Reutilisation of Water Contaminated by Mining Waste for the Encapsulation of Potentially Toxic Elements

Mining activities are essential for a population’s development; however, they also produce negative effects such as the production of waste, an impact on flora and water pollution. On the other hand, construction is one of the sectors which is most demanding of raw materials, with one of the main such materials being water. For this reason, this research evaluates the feasibility of incorporating water contaminated by mining waste into ceramic materials for bricks. In this way, the use of water is reduced and, on the other hand, the contaminating elements of the mining water are encapsulated in the ceramic matrix. To achieve this, the clay used and the contaminated water were first analysed, then different families of samples were conformed with different percentages of contaminated water. These samples were tested to determine their physical and mechanical properties. At the same time, leachate tests were carried out to determine that the ceramic material created did not cause environmental problems. The test results showed that the physical and mechanical properties of the ceramics were not influenced by the addition of contaminated water. On the other hand, the leachate tests showed that encapsulation of most of the potentially toxic elements occurred. However, the use of contaminated water as mixing water for ceramics could only be performed up to 60%, as higher percentages would leach impermissible arsenic concentrations. Accordingly, a new way of reusing water contaminated by mining activities is developed in this study, taking advantage of resources, avoiding environmental pollution and creating economic and environmentally friendly end products.     

Social Cognition in Chiari Malformation Type I: a Preliminary Characterization

Chiari malformation type I (CM-I) is a neurological disorder in which cerebellar tonsils are herniated through the foramen magnum into the spinal canal. A     

Cefepime-Induced Encephalopathy: A Possible Additional Mechanism of Neurotoxicity

Neurocritical Care -     

Prevalence and risk factors of silent brain infarcts in patients with AF detected by 3T-MRI

Journal of Neurology - Silent brain infarcts (SBI), a finding on neuroimaging, are associated with higher risk of future stroke. Atrial Fibrillation (AF) has been previously identified as a cause...     

D2 autoreceptor switches CB2 receptor effects on [3H]-dopamine release in the striatum

CB₂ receptors (CB₂R) are expressed in midbrain neurons. To evidence the control of dopamine release in dorsal striatum by CB₂R, we performed experiments of [³H]-dopamine release in dorsal striatal slices. We found a paradoxical increase in K⁺-induced [³H]-dopamine release by CB₂R activation with GW 833972A and JWH 133 two selective agonist. To understand the mechanism involved, we tested for a role of the D₂ autoreceptor in this effect; because in pallidal structures, the inhibitory effect of CB₁ receptors (CB₁R) on GABA release is switched to a stimulatory effect by D₂ receptors (D₂R). We found that the blockade of D₂ autoreceptors with sulpiride prevented the stimulatory effect of CB₂R activation; in fact, under this condition, CB₂R decreased dopamine release, indicating the role of the D₂ autoreceptor in the paradoxical increase. We also found that the effect occurs in nigrostriatal terminals, since lesions with 6-OH dopamine in the middle forebrain bundle prevented CB₂R effects on release. In addition, D₂–CB₂R interaction promoted cAMP accumulation, and the increase in [³H]-dopamine release was prevented by PKA blockade. D₂–CB₂R coprecipitation and proximity ligation assay studies indicated a close interaction of receptors that could participate in the observed effects. Finally, intrastriatal injection of CB₂R agonist induced contralateral turning in amphetamine-treated rats, which was prevented by sulpiride, indicating the role of the interaction in motor behavior. Thus, these data indicate that the D₂ autoreceptor switches, from inhibitory to stimulatory, the CB₂R effects on dopamine release, involving the cAMP → PKA pathway in nigrostriatal terminals.