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Research studies clearly indicate that age-related changes in cellular and tissue function are linked to decreases in the anabolic hormones, growth hormone and insulin-like growth factor (IGF)-1. Although there has been extensive research on the effects of these hormones on bone and muscle mass, their effect on cerebrovascular and brain ageing has received little attention. We have also observed that in response to moderate calorie restriction (a treatment that increases mean and maximal lifespan by 30-40%), age-related decreases in growth hormone secretion are ameliorated (despite a decline in plasma levels of IGF-1) suggesting that some of the effects of calorie restriction are mediated by modifying the regulation of the growth hormone/IGF-1 axis. Recently, we have observed that microvascular density on the surface of the brain decreases with age and that these vascular changes are ameliorated by moderate calorie restriction. Analysis of cerebral blood flow paralleled the changes in vasculature in both groups. Administration of growth hormone for 28 d was also found to increase microvascular density in aged animals and further analysis indicated that the cerebral vasculature is an important paracrine source of IGF-1 for the brain. In subsequent studies, administration of GHRH (to increase endogenous release of growth hormone) or direct administration of IGF-I was shown to reverse the age-related decline in spatial working and reference memory. Similarly, antagonism of IGF-1 action in the brains of young animals impaired both learning and reference memory. Investigation of the mechanisms of action of IGF-1 suggested that this hormone regulates age-related alterations in NMDA receptor subtypes (e.g. NMDAR2A and R2B). The beneficial role of growth hormone and IGF-1 in ameliorating vascular and brain ageing are counterbalanced by their well-recognised roles in age-related pathogenesis. Although research in this area is still evolving, our results suggest that decreases in growth hormone and IGF-1 with age have both beneficial and deleterious effects. Furthermore, part of the actions of moderate calorie restriction on tissue function and lifespan may be mediated through alterations in the growth hormone/IGF-1 axis.

Numerous studies have been conducted examining nitrate (NO 3 ) leaching losses from agricultural land. Simulation models have been developed that allow one to predict the potential of NO 3 to leach to groundwater. However, many of these models treat NO 3 as a conservative tracer and do not evaluate surface chemistry. This study evaluated the surface charge properties and NO 3 adsorption capacity of four acid southeastern subsoils. Significant anion exchange capacity and NO 3 retention was found for two of the soils. Point of zero net charge (PZNC) was determined using an ion exchange method. Values of 3.1 and 3.6 were determined for two of the soils while PZNC values were not quantifiable for the other two soils in the pH range of 3 to 7. Nitrate adsorption isotherms were measured on untreated and chloride-saturated soils. Nitrate adsorption maxima determined from the linearized form of the Langmuir equation ranged from 1.40 to 2.13 cmol c kg -1 . Coefficients of determination (R 2 ) and adsorption maxima increased after chloride saturation. This was attributed to competition from anions such as sulfate, fluoride, and phosphate. Net positive charge and NO 3 retention were found to depend on the type and quantity of both variable and permanent charged minerals present in the soil and the composition of the exchange complex. These results demonstrated that acid subsoils high in variable charge minerals may have the potential to retard NO 3 movement to groundwater. Therefore, simulation models may need to account for NO 3 adsorption when modeling NO 3 movement in acid soils dominated by variable charge minerals.