No abstract

Soil and climatic variability contribute in an unknown manner to the leaching of pesticides below the surface soil zone where degradation occurs at maximum levels. In this paper we couple the climatic variability model of Eagleson (1978) to the soil variability transport model of Jury (1982) to produce a probability density distribution of residual mass fraction (RMF) remaining after leaching below the surface degradation zone. Estimates of the RMF distribution are shown to be much more sensitive to soil variability than climatic variability, except when the residence time of the chemical is shorter than one year. When soil variability dominates climatic variability, the applied water distribution may be replaced by a constant average water application rate without serious error. Simulations of leaching are run with 10 pesticides in two climates and in two representative soil types with a range of soil variability. Variability in soil or climate act to produce a nonnegligible probability of survival of a small value of residual mass even for relatively immobile compounds which are predicted to degrade completely by a simple model which neglects variability. However, the simpler model may still be useful for screening pesticides for groundwater pollution potential if somewhat larger residual masses of a given compound are tolerated. Monte Carlo simulations of the RMF distribution agreed well with model predictions over a wide range of pesticide properties.

No abstract

Post-stroke Epilepsy (PSE) is one of the most common forms of acquired epilepsy, especially in the elderly population. As people get increasingly older, the number of stroke patients is expected to rise and concomitantly the number of people with PSE. Although many patients are affected by post-ischemic epileptogenesis, not much is known about the underlying pathomechanisms resulting in the development of chronic seizures. A common hypothesis is that persistent neuroinflammation and glial scar formation cause aberrant neuronal firing. Here, we summarize the clinical features of PSE and describe in detail the inflammatory changes after an ischemic stroke as well as the chronic changes reported in epilepsy. Moreover, we discuss alterations and disturbances in blood-brain-barrier leakage, astrogliosis, and extracellular matrix changes in both, stroke and epilepsy. In the end, we provide an overview of commonalities of inflammatory reactions and cellular processes in the post-ischemic environment and epileptic brain and discuss how these research questions should be addressed in the future.