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Background: Pipamperone is prescribed to prevent impulsive aggressive behaviour in patients with intermittent explosive disorder, personality disorders or mental retardation., Aim: To investigate the scientific basis of this treatment., Method: Various databases were searched using the terms 'pipamperon', 'pipamperone' and 'Dipiperon'. Located articles were reviewed in order to discover whether they dealt with the relationship between the drug and impulsiveness and aggression. results Six publications were found, all dating from before 1979., Conclusion: In view of the limited amount of research on the subject and the adverse side effects it is concluded that pipamperone is not the drug of first choice considering the treatment of impulsive aggressive behaviour.

Loess soils have always been among the most problematic soils, according to engineers. Due to the sensitivity and vulnerability of this soil type, researchers are constantly looking for different solutions to improve and stabilize this soil using different methods. In the present study, a mixture of lime and rice husk ash (LRHA) was used to modify the loess soil of the Golestan province, Iran. Lime and RHA were mixed in a ratio of 2:4 and with different contents of 2.5, 5, 7.5, 10 and 12.5% of the dry weight of the soil. To study the effect of curing on the strength properties, the samples were cured and tested for 7, 18 and 28 days. Atterberg limits, modified Proctor, unconfined compressive strength (UCS) and scanning electron microscope tests (SEM) were performed. It was found that increasing LRHA content increased the value of UCS at different curing times, such that UCS increased about five times by the addition of 5% LRHA to the loess at the end of 28 days. As the curing time increased, the optimum amount of the additive also decreased. The results showed that combining the soil with LRHA is an effective method for improving and stabilizing loess soil. According to the results of the study, the optimum value of 5% additive is economically and technically recommended. [ABSTRACT FROM AUTHOR]

The dyskinesia of Parkinson's Disease is most likely due to excess levels of dopamine in the striatum. The mechanism may be due to aberrant synthesis but also, a deficiency or absence of the Dopamine Transporter. In this study we have examined the proposition that reinstating Dopamine Transporter expression in the striatum would reduce dyskinesia. We transplanted c17.2 cells that stably expressed the Dopamine Transporter into dyskinetic rats. There was a reduction in dyskinesia in rats that received grafts expressing the Dopamine Transporter. Strategies designed to increase Dopamine Transporter in the striatum may be useful in treating the dyskinesia associated with human Parkinson's Disease. [ABSTRACT FROM AUTHOR]

Failed storage capacity, leading to pulsatile delivery of dopamine (DA) in the striatum, is used to explain the emergence of ‘wearing off’ and dyskinaesia in Parkinsons disease. In this study, we show that surviving DA neurons in 6-OHDA lesioned rats sprout to re-innervate the striatum, and maintain terminal density until ∼60% of neurons are lost. We demonstrate that DA terminal density correlates with baseline striatal DA concentration ([DA]). Electrochemical and synaptosome studies in 6-OHDA lesioned rats and primates suggest that impaired striatal DA re-uptake and increased DA release from medial forebrain bundle fibres contribute to maintaining striatal DA levels. In lesioned rats where terminal density fell by 60% or more, l-DOPA administration increased striatal DA levels markedly. The striatal [DA] produced by l-DOPA directly correlated with the extent of dyskinaesia, suggesting that dyskinaesia was related to high striatal [DA]. While sprouting and decreased dopamine uptake transporter function would be expected to contribute to the marked increase in l-DOPA induced [DA], the increased [DA] was most marked when DAergic fibres were >60% denervated, suggesting that other release sites, such as serotonergic fibres might be contributing. In conclusion, the extent of dyskinaesia was directly proportional to the extent of DA terminal denervation and levels of extra-synaptic striatal DA. We propose that sprouting of DA terminals and decreased dopamine uptake transporter function prevent the appearance of Parkinsonian symptoms until about 60% loss of nigral neurons, but also contribute to dysregulated striatal DA release that is responsible for the emergence of dyskinaesia and ‘wearing off’. [ABSTRACT FROM AUTHOR]