climate and decreases nutrient recycling. In this study, wave transformation in reed (Phragmites australis) was measured in a shallow lake. Theoretical models of wave height decay, based on linear wave theory, and transformation of the probability density function (PDF), using a wave-by-wave approach, were developed and compared to the collected data. Field data showed an average decrease in wave height of 4–5%?m?1 within the first 5–14 m of the vegetation. Incident root-mean-square wave height was 1–8 cm. A species-specific drag coefficient CD was found to be about 9 (most probable range: 3–25). CD showed little correlation with a Reynolds number or a Keulegan-Carpenter number. The PDF for the wave heights did not change significantly, but for longer distances into the vegetation and higher waves it tended to be more similar to the developed transformed distribution than to a Rayleigh distribution. Relationships developed in this study can be employed for management purposes to reduce resuspension and erosion.     

The regulation of reactive oxygen species production during programmed cell death

Reactive oxygen species (ROS) are thought to be involved in many forms of programmed cell death. The role of ROS in cell death caused by oxidative glutamate toxicity was studied in an immortalized mouse hippocampal cell line (HT22). The causal relationship between ROS production and glutathione (GSH) levels, gene expression, caspase activity, and cytosolic Ca2+ concentration was examined. An initial 5-10-fold increase in ROS after glutamate addition is temporally correlated with GSH depletion. This early increase is followed by an explosive burst of ROS production to 200-400-fold above control values. The source of this burst is the mitochondrial electron transport chain, while only 5-10% of the maximum ROS production is caused by GSH depletion. Macromolecular synthesis inhibitors as well as Ac-YVAD-cmk, an interleukin 1beta-converting enzyme protease inhibitor, block the late burst of ROS production and protect HT22 cells from glutamate toxicity when added early in the death program. Inhibition of intracellular Ca2+ cycling and the influx of extracellular Ca2+ also blocks maximum ROS production and protects the cells. The conclusion is that GSH depletion is not sufficient to cause the maximal mitochondrial ROS production, and that there is an early requirement for protease activation, changes in gene expression, and a late requirement for Ca2+ mobilization.     

Insulin-like growth factors prevent apoptosis in cortical neurons isolated from stroke-prone spontaneously hypertensive rats

Cerebral ischemia induces a massive efflux of glutamate causing delayed neuronal death in stroke-prone spontaneously hypertensive rats (SHRSP) but not in Wistar Kyoto rats (WKY). It is obvious that L-N-nitroarginine (L-NNA; NO synthase (NOS) inhibitor), benzamide (poly(ADP-ribose) synthetase inhibitor), and growth factors are involved in reducing neuronal cell death due to toxic conditions, especially phosphatidylinositol 3 (PI3)-kinase activity; however, no studies have clarified whether genetic vulnerability to neurotoxic states is present in cortical neurons isolated from SHRSP. For this purpose, we prepared cortical neurons from WKY and SHRSP (15 weeks of gestation) to test the genetic vulnerability involved in the pathogenesis of stroke as well as apoptosis of cortical neurons isolated from SHRSP. We also examined the mechanisms necessary to reduce apoptosis under neurotoxic states using ultrastructural and biochemical techniques. Cortical neurons from SHRSP were in fact found to be more vulnerable than neurons from WKY and resulted in apoptosis when treated with nitric oxide (NO)- and N-methyl-D-aspartate (NMDA)-mediated neurotoxic agents. Growth factors, especially insulin-like growth factor (IGF), rescued neurons from NO- and NMDA-mediated neurotoxicity, particularly those from SHRSP. Conversely, benzamide and L-NNA reduced NMDA-mediated neurotoxicity but not NO-mediated toxicity. The ability to protect neurons from neurotoxicity was as follows: IGF-->nerve growth factor epidermal growth factor-->L-NNA-->benzamide. In addition, it was demonstrated that wortmannin, a PI3-kinase inhibitor, lessened the protective effects of these growth factors against NO-mediated toxicity. The data thus indicate that genetic factors related to neuronal vulnerability to apoptosis are involved in the pathogenesis of stroke lesions in SHRSP. PI3-kinase activity, which is stimulated by growth factors, is closely related to protective effects against NO- and NMDA-mediated toxicity in cortical neurons, especially those isolated from SHRSP. Moreover, the genetic vulnerability observed in SHRSP neurons is possibly linked to the inadequate activation of signaling pathways in the downstream of protein tyrosine kinases.     

Effects of gastric mucosal blood flow (GMBF) on the role of adaptive cytoprotection of rat gastric mucosa

It has been reported that ingestion of an ammonium-containing diet produces hyperammonemia without encephalopathy, thus permitting the study of the specific effects of ammonia toxicity. The present study investigated the rat cerebral somatostatinergic system using this experimental model of hyperammonemia. Wistar rats were fed a high ammonia diet prepared by mixing a standard diet with ammonium acetate (20% w/w); in addition, 5 mM of ammonium acetate was added to their water supply. Control rats were fed with a standard diet. The animals were sacrificed at 3, 7 and 15 days of ammonia ingestion. Ammonia levels in blood had increased approximately 3-fold at 7 days of ammonia ingestion. These changes were associated with a significant decrease in the specific binding of somatostatin (SS) to putative receptors sites in the frontoparietal cortex and hippocampus at 7 and 15 days after starting the high ammonia diet. Scatchard analysis shows that the decrease in SS binding resulted from a decrease in the number of available SS receptors rather than a change in receptor affinity. No changes in the somatostatin-like immunoreactivity content (SSLI) were detected in either brain area at the three study times. These results suggest that hyperammonemia alone can affect the rat brain somatostatinergic system. However, the animal model of hyperammonemia used here is insufficient to produce encephalopathy despite the significant increase in serum ammonia.     

Saturation of ecosystems with toxic metals in Sudbury basin, Ontario, Canada

Mining and resource recovery activities have not been kind to ecosystems in the Sudbury basin, Ontario. The combination of logging, smelting, fires and erosion resulted in an unusual anthropogenic ecosystem of denuded barren land with lifeless lakes, or a micro-desert. Since the 1970s, however, the concerted efforts made to reduce the emissions and rehabilitate parts of the degraded ecosystem have resulted in improvements in water quality, and recoveries in phytoplankton, zooplankton, zoobenthos and fish communities but have had little impact on toxic metal concentrations in many lakes. We show that most of the catchments in the Sudbury basin have become saturated with Cu and Ni, and some with Zn and Pb. It is estimated that mobilization of metals stored in soils and glacial overburden by surface runoff, groundwater drainage and wind re-working of tailings can sustain the high concentrations of Cu and Ni in many lakes for well over 1000 years. Strategies to immobilize the pollutant metals in the watershed rather than further emission controls may be required for dealing with high levels of toxic metals in surface waters of the saturated ecosystems.     

Quantitative Comparison of Models for Barotropic Response of Homogeneous Basins

Numerous three-dimensional models that solve the shallow water equations have been proposed to describe the processes of circulation and mixing in large bodies of water. The utility of those models is often demonstrated by comparison of computed variables with field observations. However, both the hydrodynamic data and the boundary conditions that drive the model have unknown measurement uncertainties and a limited spatial coverage, which limit the validity of this approach. A series of simple benchmark problems with analytical solutions is proposed to evaluate a particular model’s suitability to efficiently and accurately reproduce a wide range of characteristic hydrodynamic phenomena in natural lakes. The test problems focus on the representation of free and forced oscillations in homogeneous water bodies (barotropic response). This is not intended as a substitute for model validation against field data but, rather, as a necessary step in the initial model testing and selection. To illustrate this approach, the proposed test problems are used to compare a finite-element and a finite-difference free-surface hydrostatic model.     

3D Numerical Modeling of MICROCYSTIS Distribution in a Water Reservoir

A 3D computational fluid dynamics program was used to calculate the wind-induced accumulation of phytoplankton in Eglwys Nynydd, a water supply reservoir in Wales. The computational fluid dynamics model solved the Navier-Stokes equations for the water velocities using the SIMPLE method to calculate the pressure. Two turbulence models were tested: a zero-equation model and the k-ε model. An unstructured nonorthogonal 3D grid with hexahedral cells was used. The distribution of the blue-green algae Microcystis was calculated by solving the transient convection-diffusion equation for phytoplankton concentration, based on the modeled flow field. The numerical model included algorithms for calculating the growth rate of phytoplankton and simulating the response of the algae to changes in underwater light intensity. The model was validated by comparing the horizontal distribution patterns produced by simulation with those recorded during a field survey of surface concentrations. The results demonstrated reasonable agreement, particularly when using the k-ε turbulence model. The main parameter affecting the results was the effective diameter of the Microcystis colonies.     

Incorporating Reservoir Transfer into Treatment Optimization Decisions

The Massachusetts Water Resources Authority (MWRA) supplies unfiltered water from two large surface water reservoirs to the metropolitan Boston area, as well as to three smaller communities in central Massachusetts [the Chicopee Valley Aqueduct (CVA) communities]. Quabbin Reservoir is larger than Wachusett Reservoir, and has traditionally been used to supplement the Wachusett during the summer period. Quabbin water is also of better quality, with lower reactive natural organic matter (NOM). The MWRA began to add chlorine at Wachusett in 1997, and a new facility for adding chlorine at Quabbin for the CVA was also started up in 2000 to meet primary disinfection regulations to meet pathogen inactivation. The reaction of chlorine with NOM produces undesirable disinfection by-products (DBPs). The absorption of ultraviolet light at a wavelength of 254 nm was identified in chlorine decay studies to be the most important raw water quality parameter for predicting chlorine decay and DBP formation. This technical note summarizes the chlorine decay model for Wachusett and Quabbin water. The model is extended to ozonation of Wachusett water for the future Walnut Hill treatment plant. The models allowed the development of a trigger using UV-254 to time the Quabbin transfer to optimize treatment results. It is believed that the model for disinfectant decay and the use of UV-254 as a trigger for water treatment decisions are generalized and applicable to other water utilities.     

Some properties of late after-potential in frog skeletal muscle fiber

Some properties of late after-potentials which appear following a train of impulses were examined in frog skeletal muscle fiber. The decay of the late after-potential followed a simple exponential time course. The time constant of the decay was larger in a viscous solution than in normal Ringer solution. It was proved by physical experiments that the diffusion of K ions was delayed in the viscous medium at the same rate as the decay. The effect of temperature on the decay was low and the Q10 for the time constant was 1.2. When the late after-potentials were recorded at membrane potentials variedly controlled by the polarizing current, the reversal potential shifted in the positive direction with the increase of impulses. These results suggest that the late after-potential may be dependent on K ions accumulated in the T system. During the initial 300 msec period immediately after the onset of the decay, the amplitude was smaller than expected by a simple exponential time course. This effect was especially apparent in the sucrose hypertonic Ringer solution in which the decay was extremely extended. The cause of this non-exponential component was discussed with respect to the K accumulation hypothesis.