Assessment of metal exposure (uranium and copper) in fatty acids and carbohydrates profiles of Calamoceras marsupus larvae (Trichoptera) and Alnus glutinosa

Physiological changes were explored in fatty acids (FA) and carbohydrate (CHO) composition in the shredder Calamoceras marsupus larvae (Trichoptera) and leaf litter (C. marsupus food) exposed to copper and uranium under natural and experimental conditions. We measured FA and CHO content in leaf litter and larvae specimens from reference and impacted streams, and exposed for 5 weeks to four realistic environmental concentrations of copper (35 μg L−1 and 70 μg L−1) and uranium (25 μg L−1 and 50 μg L−1). Regarding FA, (1) leaf litter had a reduced polyunsaturated FA (PUFA) content in metal treatments, s (14 to 33% of total FA), compared to natural conditions (≥39% of total FA). Leaf litter exposed to uranium also differed in saturated FA (SFA) composition, with lower values in natural conditions and higher values under low uranium concentrations. (2) C. marsupus had/showed low PUFA content under Cu and U exposure, particularly in high uranium concentrations. Detritivores also decreased in PUFA under exposure to both metals, particularly in high uranium concentrations. On the other hand, (1) microorganisms of the biofilm colonizing leaf litter differed in CHO composition between natural (impacted and reference) and experimental conditions, with glucose and galactose being consistently the most abundant sugars, found in different amounts under copper or uranium exposure; (2) CHO of detritivores showed similar high galactose and fucose concentrations in contaminated streams and high copper treatments, whereas low copper treatment showed distinct CHO profiles, with higher mannose, glucose, arabinose, and fucose concentrations. Our study provides evidence of metal exposure effects on FA and CHO contents at different trophic levels, which might alter the quality of food flow in trophic websFil: Tagliaferro, Marina Beatriz. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Austral de Investigaciones Científicas; ArgentinaFil: Rocha, Carolina. Universidad de Coimbra. Facultad de Ciencias E Tecnología. Departamento de Ciencias Da Vida; PortugalFil: Marques, Joao Carlos. Universidad de Coimbra. Facultad de Ciencias E Tecnología. Departamento de Ciencias Da Vida; Portugal. Marine And Environmental Sciences Centre; PortugalFil: Goncalves, Ana Marta. Universidad de Coimbra. Facultad de Ciencias E Tecnología. Departamento de Ciencias Da Vida; Portugal. Marine And Environmental Sciences Centre; PortugalVIII Congreso Argentino de la Sociedad de Toxicología y Química AmbientalMar del PlataArgentinaSociedad de Toxicología y Química Ambienta

Effects of dexamethasone on the Li-pilocarpine model of epilepsy : protection against hippocampal inflammation and astrogliosis

Background: Temporal lobe epilepsy (TLE) is the most common form of partial epilepsy and is accompanied, in one third of cases, by resistance to antiepileptic drugs (AED). Most AED target neuronal activity modulated by ionic channels, and the steroid sensitivity of these channels has supported the use of corticosteroids as adjunctives to AED. Assuming the importance of astrocytes in neuronal activity, we investigated inflammatory and astroglial markers in the hippocampus, a key structure affected in TLE and in the Li-pilocarpine model of epilepsy. Methods: Initially, hippocampal slices were obtained from sham rats and rats subjected to the Li-pilocarpine model of epilepsy, at 1, 14, and 56 days after status epilepticus (SE), which correspond to the acute, silent, and chronic phases. Dexamethasone was added to the incubation medium to evaluate the secretion of S100B, an astrocyte-derived protein widely used as a marker of brain injury. In the second set of experiments, we evaluated the in vivo effect of dexamethasone, administrated at 2 days after SE, on hippocampal inflammatory (COX-1/2, PGE2, and cytokines) and astroglial parameters: GFAP, S100B, glutamine synthetase (GS) and water (AQP-4), and K+ (Kir 4.1) channels. Results: Basal S100B secretion and S100B secretion in high-K+ medium did not differ at 1, 14, and 56 days for the hippocampal slices from epileptic rats, in contrast to sham animal slices, where high-K+ medium decreased S100B secretion. Dexamethasone addition to the incubation medium per se induced a decrease in S100B secretion in sham and epileptic rats (1 and 56 days after SE induction). Following in vivo dexamethasone administration, inflammatory improvements were observed, astrogliosis was prevented (based on GFAP and S100B content), and astroglial dysfunction was partially abrogated (based on Kir 4.1 protein and GSH content). The GS decrease was not prevented by dexamethasone, and AQP-4 was not altered in this epileptic model. Conclusions: Changes in astroglial parameters emphasize the importance of these cells for understanding alterations and mechanisms of epileptic disorders in this model. In vivo dexamethasone administration prevented most of the parameters analyzed, reinforcing the importance of anti-inflammatory steroid therapy in the Li-pilocarpine model and possibly in other epileptic conditions in which neuroinflammation is present

Stress e coping académico: Contributos para a adaptação da escala MMC

Este estudo enquadra-se na investigação do coping perante dificuldades associadas ao quotidiano escolar. Utilizando entrevistas a 30 alunos, o estudo (1) identificou as principais situações geradoras de stress, reconhecendo a importância relativa do stress académico na vida dos alunos, e (2) analisou a validade cultural para o contexto português das situações stressantes usadas na escala Multidimensional Measure of Coping (MMC), avaliando as perceções dos alunos quanto ao nível de stress induzido e controlo percebido relativamente a essas situações. Os resultados confirmaram a importância da escola enquanto fonte significativa de stress, e a adequação da MMC ao contexto português

Academic stress and coping: Contributions to the adaptation of the MMC

Este estudo enquadra-se na investiga??o das estrat?gias de coping utilizadas perante dificuldades associadas ao quotidiano escolar. Utilizando entrevistas a 30 alunos, o estudo (1) identificou as principais situa??es geradoras de stress, reconhecendo a import?ncia relativa do stress acad?mico na vida dos alunos, e (2) analisou a validade cultural para o contexto portugu?s das situa??es stressantes usadas na escala Multidimensional Measure of Coping (MMC), avaliando as perce??es dos alunos quanto ao n?vel de stress induzido e controlo percebido relativamente a essas situa??es. Os resultados confirmaram a import?ncia da escola enquanto fonte significativa de stress, e a adequa??o da MMC ao contexto portugu?s.8C1E-AFB9-6BE1 | Maria Teresa Martins Gon?alvesN/

Macular phototoxicity after corneal cross-linking

Purpose: To assess potential vascular, structural, and functional changes to the macula in patients with keratoconus that underwent ultraviolet A (UVA)-riboflavin-mediated corneal collagen cross-linking (CXL) therapy. Patients and methods: Seventeen eyes from 17 patients of age 16 years or older with keratoconus undergoing CXL treatment were studied. The same eye served as its own control (before CXL vs after CXL). Eyes were evaluated in terms of best-corrected visual acuity (BCVA), refractive error, intraocular pressure, Amsler grid, retinography, fluorescein angiography, autofluorescence, and spectral domain optical coherence tomography (SD-OCT) prior to CXL and 7 and 30 days after treatment. Multifocal electroretinography (mfERG) was recorded prior to and 7 days after CXL. Results: Mean (SD) BCVA by logMAR chart was 0.47 (+/-0.12) pre-CXL, 0.55 (+/-0.15) 7 days post-CXL (P=0.57), and 0.46 (+/-0.10) 30 days post-CXL (P=0.87). Mean (SD) SD-OCT central macular thickness (microm) was 253.62 (+/-20.9) pre-CXL, 260.5 (+/-18.7) 7 days post-CXL (P=0.48), and 256.44 (+/-21.6) 30 days post-CXL (P=0.69). In 12 eyes, mfERG revealed a statistically significant increase (P=0.0353) in P1 latency (ms) of ring four from the pre-CXL period (39.45+/-2.05) to 7 days post-CXL (41.04+/-1.28) period. Regression analysis showed that the increase in P1 latency was correlated with the increase in central macular thickness (P=0.027). Furthermore, nine patients experienced a significant decrease in P1 amplitudes of rings 1 (P=0.0014), 2 (P=0.0029), 3 (P=0.0037), 4 (P=0.0014), and 5 (P=0.0012) from pre-CXL to 7 days post-CXL. Conclusion: In this pilot study, most of the patients exhibited slight changes in their mfERG parameters and OCT thickness, despite a lack of vascular abnormalities observed on fluorescein angiography/autofluorescence imaging, no alteration in BCVA, and no reports of symptoms. These changes could, therefore, be categorized as a mild subclinical effect of the corneal cross-linking procedure

Early effects of LPS-induced neuroinflammation on the rat hippocampal glycolytic pathway

Neuroinflammation is a common feature during the development of neurological disorders and neurodegenerative diseases, where glial cells, such as microglia and astrocytes, play key roles in the activation and maintenance of inflammatory responses in the central nervous system. Neuroinflammation is now known to involve a neurometabolic shift, in addition to an increase in energy consumption. We used two approaches (in vivo and ex vivo) to evaluate the effects of lipopolysaccharide (LPS)-induced neuroinflammation on neurometabolic reprogramming, and on the modulation of the glycolytic pathway during the neuroinflammatory response. For this, we investigated inflammatory cytokines and receptors in the rat hippocampus, as well as markers of glial reactivity. Mitochondrial respirometry and the glycolytic pathway were evaluated by multiple parameters, including enzymatic activity, gene expression and regulation by protein kinases. Metabolic (e.g., metformin, 3PO, oxamic acid, fluorocitrate) and inflammatory (e.g., minocycline, MCC950, arundic acid) inhibitors were used in ex vivo hippocampal slices. The induction of early inflammatory changes by LPS (both in vivo and ex vivo) enhanced glycolytic parameters, such as glucose uptake, PFK1 activity and lactate release. This increased glucose consumption was independent of the energy expenditure for glutamate uptake, which was in fact diverted for the maintenance of the immune response. Accordingly, inhibitors of the glycolytic pathway and Krebs cycle reverted neuroinflammation (reducing IL-1β and S100B) and the changes in glycolytic parameters induced by LPS in acute hippocampal slices. Moreover, the inhibition of S100B, a protein predominantly synthesized and secreted by astrocytes, inhibition of microglia activation and abrogation of NLRP3 inflammasome assembly confirmed the role of neuroinflammation in the upregulation of glycolysis in the hippocampus. Our data indicate a neurometabolic glycolytic shift, induced by inflammatory activation, as well as a central and integrative role of astrocytes, and suggest that interference in the control of neurometabolism may be a promising strategy for downregulating neuroinflammation and consequently for diminishing negative neurological outcomes