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This paper presents a strategy based on binary labelling of nodes for the creation of anti-loop formulations from existing strategies. This strategy prevents by default the formation of odd cycles, therefore it can have important role in iterative procedures based on generating subtour elimination constraints. It can also be used to modify the classic strategies used in problems associated to graphs. In this paper we focus on this last application. The behavior of this strategy is analyzed with two problems associated with graphs, the Asymmetric Traveling Salesman Problem (ATSP) and the Steiner Problem, where two configurations that modify the Miller-Tucking-Zem- lig proposal to avoid cycles are compared. The experimental analysis shows that this strategy keep a good convergence, highlighting its use for the Steiner problem.

This paper presents two novel formulations for scheduling problems, namely order- position hybrid formulation (OPH) and order-disjunctive hybrid formulation (ODH), which extend and combine parts of existing formulation strategies. The first strategy (OPH) is based on sequence position and linear ordering formulations, adding relationships between constraints that allow relaxing some decision variables. The second approach (ODH) is based on linear ordering and disjunctive formulations. In this work, we prove ODH to be the most efficient formulation known so far. The experiments have been carried out with a large set of problems, which consider single machines and identical parallel machines. Computational results show that OPH is better than the rest of the existing formulations for the case of weighted completion objectives, while ODH turns out to be the best approach for most scenarios studied.

Manganese (Mn) induces cognitive disorders and basal forebrain (BF) cholinergic neuronal loss, involved on learning and memory regulation, which could be the cause of such cognitive disorders. However, the mechanisms through which it induces these effects are unknown. We hypothesized that Mn could induce BF cholinergic neuronal loss through oxidative stress generation, cholinergic transmission and AChE variants alteration that could explain Mn cognitive disorders. This study shows that Mn impaired cholinergic transmission in SN56 cholinergic neurons from BF through alteration of AChE and ChAT activity and CHT expression. Moreover, Mn induces, after acute and long-term exposure, AChE variants alteration and oxidative stress generation that leaded to lipid peroxidation and protein oxidation. Finally, Mn induces cell death on SN56 cholinergic neurons and this effect is independent of cholinergic transmission alteration, but was mediated partially by oxidative stress generation and AChE variants alteration. Our results provide new understanding of the mechanisms contributing to the harmful effects of Mn on cholinergic neurons and their possible involvement in cognitive disorders induced by Mn., Banco Santander, Universidad Complutense de Madrid, Depto. de Farmacología y Toxicología, Fac. de Veterinaria, TRUE, pub

Paraquat (PQ) is a widely used non-selective contact herbicide shown to produce memory and learning deficits after acute and repeated exposure similar to those induced in Alzheimer's disease (AD). However, the complete mechanisms through which it induces these effects are unknown. On the other hand, cholinergic and glutamatergic systems, mainly in the hippocampus, are involved on learning, memory and cell viability regulation. An alteration of hippocampal cholinergic or glutamatergic transmissions or neuronal cell loss may induce these effects. In this regard, it has been suggested that PQ may induce cell death and affect cholinergic and glutamatergic transmission, which alteration could produce neuronal loss. According to these data, we hypothesized that PQ could induce hippocampal neuronal loss through cholinergic and glutamatergic transmissions alteration. To prove this hypothesis, we evaluated in hippocampal primary cell culture, the PQ toxic effects after 24h and 14 consecutive days exposure on neuronal viability and the cholinergic and glutamatergic mechanisms related to it. This study shows that PQ impaired acetylcholine levels and induced AChE inhibition and increased CHT expression only after 14days exposure, which suggests that acetylcholine levels alteration could be mediated by these actions. PQ also disrupted glutamate levels through induction of glutaminase activity. In addition, PQ induced, after 24h and 14days exposure, cell death on hippocampal neurons that was partially mediated by AChE variants alteration and cholinergic and gultamatergic transmissions disruption. Our present results provide new view of the mechanisms contributing to PQ neurotoxicity and may explain cognitive dysfunctions observed after PQ exposure., Banco Santander, Universidad Complutense de Madrid, Depto. de Farmacología y Toxicología, Fac. de Veterinaria, TRUE, pub