Quantifying the effect of wind on internal wave resonance in Lake Villarrica, Chile

Artículo de publicación ISILake Villarrica, located in south central Chile, has amaximum depth of 167mand amaximum fetch of about 20 km.The lake is monomictic, with a seasonal thermocline located at a depth of approximately 20 m. Field data show the presence of basin-scale internal waves that are forced by daily winds and affected by Coriolis acceleration. A modal linear and nonlinear analysis of internal waves has been used, assuming a two-layer system. The numerical simulations show good agreement with the internal wave field observations. The obtained modes were used to study the energy dissipation within the system, which is necessary to control the amplitude growth. Field data and numerical simulations identify (1) the occurrence of a horizontal mode 1 Kelvin wave, with a period of about a day that coincides with the frequency of daily winds, suggesting that this mode of the Kelvin waves is in a resonant state (subject to damping and controlled by frictional effects in the field) and (2) the presence of higher-frequency internal waves, which are excited by non-linear interactions between basinscale internal waves. The non-linear simulation indicates that only 10% of the dissipation rate of the Kelvin wave is because of bottom friction, while the rest 90% represents the energy that is radiated from the Kelvin wave to other modes. Also, this study shows that modes with periods between 5 and 8 h are excited by non-linear interactions between the fundamental Kelvin wave and horizontal Poincaré-type waves. A laboratory study of the resonant interaction between a periodic forcing and the internal wave field response has also been performed, confirming the resonance for the horizontal mode 1 Kelvin wave.The authors acknowledge support of the Civil Engineering Department, Universidad de Chile, FONDECYT Project 1080617 and the Civil Engineering Department, University of Dundee. The first author acknowledges financial support from Department of Graduate and Postgraduate Degree, Universidad de Chile

Striatal implants protect the host striatum against quinolinic acid toxicity.

Quinolinic acid (QA) and related excitotoxins produce a pattern of neuronal loss and neurochemical changes in the rat striatum similar to that of patients suffering from Huntington's disease, suggesting neurotoxicity is important in the etiology of that disease. Thus, strategies for limiting excitotoxin-induced striatal damage, like that caused by QA, may be of great benefit to these individuals. Accordingly, we tested the ability of both neural and non-neural tissue implants to protect the rat striatum against a subsequent QA challenge. Our results demonstrated that recipients of fetal striatal grafts were significantly less affected by striatal injections of QA than non-grafted animals. In contrast to the latter, fetal striatal tissue recipients did not exhibit apomorphine-induced rotation behavior and showed a sparing of cholinergic and enkephalinergic systems normally lost following QA injections. Animals grafted with adult rat sciatic nerve, adrenal medulla or adipose tissue all showed a less dramatic behavioral protection and sparing of cholinergic and enkephalinergic systems. These results suggest that fetal striatal tissue exerts an optimal, and perhaps specific protective influence on the host brain

Effects of aluminum sulfate on delta-aminolevulinate dehydratase from kidney, brain, and liver of adult mice

The purpose of the present study was to investigate the in vitro and in vivo effects of aluminum sulfate on delta-aminolevulinic acid dehydratase (ALA-D) activity from the brain, liver and kidney of adult mice (Swiss albine). In vitro experiments showed that the aluminum sulfate concentration needed to inhibit the enzyme activity was 1.0-5.0 mM (N = 3) in brain, 4.0-5.0 mM (N = 3) in liver and 0.0-5.0 mM (N = 3) in kidney. The in vivo experiments were performed on three groups for one month: 1) control animals (N = 8); 2) animals treated with 1 g% (34 mM) sodium citrate (N = 8) and 3) animals treated with 1 g% (34 mM) sodium citrate plus 3.3 g% (49.5 mM) aluminum sulfate (N = 8). Exposure to aluminum sulfate in drinking water inhibited ALA-D activity in kidney (23.3 ± 3.7%, mean ± SEM, P<0.05 compared to control), but enhanced it in liver (31.2 ± 15.0%, mean ± SEM, P<0.05). The concentrations of aluminum in the brain, liver and kidney of adult mice were determined by graphite furnace atomic absorption spectrometry. The aluminum concentrations increased significantly in the liver (527 ± 3.9%, mean ± SEM, P<0.05) and kidney (283 ± 1.7%, mean ± SEM, P<0.05) but did not change in the brain of aluminum-exposed mice. One of the most important and striking observations was the increase in hepatic aluminum concentration in the mice treated only with 1 g% sodium citrate (34 mM) (217 ± 1.5%, mean ± SEM, P<0.05 compared to control). These results show that aluminum interferes with delta-aminolevulinate dehydratase activity in vitro and in vivo. The accumulation of this element was in the order: liver > kidney > brain. Furthermore, aluminum had only inhibitory properties in vitro, while in vivo it inhibited or stimulated the enzyme depending on the organ studied