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Your search keyword '"Garcia-Moreno H"' showing total 3 results
Start Over Author "Garcia-Moreno H" Publisher elsevier
3 results on '"Garcia-Moreno H"'

1. Melatonin protects mast cells against cytotoxicity mediated by chemical stimuli PMACI: Possible clinical use

Author

Universidad de Sevilla. Departamento de Bioquímica Médica y Biología Molecular e Inmunología, Maldonado y Aibar, María Dolores, Garcia-Moreno, H., Calvo Gutiérrez, Juan Ramón, Universidad de Sevilla. Departamento de Bioquímica Médica y Biología Molecular e Inmunología, Maldonado y Aibar, María Dolores, Garcia-Moreno, H., and Calvo Gutiérrez, Juan Ramón

Abstract

Melatonin has documented cytoprotective effects on a wide variety of immune cells. The mechanism of action on mast cells (RBL-2H3) still remains in the dark. We found that melatonin significantly attenuated phorbol 12-myristate 13-acetate plus calcium ionophore A23187 (PMACI)-induced cytotoxicity in a concentration and time-dependent manner. It appears that the effect of melatonin on mast cells is two-fold: dependent (MT1 and MT2) and independent membrane receptors. In conclusion, melatonin treatment reduced the cytotoxicity, mediated by PMACI, and could provide a useful therapeutic option in processes where an excessive activation of mast cells occurs.

Published
2013

2. Melatonin administrated immediately before an intense exercise reverses oxidative stress, improves immunological defenses and lipid metabolism in football players

Author

Universidad de Sevilla. Departamento de Bioquímica Médica y Biología Molecular e Inmunología, Maldonado y Aibar, María Dolores, Manfredi, M., Ribas Serna, Juan, Garcia-Moreno, H., Calvo Gutiérrez, Juan Ramón, Universidad de Sevilla. Departamento de Bioquímica Médica y Biología Molecular e Inmunología, Maldonado y Aibar, María Dolores, Manfredi, M., Ribas Serna, Juan, Garcia-Moreno, H., and Calvo Gutiérrez, Juan Ramón

Abstract

Acute sport exercise leads to a strong stimulation of muscle tissue and a change in the organism energy demands. This study was designed to investigate the effect of oral melatonin supplementation on human physiological functions associated with acute exercise. Immune, endocrine and metabolic parameters were measured in 16 young male football players, who were divided into two groups, an experimental group (supplementation with 6 mg of melatonin administered 30 min prior to exercise) and a control group (placebo without melatonin). They performed a continuous exercise of high intensity (135 beats/min). Samples were collected 30 min before the exercise and 3, 15 and 60 min during the exercise. The results indicated that the acute sport training presented: a) increased lipid peroxidation products (MDA) in both groups, control and experimental, with levels significantly decreased in the group treated with melatonin after 15 and 60 min of high-intensity exercise, b) the total antioxidant activity (TAS) was lower in the control group than in the experimental, the latter showing significant differences at 60 min of high-intensity exercise c) the lipid profile of subjects in the experimental group showed lower triglyceride levels than the control group after 15 and 60 min of high-intensity exercise, d) immunological studies only showed, in the experimental group, an increase in IgA levels at 60 min after the exercise, and finally there were no significant differences between the groups for any of the other variables. In conclusion these results indicated that treatment with melatonin in acute sports exercise reversed oxidative stress, improved defenses and lipid metabolism, which would result in an improvement in fitness

Published
2012

3. Expanding SPTAN1 monoallelic variant associated disorders: From epileptic encephalopathy to pure spastic paraplegia and ataxia.

Author

Morsy H, Benkirane M, Cali E, Rocca C, Zhelcheska K, Cipriani V, Galanaki E, Maroofian R, Efthymiou S, Murphy D, O'Driscoll M, Suri M, Banka S, Clayton-Smith J, Wright T, Redman M, Bassetti JA, Nizon M, Cogne B, Jamra RA, Bartolomaeus T, Heruth M, Krey I, Gburek-Augustat J, Wieczorek D, Gattermann F, Mcentagart M, Goldenberg A, Guyant-Marechal L, Garcia-Moreno H, Giunti P, Chabrol B, Bacrot S, Buissonnière R, Magry V, Gowda VK, Srinivasan VM, Melegh B, Szabó A, Sümegi K, Cossée M, Ziff M, Butterfield R, Hunt D, Bird-Lieberman G, Hanna M, Koenig M, Stankewich M, Vandrovcova J, and Houlden H

Subjects
Humans, Spectrin genetics, Mutation, Phenotype, Ataxia, Seizures, Paraplegia, Pedigree, Epilepsy genetics, Spastic Paraplegia, Hereditary genetics
Abstract

Purpose: Nonerythrocytic αII-spectrin (SPTAN1) variants have been previously associated with intellectual disability and epilepsy. We conducted this study to delineate the phenotypic spectrum of SPTAN1 variants., Methods: We carried out SPTAN1 gene enrichment analysis in the rare disease component of the 100,000 Genomes Project and screened 100,000 Genomes Project, DECIPHER database, and GeneMatcher to identify individuals with SPTAN1 variants. Functional studies were performed on fibroblasts from 2 patients., Results: Statistically significant enrichment of rare (minor allele frequency < 1 × 10 -5 ) probably damaging SPTAN1 variants was identified in families with hereditary ataxia (HA) or hereditary spastic paraplegia (HSP) (12/1142 cases vs 52/23,847 controls, p = 2.8 × 10 -5 ). We identified 31 individuals carrying SPTAN1 heterozygous variants or deletions. A total of 10 patients presented with pure or complex HSP/HA. The remaining 21 patients had developmental delay and seizures. Irregular αII-spectrin aggregation was noted in fibroblasts derived from 2 patients with p.(Arg19Trp) and p.(Glu2207del) variants., Conclusion: We found that SPTAN1 is a genetic cause of neurodevelopmental disorder, which we classified into 3 distinct subgroups. The first comprises developmental epileptic encephalopathy. The second group exhibits milder phenotypes of developmental delay with or without seizures. The final group accounts for patients with pure or complex HSP/HA., Competing Interests: Conflict of Interest The authors declare no conflicts of interest., (Copyright © 2022 The Authors. Published by Elsevier Inc. All rights reserved.)

Published
2023
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