Temporal Variations in the Usefulness of Normalized Difference Vegetation Index as a Predictor for Ixodes ricinus (Acari: Ixodidae) in a Borrelia lusitaniae Focus in Tuscany, Central Italy

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Alcohol-induced blood-brain barrier impairment: An in vitro study

In recent years, alcohol abuse has dramatically grown with deleterious consequence for people’s health and, in turn, for health care costs. It has been demonstrated, in humans and animals, that alcohol intoxication induces neuroinflammation and neurodegeneration thus leading to brain impairments. Furthermore, it has been shown that alcohol consumption is able to impair the blood– brain barrier (BBB), but the molecular mechanisms underlining this detrimental effect have not been fully elucidated. For this reason, in this study we investigated the effects of alcohol exposure on a rat brain endothelial (RBE4) cell line, as an in vitro-validated model of brain microvascular endothelial cells. To assess whether alcohol caused a concentration-related response, the cells were treated at different times with increasing concentrations (10–1713 mM) of ethyl alcohol (EtOH). Microscopic and molecular techniques, such as cell viability assay, immunofluorescence and Western blotting, were used to examine the mechanisms involved in alcohol-induced brain endothelial cell alterations including tight junction distribution, apoptosis, and reactive oxygen species production. Our findings clearly demonstrate that alcohol causes the formation of gaps between cells by tight junction disassembly, triggered by the endoplasmic reticulum and oxidative stress, highlighted by GRP78 chaperone upregulation and increase in reactive oxygen species production, respectively. The results from this study shed light on the mechanisms underlying alcohol-induced blood–brain barrier dysfunction and a better understanding of these processes will allow us to take advantage of developing new therapeutic strategies in order to prevent the deleterious effects of alcohol

Biological Tools to Study the Effects of Environmental Contaminants at the Feto–Maternal Interface

The identification of reproductive toxicants is a major scientific challenge for human health. Pre-natal life is the most vulnerable and important time-span of human development. For obvious ethical reasons, in vivo models cannot be used in human pregnancy and animal models do not perfectly reflect human physiology. This review describes the in vitro test models representative of the human feto-maternal interface and the effects of environmental chemicals with estrogen-like activity, mainly bisphenol A (BPA) and para-nonylphenol (p-NP), with a particular emphasis to the effects at low, non-toxic doses, similar to concentrations commonly detected in the population

Flow synthesis and biological studies of an analgesic adamantane derivative that inhibits P2X7-evoked glutamate release

We report the biological evaluation of a class of adamantane derivatives, which were achieved via modified telescoped machine-assisted flow procedure. Among the series of compounds tested in this work, 5 demonstrated outstanding analgesic properties. This compound showed that its action was not mediated through direct interaction with opioid and/or cannabinoid receptors. Moreover, it did not display any significant anti-inflammatory properties. Experiments carried out on rat cerebrocortical purified synaptosomes indicated that 5 inhibits the P2X7-evoked glutamate release, which may contribute to its antinociceptive properties. Nevertheless, further experiments are ongoing to characterize the pharmacological properties and mechanism of action of this molecule