124 results on '"Gomez-Cabrera M"'
Search Results
2. 1469 - EVALUACIÓN DEL DAÑO OXIDATIVO COMO PREDICTOR DE GRAVEDAD EN LA NEUMONÍA POR SARS-COV-2
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García-Domínguez, Cristina, Carretero, Aitor, García-Domínguez, Esther, Fernández-Presa, Lucía, Signes-Costa, Jaime, Gómez-Cabrera, M. Carmen, and Viña, José
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- 2024
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3. Glucose 6-P Dehydrogenase-An Antioxidant Enzyme with Regulatory Functions in Skeletal Muscle during Exercise
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Garcia-Dominguez E, Carretero A, Vina-Almunia A, Domenech-Fernandez J, Olaso-Gonzalez G, Vina J, and Gomez-Cabrera M
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physical training ,aging ,pentose phosphate pathway ,NADPH ,skeletal muscle ,G6PD - Abstract
Hypomorphic Glucose 6-P dehydrogenase (G6PD) alleles, which cause G6PD deficiency, affect around one in twenty people worldwide. The high incidence of G6PD deficiency may reflect an evolutionary adaptation to the widespread prevalence of malaria, as G6PD-deficient red blood cells (RBCs) are hostile to the malaria parasites that infect humans. Although medical interest in this enzyme deficiency has been mainly focused on RBCs, more recent evidence suggests that there are broader implications for G6PD deficiency in health, including in skeletal muscle diseases. G6PD catalyzes the rate-limiting step in the pentose phosphate pathway (PPP), which provides the precursors of nucleotide synthesis for DNA replication as well as reduced nicotinamide adenine dinucleotide phosphate (NADPH). NADPH is involved in the detoxification of cellular reactive oxygen species (ROS) and de novo lipid synthesis. An association between increased PPP activity and the stimulation of cell growth has been reported in different tissues including the skeletal muscle, liver, and kidney. PPP activity is increased in skeletal muscle during embryogenesis, denervation, ischemia, mechanical overload, the injection of myonecrotic agents, and physical exercise. In fact, the highest relative increase in the activity of skeletal muscle enzymes after one bout of exhaustive exercise is that of G6PD, suggesting that the activation of the PPP occurs in skeletal muscle to provide substrates for muscle repair. The age-associated loss in muscle mass and strength leads to a decrease in G6PD activity and protein content in skeletal muscle. G6PD overexpression in Drosophila Melanogaster and mice protects against metabolic stress, oxidative damage, and age-associated functional decline, and results in an extended median lifespan. This review discusses whether the well-known positive effects of exercise training in skeletal muscle are mediated through an increase in G6PD.
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- 2022
4. Glucosamine Supplementation Improves Physical Performance in Trained Mice
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De la Rosa A, Olaso-Gonzalez G, Garcia-Dominguez E, Mastaloudis A, Hester S, Wood S, Gomez-Cabrera M, and Vina J
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INTRODUCTION: D-Glucosamine (GlcN) is one of the most widely consumed dietary supplements and complementary medicines in the world and has been traditionally used to attenuate osteoarthritis in humans. GlcN extends lifespan in different animal models. In humans, its supplementation has been strongly associated with decreased total mortality and improved vascular endothelial function. GlcN acts as a suppressor of inflammation and by inhibiting glycolysis, it can activate the metabolism of stored fat and mitochondrial respiration. METHODS: The conventional human GlcN dose is 1,500 mg x day-1 but extensive evidence indicates that much higher doses are well tolerated. GlcN is one of the supplements that has experienced a greater use in the last years in elite athletes mainly due to its potential chondroprotective effects that may promote cartilage health. However, the possibility of it being an ergogenic aid has not been explored. We aimed to study the potential beneficial effects of GlcN on mitochondrial content, on physical performance and oxidative stress in mice that were aerobically trained and supplemented with three different doses of glucosamine (250, 500, and 1,000 mg x Kg-1) for six weeks. We measured exercise performance (grip strength, motor coordination and running capacity) before and after the training period. Proteins involved in mitochondrial biogenesis (AMPK, PGC-1, NRF-1, SIRT-1, cytochrome c, citrate synthase), markers of oxidative stress (GSSG/GSH) or damage (MDA, carbonylated proteins), antioxidant enzymes (NRF-2, SOD1, SOD2, Catalase and PRDX6) and MAPKs (p38 and ERK ) were also determined in skeletal muscle. RESULTS AND CONCLUSIONS: Our results show that GlcN supplementation in aerobically trained mice, at doses equivalent to those conventionally used in humans, increases the protein levels of mitochondrial biogenesis markers, improves motor coordination and may have a synergistic effect with exercise training on running distance.
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- 2022
5. Transcriptomic profile of epileptic children treated with ketogenic therapies
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Ruiz-Herrero J, Olaso-Gonzalez G, Serna E, Canedo-Villarroya E, Correas A, Gambini J, Gomez-Cabrera M, Pedron-Giner C, and Vina J
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Background: Ketogenic dietary therapies (KDT) are used as a treatment in childhood epilepsy. However, their mechanism has not yet been established. The main objective of this study was to determine the changes in the transcriptomic profile induced by KDT in children with epilepsy in order to shed light on its possible mechanisms. Methods: Eight children with refractory epilepsy were enrolled in the study. Peripheral blood mononuclear cells were obtained before and after the children were treated with KDT for a minimum of 6 months. RNA was extracted and mRNA and miRNA profiling were performed and analyzed. Results: Our intervention with KDT significantly reduced the seizure number in seven of the eight paediatric patients treated and caused important changes in their gene expression profile. Our study reveals modifications in the transcription of 4630 genes and 230 miRNAs. We found that the genes involved in the protection against epileptic crises were among those mainly changed. These genes collectively encode for ion channels, neurotransmitter receptors, and synapse structural proteins. Conclusions: Together our results explain the possible mechanisms of KDT and reinforce its clinical importance in the treatment of epilepsy. © 2022 The Author(s). Published by IMR Press.
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- 2022
6. Exercise training as a modulator of epigenetic events in prostate tumors
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Dufresne S, Gueritat J, Wong C, Isanejad A, Ho E, Serna E, Gomez-Cabrera M, and Rebillard A
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Background Exercise is increasingly recognized as an effective strategy to improve cancer prevention and prognosis. Several biological mechanisms mediating these benefits have been proposed, but the role of epigenetics remains largely unknown. Since epigenetics is highly susceptible to lifestyle factors, we hypothesized that exercise could affect the epigenome landscape in cancer tissues. Methods Rats implanted with AT1 prostate tumors were randomized to either control or exercise training. microRNA expression, DNA methylation and histone acetylation were analyzed in the tumor tissue. Results MiR-27a-5p appeared to be differently expressed between sedentary and trained rats. Furthermore, exercise increased global DNA methylation and decreased DNA methyltransferases mRNA expression in the tumor tissue. Histone acetylation however remained unaltered. Conclusion Overall, exercise might reverse some of the cancer-related epigenetic alterations in the prostate tumor tissue.
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- 2022
7. Allopurinol prevents cardiac and skeletal muscle damage in professional soccer players
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Sanchis-Gomar, F., Pareja-Galeano, H., Gomez-Cabrera, M. C., Candel, J., Lippi, G., Salvagno, G. L., Mann, G. E., and Viña, J.
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- 2015
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8. Growth Hormone Replacement Therapy Prevents Sarcopenia by a Dual Mechanism: Improvement of Protein Balance and of Antioxidant Defenses
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Brioche, T., Kireev, R. A., Cuesta, S., Gratas-Delamarche, A., Tresguerres, J. A., Gomez-Cabrera, M. C., and Viña, J.
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- 2014
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9. Effect of colony size and surrounding substrate on corals experiencing a mild bleaching event on Heron Island reef flat (southern Great Barrier Reef, Australia)
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Ortiz, J. C., Gomez-Cabrera, M. del C., and Hoegh-Guldberg, O.
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- 2009
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10. Glucose 6-P dehydrogenase delays the onset of frailty by protecting against muscle damage
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Arc-Chagnaud C, Salvador-Pascual A, Garcia-Dominguez E, Olaso-Gonzalez G, Correas A, Serna E, Brioche T, Chopard A, Fernandez-Marcos P, Serrano M, Serrano A, Munoz-Canoves P, Sebastia V, Vina J, and Carmen Gomez-Cabrera M
- Abstract
Background Frailty is a major age-associated syndrome leading to disability. Oxidative damage plays a significant role in the promotion of frailty. The cellular antioxidant system relies on reduced nicotinamide adenine dinucleotide phosphate (NADPH) that is highly dependent on glucose 6-P dehydrogenase (G6PD). The G6PD-overexpressing mouse (G6PD-Tg) is protected against metabolic stresses. Our aim was to examine whether this protection delays frailty. Methods Old wild-type (WT) and G6PD-Tg mice were evaluated longitudinally in terms of frailty. Indirect calorimetry, transcriptomic profile, and different skeletal muscle quality markers and muscle regenerative capacity were also investigated. Results The percentage of frail mice was significantly lower in the G6PD-Tg than in the WT genotype, especially in 26-month-old mice where 50% of the WT were frail vs. only 13% of the Tg ones (P < 0.001). Skeletal muscle transcriptomic analysis showed an up-regulation of respiratory chain and oxidative phosphorylation (P = 0.009) as well as glutathione metabolism (P = 0.035) pathways in the G6PD-Tg mice. Accordingly, the Tg animals exhibited an increase in reduced glutathione (34.5%, P < 0.01) and a decrease on its oxidized form (-69%, P < 0.05) and in lipid peroxidation (4-HNE: -20.5%, P < 0.05). The G6PD-Tg mice also showed reduced apoptosis (BAX/Bcl2: -25.5%, P < 0.05; and Bcl-xL: -20.5%, P < 0.05), lower levels of the intramuscular adipocyte marker FABP4 (-54.7%, P < 0.05), and increased markers of mitochondrial content (COX IV: 89.7%, P < 0.05; Grp75: 37.8%, P < 0.05) and mitochondrial OXPHOS complexes (CII: 81.25%, P < 0.01; CIII: 52.5%, P < 0.01; and CV: 37.2%, P < 0.05). Energy expenditure (-4.29%, P < 0.001) and the respiratory exchange ratio were lower (-13.4%, P < 0.0001) while the locomotor activity was higher (43.4%, P < 0.0001) in the 20-month-old Tg, indicating a major energetic advantage in these mice. Short-term exercise training in young C57BL76J mice induced a robust activation of G6PD in skeletal muscle (203.4%, P < 0.05), similar to that achieved in the G6PD-Tg mice (142.3%, P < 0.01). Conclusions Glucose 6-P dehydrogenase deficiency can be an underestimated risk factor for several human pathologies and even frailty. By overexpressing G6PD, we provide the first molecular model of robustness. Because G6PD is regulated by pharmacological and physiological interventions like exercise, our results provide molecular bases for interventions that by increasing G6PD will delay the onset of frailty.
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- 2021
11. Overexpression of glucose 6 phosphate dehydrogenase preserves mouse pancreatic beta cells function until late in life
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De la Rosa A, Gomez-Cabrera M, Vinue A, Gonzalez-Navarro H, Sanchez-Andres J, and Vina J
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hemic and lymphatic diseases ,parasitic diseases ,nutritional and metabolic diseases - Abstract
NAD(P)H donates electrons for reductive biosynthesis and antioxidant defense across all forms of life. Glucose-6-phosphate dehydrogenase (G6PD) is a critical enzyme to provide NADPH. G6PD deficiency is present in more than 400 million people worldwide. This enzymopathy provides protection against malaria but sensitizes cells to oxidative stressors. Oxidative stress has been involved in the pathogenesis of the diabetic complications and several studies have provided evidences of a link between G6PD deficiency and type 2 diabetes (T2D). We hypothesized that a moderate overexpression of G6PD (G6PD-Tg) could protect beta-cells from age-associated oxidative stress thus reducing the risk of developing T2D. Here we report, that G6PD-Tg mice show an improved glucose tolerance and insulin sensitivity when compared to old age-matched Wild Type (WT) ones. This is accompanied by a decrease in oxidative damage and stress markers in the pancreas of the old Tg animals (20-24month-old). Pancreatic beta-cells progress physiologically towards a state of reduced responsiveness to glucose. In pancreatic islets isolated from G6PD-Tg and WT animals at different ages, and using electrophysiological techniques, we demonstrate a wider range of response to glucose in the G6PD-Tg cells that may explain the improvements in glucose tolerance and insulin sensitivity. Together, our results show that overexpression of G6PD maintains pancreatic beta-cells from old mice in a "juvenile-like" state and points to the G6PD dependent generation of NADPH as an important factor to improve the natural history of diabetes.
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- 2021
12. Muscle repair after physiological damage relies on nuclear migration for cellular reconstruction
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Roman W, Pinheiro H, Pimentel M, Segales J, Oliveira L, Garcia-Dominguez E, Gomez-Cabrera M, Serrano A, Gomes E, and Munoz-Canoves P
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ComputingMethodologies_DOCUMENTANDTEXTPROCESSING ,ComputingMilieux_MISCELLANEOUS - Abstract
[Figure: see text].
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- 2021
13. Redox-related biomarkers in physical exercise
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Gomez-Cabrera M, Carretero A, Millan-Domingo F, Garcia-Dominguez E, Correas A, Olaso-Gonzalez G, and Vina J
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Free radical ,Oxidative stress ,Exercise ,Biomarkers ,Antioxidants - Abstract
Research in redox biology of exercise has made considerable advances in the last 70 years. Since the seminal study of George Pake?s group calculating the content of free radicals in skeletal muscle in resting conditions in 1954, many discoveries have been made in the field. The first section of this review is devoted to highlight the main research findings and fundamental changes in the exercise redox biology discipline. It includes: i) the first steps in free radical research, ii) the relation between exercise and oxidative damage, iii) the redox regulation of muscle fatigue, iv) the sources of free radicals during muscle contractions, and v) the role of reactive oxygen species as regulators of gene transcription and adaptations in skeletal muscle. In the second section of the manuscript, we review the available biomarkers for assessing health, performance, recovery during exercise training and overtraining in the sport population. Among the set of biomarkers that could be determined in exercise studies we deepen on the four categories of redox biomarkers: i) oxidants, ii) antioxidants, iii) oxidation products (markers of oxidative damage), and iv) measurements of the redox balance (markers of oxidative stress). The main drawbacks, strengths, weaknesses, and methodological considerations of every biomarker are also discussed.
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- 2021
14. Implementing Precision Medicine in Human Frailty through Epigenetic Biomarkers
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Garcia-Gimenez J, Mena-Molla S, Tarazona-Santabalbina F, Vina J, Gomez-Cabrera M, and Pallardo F
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The main epigenetic features in aging are: reduced bulk levels of core histones, altered pattern of histone post-translational modifications, changes in the pattern of DNA methylation, replacement of canonical histones with histone variants, and altered expression of non-coding RNA. The identification of epigenetic mechanisms may contribute to the early detection of age-associated subclinical changes or deficits at the molecular and/or cellular level, to predict the development of frailty, or even more interestingly, to improve health trajectories in older adults. Frailty reflects a state of increased vulnerability to stressors as a result of decreased physiologic reserves, and even dysregulation of multiple physiologic systems leading to adverse health outcomes for individuals of the same chronological age. A key approach to overcome the challenges of frailty is the development of biomarkers to improve early diagnostic accuracy and to predict trajectories in older individuals. The identification of epigenetic biomarkers of frailty could provide important support for the clinical diagnosis of frailty, or more specifically, to the evaluation of its associated risks. Interventional studies aimed at delaying the onset of frailty and the functional alterations associated with it, would also undoubtedly benefit from the identification of frailty biomarkers. Specific to the article yet reasonably common within the subject discipline.
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- 2021
15. Frailty Is Associated with Oxidative Stress in Older Patients with Type 2 Diabetes
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Alabadi B, Civera M, De la Rosa A, Martinez-Hervas S, Gomez-Cabrera M, and Real J
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body composition ,diabetes ,aging ,oxidative stress ,frailty - Abstract
Aging has increased the prevalence of frailty, and type 2 diabetes (T2D) has also increased in prevalence. Diabetes and oxidative stress (OS) have been shown to be related to frailty. However, the exact mechanism by which it occurs is not fully known. Our aim was to analyze body composition in community-dwelling older diabetic people treated in our center and to evaluate the possible relation between OS, frailty, and body composition. We included 100 adults older than 65 years with T2D. We found that 15% were frail and 57% were prefrail. The patients included in the nonrobust group showed increased levels of OS. Our study shows that the presence of T2D in the geriatric population is associated with a high prevalence of frailty and high OS levels, conditions that cause greater morbidity and mortality and that highlight the importance of the diagnosis of frailty in this population.
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- 2021
16. Activation of the Constitutive Androstane Receptor Inhibits Leukocyte Adhesiveness to Dysfunctional Endothelium
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Lopez-Riera M, Ortega R, Hueso L, Montesinos M, Gomez-Cabrera M, Sanz M, Real J, and Piqueras L
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constitutive androstane receptor ,leukocyte recruitment ,endothelial dysfunction - Abstract
Leukocyte cell recruitment into the vascular subendothelium constitutes an early event in the atherogenic process. As the effect of the constitutive androstane receptor (CAR) on leukocyte recruitment and endothelial dysfunction is poorly understood, this study investigated whether the role of CAR activation can affect this response and the underlying mechanisms involved. Under physiological flow conditions, TNF alpha-induced endothelial adhesion of human leukocyte cells was concentration-dependently inhibited by preincubation of human umbilical arterial endothelial cells with the selective human CAR ligand CITCO. CAR agonism also prevented TNF alpha induced VCAM-1 expression, as well as MCP-1/CCL-2 and RANTES/CCL-5 release in endothelial cells. Suppression of CAR expression with a small interfering RNA abrogated the inhibitory effects of CITCO on these responses. Furthermore, CITCO increased interaction of CAR with Retinoid X Receptor (RXR) and reduced TNF alpha-induced p38-MAPK/NF-kappa B activation. In vivo, using intravital microscopy in the mouse cremasteric microcirculation treatment with the selective mouse CAR ligand TCPOBOP inhibited TNF alpha-induced leukocyte rolling flux, adhesion, and emigration and decreased VCAM-1 in endothelium. These results reveal that CAR agonists can inhibit the initial inflammatory response that precedes the atherogenic process by targeting different steps in the leukocyte recruitment cascade. Therefore, CAR agonists may constitute a new therapeutic tool in controlling cardiovascular disease-associated inflammatory processes.
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- 2021
17. 1552 - PAPEL DEL DAÑO OXIDATIVO EN PACIENTES CON NEUMONÍA POR SARS-COV-2
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García-Domínguez, Cristina, Carretero, Aitor, García-Domínguez, Esther, Fernández-Presa, Lucía, Signes-Costa, Jaime, Gómez-Cabrera, M. Carmen, and Viña, José
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- 2023
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18. The hybrid algorithm (Hbmr) to fight against blood doping in sports
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Sanchis-Gomar, F., Martinez-Bello, V. E., Gomez-Cabrera, M. C., and Viña, J.
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- 2010
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19. Continuous Compared to Accumulated Walking-Training on Physical Function and Health-Related Quality of Life in Sedentary Older Persons
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Monteagudo P, Roldan A, Cordellat A, Gomez-Cabrera M, and Blasco-Lafarga C
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The present study aimed to analyze the impact of overground walking interval training (WIT) in a group of sedentary older adults, comparing two different dose-distributions. In this quasi-experimental and longitudinal study, we recruited twenty-three sedentary older adults (71.00 ± 4.10 years) who were assigned to two groups of WIT. The continuous group (CWIT) trained for 60 min/session in the morning, while the accumulated group (AWIT) performed the same duration and intensity of exercise, but it was distributed twice a day (30 min in the morning and 30 more in the afternoon). After 15 weeks of an equal external-load training (3 days/week), Bonferroni post-hoc comparisons revealed significant (p < 0.050) and similar large improvements in both groups in cardiorespiratory fitness and lower limb strength; even larger gains in preferred walking speed and instrumental daily life activity, which was slightly superior for CWIT; and improvements in agility, which were moderate for CWIT and large for AWIT. However, none of the training protocols had an impact on the executive function in the individuals, and only the AWIT group improved health-related quality of life. Although both training protocols induced a general significant improvement in physical function in older adults, our results showed that the accumulative strategy should be recommended when health-related quality of life is the main target, and the continuous strategy should be recommended when weakness may be a threat in the short or medium term.
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- 2020
20. Physical exercise in the prevention and treatment of Alzheimer's disease
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De la Rosa A, Olaso-Gonzalez G, Arc-Chagnaud C, Millan F, Salvador-Pascual A, Garcia-Lucerga C, Blasco-Lafarga C, Garcia-Dominguez E, Carretero A, Correas A, Vina J, and Gomez-Cabrera M
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Dementia is one of the greatest global challenges for health and social care in the 21st century. Alzheimer's disease (AD), the most common type of dementia, is by no means an inevitable consequence of growing old. Several lifestyle factors may increase, or reduce, an individual's risk of developing AD. Much has been written overthe ages about the benefits of exercise and physical activity. Among the risk factors associated with AD is a low level of physical activity. The relationship between physical and mental health was established several years ago. In this review, we discuss the role of exercise (aerobic and resistance) training as a therapeutic strategy for the treatment and prevention of AD. Older adults who exercise are more likely to maintain cognition. We address the main protective mechanism on brain function modulated by physical exercise by examining both human and animal studies. We will pay especial attention to the potential role of exercise in the modulation of amyloid beta turnover, inflammation, synthesis and release of neurotrophins, and improvements in cerebral blood flow. Promoting changes in lifestyle in presymptomatic and predementia disease stages may have the potential for delaying one-third of dementias worldwide. Multimodal interventions that include the adoption of an active lifestyle should be recommended for older populations. Copyright © 2020. Production and hosting by Elsevier B.V.
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- 2020
21. Modulating Oxidant Levels to Promote Healthy Aging
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Vina J, Olaso-Gonzalez G, Arc-Chagnaud C, De la Rosa A, and Gomez-Cabrera M
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mitochondria ,exercise ,glucose-6-phosphate dehydrogenase ,skeletal muscle ,health span - Abstract
Recent Advances: This review discusses the importance of the modulation of the oxidant levels through physiological strategies such as physical exercise or genetic manipulations such as the overexpression of antioxidant enzymes, in the promotion of healthy aging. Critical Issues: We have divided the review into five different sections. In the first two sections of the article "Oxidants are signals" and "Exercise training is an antioxidant," we discuss the main sources of free radicals during muscle contraction and their role, as hormetic substances, in the regulation of two main muscle adaptations to exercise in skeletal muscle; that is, mitochondrial biogenesis and the endogenous antioxidant defense. In the third section of the review, we deal with "the energy collapse in aging." The increased rate of reactive oxygen species (ROS) production and the low rate of mitochondria biosynthesis in the old cells are examined. Finally, in the fourth and fifth sections entitled "Overexpression of antioxidants enzymes in healthy aging" and "Exercise, longevity, and frailty," we consider the importance of the potentiation of the cellular defenses in health span and in life span. Future Directions: A correct manipulation of the ROS generation, directing these species to their physiological signaling role and preventing their deleterious effects, would allow the promotion of healthy aging.
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- 2020
22. A polymorphism in the agouti signalling protein (ASIP) is associated with decreased levels of mRNA
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Voisey, J., Gomez-Cabrera, M. del C., Smit, D. J., Leonard, J. H., Sturm, R. A., and van Daal, A.
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- 2006
23. ACTIVATION OF NFKB IN RAT SKELETAL MUSCLE: EFFECTS OF EXERCISE, HYDROPEROXIDE AND LIPOPOLYSACCHARIDE
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Gomez-Cabrera, M C., Steinhafel, N, Vina, J, and Ji, L L.
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- 2003
24. EXERCISE ACTIVATION OF NUCLEAR FACTOR (NF) KB SIGNALING CASCADES IN RAT SKELETAL MUSCLE
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Ji, L L., Steinhafel, N, Hollander, J, Gomez-Cabrera, M-C, Vina, J, Lee, J M., and Johnson, J A.
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- 2003
25. Beneficial Effects of Inspiratory Muscle Training Combined With Multicomponent Training in Elderly Active Women
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Roldan A, Cordellat A, Monteagudo P, Garcia-Lucerga C, Blasco-Lafarga N, Gomez-Cabrera M, and Blasco-Lafarga C
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respiratory muscle training ,primary prevention ,short-term interventions ,Cardiovascular fitness - Abstract
Purpose: This study aims to analyze changes in Maximum Inspiratory Pressure (MIP), lung function, cardiorespiratory fitness, and blood pressure, in 10 healthy active elderly women, following 7 weeks of inspiratory muscle training (IMT) combined with a multicomponent training program (MCTP). The association among these health parameters, their changes after training (deltas), and the influence of MIP at baseline (MIPpre) are also considered. Methods: IMT involved 30 inspirations at 50% of the MIP, twice daily, 7 days a week, while MCTP was 1 hr, twice a week. MIP, lung function (FVC, FEV1, FEV1/FVC, FEF25-75%, PEF), 6MWT, and blood pressure (SBP, DBP), jointly with body composition, were assessed before and after the intervention. Results: Seven weeks were enough to improved MIP (p = .019; d = 1.397), 6MWT (p = .012; d = .832), SBP (p = .003; d = 1.035) and DBP (p = .024; d = .848). Despite the high physical fitness (VO2 peak: M = 23.38, SD = 3.39 ml center dot min center dot Kg(-1)), MIPpre was low (M = 39.00, SD = 7.63 cmH(2)O) and displayed a significant negative correlation with Delta MIPpre-post (r = -.821; p < .004), showing that women who started the intervention with lower MIP achieved higher improvements in inspiratory muscle strength after training. Conclusions: No significant changes in spirometric parameters may signal that lung function is independent of early improvements in inspiratory muscles and cardiorespiratory fitness. Absence of correlation between physical fitness and respiratory outcomes suggests that being fit does not ensure cardiorespiratory health in active elderly women, so IMT might be beneficial and should supplement the MCTP in this population.
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- 2019
26. Data on in vivo PGC-1 alpha overexpression model via local transfection in aged mouse muscle
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Yeo D, Kang C, Gomez-Cabrera M, Vina J, and Ji L
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- 2019
27. Exercise and probiotics attenuate the development of Alzheimer's disease in transgenic mice: Role of microbiome
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Abraham D, Feher J, Scuderi G, Szabo D, Dobolyi A, Cservenak M, Juhasz J, Ligeti B, Pongor S, Gomez-Cabrera M, Vina J, Higuchi M, Suzuki K, Boldogh I, and Radak Z
- Published
- 2019
28. Intensified mitophagy in skeletal muscle with aging is downregulated by PGC-1alpha overexpression in vivo
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Yeo D, Kang C, Gomez-Cabrera M, Vina J, and Ji L
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- 2019
29. Long-term exercise training improves memory in middle-aged men and modulates peripheral levels of BDNF and Cathepsin B
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De la Rosa A, Solana E, Corpas R, Bartres-Faz D, Pallas M, Vina J, Sanfeliu C, and Gomez-Cabrera M
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- 2019
30. Global, regional, and national age-sex-specific mortality and life expectancy, 1950-2017: A systematic analysis for the Global Burden of Disease Study 2017
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Dicker, D, Nguyen, G, Abate, D, Abate, K, Abay, S, Abbafati, C, Abbasi, N, Abbastabar, H, Abd-Allah, F, Abdela, J, Abdelalim, A, Abdel-Rahman, O, Abdi, A, Abdollahpour, I, Abdulkader, R, Abdurahman, A, Abebe, H, Abebe, M, Abebe, Z, Abebo, T, Aboyans, V, Abraha, H, Abrham, A, Abu-Raddad, L, Abu-Rmeileh, N, Accrombessi, M, Acharya, P, Adebayo, O, Adedeji, I, Adedoyin, R, Adekanmbi, V, Adetokunboh, O, Adhena, B, Adhikari, T, Adib, M, Adou, A, Adsuar, J, Afarideh, M, Afshin, A, Agarwal, G, Aggarwal, R, Aghayan, S, Agrawal, S, Agrawal, A, Ahmadi, M, Ahmadi, A, Ahmadieh, H, Ahmed, M, Ahmed, S, Aichour, A, Aichour, I, Aichour, M, Akanda, A, Akbari, M, Akibu, M, Akinyemi, R, Akinyemiju, T, Akseer, N, Alahdab, F, Al-Aly, Z, Alam, K, Alebel, A, Aleman, A, Alene, K, Al-Eyadhy, A, Ali, R, Alijanzadeh, M, Alizadeh-Navaei, R, Aljunid, S, Alkerwi, A, Alla, F, Allebeck, P, Allen, C, Alonso, J, Al-Raddadi, R, Alsharif, U, Altirkawi, K, Alvis-Guzman, N, Amare, A, Amini, E, Ammar, W, Amoako, Y, Anber, N, 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- Abstract
Background: Assessments of age-specifc mortality and life expectancy have been done by the UN Population Division, Department of Economics and Social Afairs (UNPOP), the United States Census Bureau, WHO, and as part of previous iterations of the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD). Previous iterations of the GBD used population estimates from UNPOP, which were not derived in a way that was internally consistent with the estimates of the numbers of deaths in the GBD. The present iteration of the GBD, GBD 2017, improves on previous assessments and provides timely estimates of the mortality experience of populations globally. Methods: The GBD uses all available data to produce estimates of mortality rates between 1950 and 2017 for 23 age groups, both sexes, and 918 locations, including 195 countries and territories and subnational locations for 16 countries. Data used include vital registration systems, sample registration systems, household surveys (complete birth histories, summary birth histories, sibling histories), censuses (summary birth histories, household deaths), and Demographic Surveillance Sites. In total, this analysis used 8259 data sources. Estimates of the probability of death between birth and the age of 5 years and between ages 15 and 60 years are generated and then input into a model life table system to produce complete life tables for all locations and years. Fatal discontinuities and mortality due to HIV/AIDS are analysed separately and then incorporated into the estimation. We analyse the relationship between age-specifc mortality and development status using the Socio-demographic Index, a composite measure based on fertility under the age of 25 years, education, and income. There are four main methodological improvements in GBD 2017 compared with GBD 2016: 622 additional data sources have been incorporated; new estimates of population, generated by the GBD study, are used; statistical methods used in diferent compon
- Published
- 2018
31. Endocrinology of Aging From a Muscle Function Point of View: Results From the Toledo Study for Healthy Aging
- Author
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Guadalupe-Grau A, Carnicero J, Losa-Reyna J, Tresguerres J, Gomez-Cabrera M, Castillo C, Alfaro-Acha A, Rosado-Artalejo C, Rodriguez-Manas L, and Garcia-Garcia F
- Published
- 2017
32. Exercise: the lifelong supplement for healthy ageing and slowing down the onset of frailty
- Author
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Vina J, Rodriguez-Manas L, Salvador-Pascual A, Tarazona-Santabalbina F, and Gomez-Cabrera M
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- 2016
33. Exercise training as a drug to treat age associated frailty
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Vina J, Salvador-Pascual A, Tarazona-Santabalbina F, Rodriguez-Manas L, and Gomez-Cabrera M
- Published
- 2016
34. G6PD protects from oxidative damage and improves healthspan in mice
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Nobrega-Pereira S, Fernandez-Marcos P, Brioche T, Gomez-Cabrera M, Salvador-Pascual A, Flores J, Vina J, and Serrano M
- Published
- 2016
35. Role of NAD(+)/NADH redox ratio in cell metabolism A tribute to Helmut Sies and Theodor Bucher and Hans A. Krebs
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Vina J, Saez G, Gambini J, Gomez-Cabrera M, and Borras C
- Published
- 2016
36. A Multicomponent Exercise Intervention that Reverses Frailty and Improves Cognition, Emotion, and Social Networking in the Community-Dwelling Frail Elderly: A Randomized Clinical Trial
- Author
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Tarazona-Santabalbina F, Gomez-Cabrera M, Perez-Ros P, Martinez-Arnau F, Cabo H, Tsaparas K, Salvador-Pascual A, Rodriguez-Manas L, and Vina J
- Published
- 2016
37. Biology of frailty: Modulation of ageing genes and its importance to prevent age-associated loss of function
- Author
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Vina J, Tarazona-Santabalbina F, Perez-Ros P, Martinez-Arnau F, Borras C, Olaso-Gonzalez G, Salvador-Pascual A, and Gomez-Cabrera M
- Published
- 2016
38. Role of Redox Signaling and Inflammation in Skeletal Muscle Adaptations to Training
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Gomez-Cabrera M, Vina J, and Ji L
- Published
- 2016
39. Global, regional, and national comparative risk assessment of 79 behavioural, environmental and occupational, and metabolic risks or clusters of risks, 1990-2015: a systematic analysis for the Global Burden of Disease Study 2015
- Author
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Popova, S., Poulton, R., Pourmalek, F., Prasad, N., Qorbani, M., Rabiee, R., Radfar, A., Rafay, A., Rahimi-Movaghar, V., Rahman, M., Rahman, S., Rai, R., Rajsic, S., Raju, M., Ram, U., Rana, S., Ranganathan, K., Rao, P., Razo Garcia, C., Refaat, A., Rehm, C., Rehm, J., Reinig, N., Remuzzi, G., Resnikoff, S., Ribeiro, A., Rivera, J., Rolm, H., Rodriguez, A., Rodriguez-Ramirez, S., Rojas-Rueda, D., Roman, Y., Ronfani, L., Roshandel, G., Rothenbacher, D., Roy, A., Saleh, M., Sanabria, J., Dolores Sanchez-Nino, M., Sanchez-Pimienta, T., Sandar, L., Santomauro, D., Santos, I., Sarmiento-Suarez, R., Sartorius, B., Satpathy, M., Savic, M., Sawhney, M., Schmidhuber, J., Schmidt, M., Schneider, I., Schoettker, B., Schutte, A., Schwebel, D., Scott, J., Seedat, S., Sepanlou, S., Servan-Mori, E., Shaheen, A., Shahraz, S., Shaikh, M., Levy, T., Sharma, R., She, J., Sheikhbahaei, S., Shen, J., Sheth, K., Shi, P., Shibuya, K., Shigematsu, M., Shin, M., Shiri, R., Shishani, K., Shiue, I., Shrime, M., Sigfusdottir, I., Silva, D., Alves Silveira, D., Silverberg, J., Simard, E., Sindi, S., Singh, A., Singh, J., Singh, P., Slepak, E., Soljak, M., Soneji, S., Sorensen, R., Sposato, L., Sreeramareddy, C., Stathopoulou, V., Steckling, N., Steel, N., Stein, D., Stein, M., Stockl, H., Stranges, S., Stroumpoulis, K., Sunguya, B., Swaminathan, S., Sykes, B., Szoeke, C., Tabares-Seisdedos, R., Takahashi, K., Talongwa, R., Landon, N., Tanne, D., Tavakkoli, M., Taye, B., Taylor, H., Tedla, B., Tefera, W., Tegegne, T., Tekle, D., Terkawi, A., Thakur, J., Thomas, B., Thomas, M., Thomson, A., Thorne-Lyman, A., Thrift, A., Thurston, G., Tillmann, T., Tobe-Gai, R., Tobollik, M., Topor-Madry, R., Topouzis, F., Towbin, J., Bach, X., Dimbuene, Z., Tsilimparis, N., Tura, A., Tuzcu, E., Tyrovolas, S., Ukwaja, K., Undurraga, E., Uneke, C., Uthman, O., van Donkelaar, A., van Os, J., Varakin, Y., Vasankari, T., Veerman, J., Venketasubramanian, N., Violante, F., Vollset, S., Wagner, G., Waller, S., Wang, J., Wang, L., Wang, Y., Weichenthal, S., Weiderpass, E., Weintraub, R., Werdecker, A., Westerman, R., Whiteford, H., Wijeratne, T., Wiysonge, C., Wolfe, C., Won, S., Woolf, A., Wubshet, M., Xavier, D., Xu, G., Yadav, A., Yakob, B., Yalew, A., Yano, Y., Yaseri, M., Ye, P., Yip, P., Yonemoto, N., Yoon, S., Younis, M., Yu, C., Zaidi, Z., Zaki, M., Zhu, J., Zipkin, B., Zodpey, S., Zuhlke, L., Murray, C., Forouzanfar, M., Afshin, A., Alexander, L., Anderson, H., Bhutta, Z., Biryukov, S., Brauer, M., Burnett, R., Cercy, K., Charlson, F., Cohen, A., Dandona, L., Estep, K., Ferrari, A., Frostad, J., Fullman, N., Gething, P., Godwin, W., Griswold, M., Kinfu, Y., Kyu, H., Larson, H., Liang, X., Lim, S., Liu, P., Lopez, A., Lozano, R., Marczak, L., Mensah, G., Mokdad, A., Moradi-Lakeh, M., Naghavi, M., Neal, B., Reitsma, M., Roth, G., Salomon, J., Sur, P., Vos, T., Wagner, J., Wang, H., Zhao, Y., Zhou, M., Aasvang, G., Abajobir, A., Abate, K., Abbafati, C., Abbas, K., Abd-Allah, F., Abdulle, A., Abera, S., Abraham, B., Abu-Raddad, L., Abyu, G., Adebiyi, A., Adedeji, I., Ademi, Z., Adou, A., Adsuar, J., Agardh, E., Agarwal, A., Agrawal, A., Kiadaliri, A., Ajala, O., Akinyemiju, T., Al-Aly, Z., Alam, K., Alam, N., Aldhahri, S., Aldridge, R., Alemu, Z., Ali, R., Alkerwi, A., Alla, F., Allebeck, P., Alsharif, U., Altirkawi, K., Alvarez Martin, E., Alvis-Guzman, N., Amare, A., Amberbir, A., Amegah, A., Amini, H., Ammar, W., Amrock, S., Andersen, H., Anderson, B., Antonio, C., Anwar, P., Arnlov, J., Al, A., Asayesh, H., Asghar, R., Assadi, R., Atique, S., Avokpaho, E., Awasthi, A., Quintanilla, B., Azzopardi, P., Bacha, U., Badawi, A., Bahit, M., Balakrishnan, K., Barac, A., Barber, R., Barker-Collo, S., Baernighausen, T., Barquera, S., Barregard, L., Barrero, L., Basu, S., Bans, C., Bazargan-Hejazi, S., Beardsley, J., Bedi, N., Beghi, E., Bell, M., Bello, A., Bennett, D., Bensenor, I., Berhane, A., Bernabe, E., Betsu, B., Beyene, A., Bhala, N., Bhansali, A., Bhatt, S., Biadgilign, S., Bikbov, B., Bisanzio, D., Bjertness, E., Blore, J., Borschmann, R., Boufous, S., Bourne, R., Brainin, M., Brazinova, A., Breitborde, N., Brenner, H., Broday, D., Brugha, T., Brunekreef, B., Butt, Z., Cahill, L., Calabria, B., Ricardo Campos-Nonato, I., Cardenas, R., Carpenter, D., Casey, D., Castaneda-Oquela, C., Castillo Rivas, J., Estanislao Castro, R., Catala-Lopez, F., Chang, J., Chiang, P., Chibalabala, M., Chimed-Ochir, O., Chisumpa, V., Chitheer, A., Choi, J., Christensen, H., Christopher, D., Ciobanu, L., Coates, M., Colquhoun, S., Cooper, L., Cooperrider, K., Cornaby, L., Cortinovis, M., Crump, J., Cuevas-Nasu, L., Damasceno, A., Dandona, R., Darby, S., Dargan, P., das Neves, J., Davis, A., Davletov, K., Filipa de Castro, E., De la Cruz-Gongora, V., De Leo, D., Degenhardt, L., Del Gobbo, L., del Pozo-Cruz, B., Dellavalle, R., Deribew, A., Des Jarlais, D., Dharmaratne, S., Dhillon, P., Diaz-Tome, C., Dicker, D., Ding, E., Dorsey, E., Doyle, K., Driscoll, T., Duan, L., Dubey, M., Duncan, B., Elyazar, I., Endries, A., Ermakov, S., Erskine, H., Eshrati, B., Esteghamati, A., Fahimi, S., Aquino Faraon, E., Farid, T., Sofia E Sa Farinha, C., Faro, A., Farvid, M., Farzadfar, F., Feigin, V., Fereshtehnejad, S., Fernandes, J., Fischer, F., Fitchett, J., Fleming, T., Foigt, N., Foreman, K., Fowkes, F., Franklin, R., Fuerst, T., Futran, N., Gakidou, E., Garcia-Basteiro, A., Gebrehiwot, T., Gebremedhin, A., Geleijnse, J., Gessner, B., Giref, A., Giroud, M., Gishu, M., Goenka, S., Carmen Gomez-Cabrera, M., Gomez-Dantes, H., Gona, P., Goodridge, A., Gopalani, S., Gotay, C., Goto, A., Gouda, H., Gugnani, H., Guillemin, F., Guo, Y., Gupta, R., Gutierrez, R., Haagsma, J., Hafezi-Nejad, N., Haile, D., Hailu, G., Halasa, Y., Hamadeh, R., Hamidi, S., Handal, A., Hankey, G., Hao, Y., Harb, H., Harikrishnan, S., Maria Haro, J., Hassanvand, M., Hassen, T., Havmoeller, R., Beatriz Heredia-Pi, I., Francisco Hernandez-Llanes, N., Heydarpour, P., Hoek, H., Hoffman, H., Horino, M., Horita, N., Hosgood, H., Hoy, D., Hsairi, M., Htet, A., Hu, G., Huang, J., Husseini, A., Hutchings, S., Huybrechts, I., Iburg, K., Idrisov, B., Ileanu, B., Inoue, M., Jacobs, T., Jacobsen, K., Jahanmehr, N., Jakovljevic, M., Jansen, H., Jassal, S., Javanbakht, M., Jayatilleke, A., Jee, S., Jeemon, P., Jha, V., Jiang, Y., Jibat, T., Jin, Y., Johnson, C., Jonas, J., Kabir, Z., Kalkonde, Y., Kamal, R., Kan, H., Karch, A., Karema, C., Karimkhani, C., Kasaeian, A., Kaul, A., Kawakami, N., Kazi, D., Keiyoro, P., Kemp, A., Kengne, A., Keren, A., Kesavachandran, C., Khader, Y., Khan, A., Khan, E., Khan, G., Khang, Y., Khatibzadeh, S., Khera, S., Khoja, T., Khubchandani, J., Kieling, C., Kim, C., Kim, D., Kimokoti, R., Kissoon, N., Kivipelto, M., Knibbs, L., Kokubo, Y., Kopec, J., Koul, P., Koyanagi, A., Kravchenko, M., Kromhout, H., Krueger, H., Ku, T., Defo, B., Kuchenbecker, R., Bicer, B., Kuipers, E., Kumar, G., Kwan, G., Lal, D., Lalloo, R., Lallukka, T., Lan, Q., Larsson, A., Latif, A., Beatriz Lawrynowicz, A., Leasher, J., Leigh, J., Leung, J., Levi, M., Li, X., Li, Y., Liang, J., Liu, S., Lloyd, B., Logroscino, G., Lotufo, P., Lunevicius, R., Maclntyre, M., Mahdavi, M., Majdan, M., Majeed, A., Malekzadeh, R., Malta, D., Manamo, W., Mapoma, C., Marcenes, W., Martin, R., Martinez-Raga, J., Masiye, F., Matsushita, K., Matzopoulos, R., Mayosi, B., McGrath, J., McKee, M., Meaney, P., Medina, C., Mehari, A., Mena-Rodriguez, F., Mekonnen, A., Melaku, Y., Memish, Z., Mendoza, W., Mensink, G., Meretoja, A., Meretoja, T., Mesfin, Y., Mhimbira, F., Miller, Ted, Mills, E., Mirarefin, M., Misganaw, A., Mock, C., Mohammadi, A., Mohammed, S., Mola, G., Monasta, L., Montanez Hernandez, J., Montico, M., Morawska, L., Mori, R., Mozaffarian, D., Mueller, U., Mullany, E., Mumford, J., Murthy, G., Nachega, J., Naheed, A., Nangia, V., Nassiri, N., Newton, J., Ng, M., Quyen, L., Nisar, M., Pete, P., Norheim, O., Norman, R., Norrving, B., Nyakarahuka, L., Obermeyer, C., Ogbo, F., Oh, I., Oladimeji, O., Olivares, P., Olsen, H., Olusanya, B., Olusanya, J., Opio, J., Oren, E., Orozco, R., Ortiz, A., Ota, E., Mahesh, P., Pana, A., Park, E., Parry, C., Parsaeian, M., Patel, T., Caicedo, A., Patil, S., Patten, S., Patton, G., Pearce, N., Pereira, D., Perico, N., Pesudovs, K., Petzold, M., Phillips, M., Piel, F., Pillay, J., Plass, D., Polinder, S., Pond, C., Pope, C., Pope, D., Popova, S., Poulton, R., Pourmalek, F., Prasad, N., Qorbani, M., Rabiee, R., Radfar, A., Rafay, A., Rahimi-Movaghar, V., Rahman, M., Rahman, S., Rai, R., Rajsic, S., Raju, M., Ram, U., Rana, S., Ranganathan, K., Rao, P., Razo Garcia, C., Refaat, A., Rehm, C., Rehm, J., Reinig, N., Remuzzi, G., Resnikoff, S., Ribeiro, A., Rivera, J., Rolm, H., Rodriguez, A., Rodriguez-Ramirez, S., Rojas-Rueda, D., Roman, Y., Ronfani, L., Roshandel, G., Rothenbacher, D., Roy, A., Saleh, M., Sanabria, J., Dolores Sanchez-Nino, M., Sanchez-Pimienta, T., Sandar, L., Santomauro, D., Santos, I., Sarmiento-Suarez, R., Sartorius, B., Satpathy, M., Savic, M., Sawhney, M., Schmidhuber, J., Schmidt, M., Schneider, I., Schoettker, B., Schutte, A., Schwebel, D., Scott, J., Seedat, S., Sepanlou, S., Servan-Mori, E., Shaheen, A., Shahraz, S., Shaikh, M., Levy, T., Sharma, R., She, J., Sheikhbahaei, S., Shen, J., Sheth, K., Shi, P., Shibuya, K., Shigematsu, M., Shin, M., Shiri, R., Shishani, K., Shiue, I., Shrime, M., Sigfusdottir, I., Silva, D., Alves Silveira, D., Silverberg, J., Simard, E., Sindi, S., Singh, A., Singh, J., Singh, P., Slepak, E., Soljak, M., Soneji, S., Sorensen, R., Sposato, L., Sreeramareddy, C., Stathopoulou, V., Steckling, N., Steel, N., Stein, D., Stein, M., Stockl, H., Stranges, S., Stroumpoulis, K., Sunguya, B., Swaminathan, S., Sykes, B., Szoeke, C., Tabares-Seisdedos, R., Takahashi, K., Talongwa, R., Landon, N., Tanne, D., Tavakkoli, M., Taye, B., Taylor, H., Tedla, B., Tefera, W., Tegegne, T., Tekle, D., Terkawi, A., Thakur, J., Thomas, B., Thomas, M., Thomson, A., Thorne-Lyman, A., Thrift, A., Thurston, G., Tillmann, T., Tobe-Gai, R., Tobollik, M., Topor-Madry, R., Topouzis, F., Towbin, J., Bach, X., Dimbuene, Z., Tsilimparis, N., Tura, A., Tuzcu, E., Tyrovolas, S., Ukwaja, K., Undurraga, E., Uneke, C., Uthman, O., van Donkelaar, A., van Os, J., Varakin, Y., Vasankari, T., Veerman, J., Venketasubramanian, N., Violante, F., Vollset, S., Wagner, G., Waller, S., Wang, J., Wang, L., Wang, Y., Weichenthal, S., Weiderpass, E., Weintraub, R., Werdecker, A., Westerman, R., Whiteford, H., Wijeratne, T., Wiysonge, C., Wolfe, C., Won, S., Woolf, A., Wubshet, M., Xavier, D., Xu, G., Yadav, A., Yakob, B., Yalew, A., Yano, Y., Yaseri, M., Ye, P., Yip, P., Yonemoto, N., Yoon, S., Younis, M., Yu, C., Zaidi, Z., Zaki, M., Zhu, J., Zipkin, B., Zodpey, S., Zuhlke, L., and Murray, C.
- Published
- 2016
40. Allopurinol prevents cardiac and skeletal muscle damage in professional soccer players
- Author
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Sanchis Gomar, F., Pareja Galeano, H., Gomez Cabrera, M. C., Candel, J., Lippi, Giuseppe, Salvagno, GIAN LUCA, Mann, G. E., and Viña, J.
- Subjects
Adult ,Male ,injury ,Allopurinol ,free radicals ,Young Adult ,Troponin T ,Malondialdehyde ,Soccer ,Creatine Kinase, MB Form ,Humans ,Xanthine oxidase ,Aspartate Aminotransferases ,Muscle, Skeletal ,Creatine Kinase ,exercise ,L-Lactate Dehydrogenase ,Myoglobin ,Myocardium ,Heart ,Free Radical Scavengers ,gamma-Glutamyltransferase ,peroxidation ,Lipid Peroxidation ,xanthine oxidase ,human activities ,performance - Abstract
Xanthine oxidase (XO), a free radical-generating enzyme, is involved in tissue damage produced during exhaustive exercise. Our aim was to test whether allopurinol, a powerful inhibitor of XO, may be effective in preventing exercise-induced tissue damage in soccer players. Twelve soccer players were randomized into two experimental groups. One received allopurinol, before a match of the premier Spanish Football League, and the other placebo. Allopurinol prevented the exercise-induced increase in all the markers of skeletal muscle damage analyzed: creatine kinase, lactate dehydrogenase, aspartate aminotransferase, and myoglobin. Creatine kinase-MB isoenzyme and highly sensitive troponin T, specific biomarkers of myocardial injury, increased significantly in the placebo but not in the allopurinol-treated group after the football match. We also found that the exercise-induced lipid peroxidation, as reflected by malondialdehyde measurements, was prevented after allopurinol administration. However, inhibition of XO did not prevent the increment in the activity of alanine aminotransferase found after the match. No changes in the serum gamma glutamyltransferase activity was found after the match on either the placebo and the allopurinol groups. These two enzymes were determined as biomarkers of liver injury. Allopurinol represents an effective and inexpensive pharmacological agent to prevent tissue damage in soccer players.
- Published
- 2014
41. Epigenetic biomarkers: A new perspective in laboratory diagnostics
- Author
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Garcia-Gimenez J, Sanchis-Gomar F, Lippi G, Mena S, Ivars D, Gomez-Cabrera M, Vina J, and Pallardo F
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Histone ,DNA methylation ,miRNAs ,Rare disease ,Cancer - Abstract
Epigenetics comprises the study of chemical modifications in the DNA and histones that regulates the gene expression or cellular phenotype. However, during the last decade this term has evolved after the elucidation of different mechanisms (microRNAs and nuclear organization of the chromosomes) involved in regulating gene expression. Epigenetics and the new designed technologies capable to analyze epigenetic changes (e.g., methylated DNA, miRNAs expression, post-translational modifications on histones among others) have disclosed an appealing scenario that will offer for the biomedical sciences new biomarkers for the study of neurodegenerative diseases, multifactorial complex diseases, rare diseases and cancer. Moreover, new technologies adapted for epigenetic studies will offer promising applications that in the next years will be common technologies in clinical laboratories. In this review we discuss epigenetic modifications used as possible biomarkers in several diseases. We also present the potential of methodologies to purify histones, and high throughput technologies as candidates to be set in clinical laboratories for their high potential analyzing epigenetic processes. (c) 2012 Elsevier B.V. All rights reserved.
- Published
- 2012
42. Active paraplegics are protected against exercise-induced oxidative damage through the induction of antioxidant enzymes
- Author
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Inglés, M, primary, Serra-Añó, P, additional, Gambini, J, additional, Abu-Sharif, F, additional, Dromant, M, additional, Garcia-Valles, R, additional, Pareja-Galeano, H, additional, Garcia-Lucerga, C, additional, and Gomez-Cabrera, M C, additional
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- 2016
- Full Text
- View/download PDF
43. Bénéfices de l'allopurinol dans la prévention de l'atrophie musculaire induite par l'immobilisation
- Author
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Derbré, Frédéric, Ferrando, B, Martinez-Bello, V, Sanchis-Gomar, F, R, Garcia-Valles, E, Garcia-Lopez, S., Ibañez, Thomas, Brioche, Gomez-Cabrera, M C, Gratas-Delamarche, Arlette, Viña, J, Laboratoire Mouvement Sport Santé (M2S), École normale supérieure - Cachan (ENS Cachan)-Université de Rennes 1 (UR1), Université de Rennes (UNIV-RENNES)-Université de Rennes (UNIV-RENNES)-Université de Rennes 2 (UR2), Université de Rennes (UNIV-RENNES)-Université de Brest (UBO)-Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique ), Jonchère, Laurent, and École normale supérieure - Cachan (ENS Cachan)-Université de Rennes (UR)-Université de Brest (UBO)-Université de Rennes 2 (UR2)-Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique )
- Subjects
[SDV] Life Sciences [q-bio] ,[SDV]Life Sciences [q-bio] ,ComputingMilieux_MISCELLANEOUS - Abstract
National audience; no abstract
- Published
- 2010
44. Age and gender mediate the small association of MIP and functional capacity in healthy active elderly.
- Author
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Roldán, A., Cordellat, A., Monteagudo, P., Blasco-Lafarga, N., Gomez-Cabrera, M., and Blasco-Lafarga, C.
- Subjects
OLDER people ,GENDER ,PILATES method ,AGE ,PEARSON correlation (Statistics) - Published
- 2019
45. Properties of Resveratrol:In VitroandIn VivoStudies about Metabolism, Bioavailability, and Biological Effects in Animal Models and Humans
- Author
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Gambini, J., primary, Inglés, M., additional, Olaso, G., additional, Lopez-Grueso, R., additional, Bonet-Costa, V., additional, Gimeno-Mallench, L., additional, Mas-Bargues, C., additional, Abdelaziz, K. M., additional, Gomez-Cabrera, M. C., additional, Vina, J., additional, and Borras, C., additional
- Published
- 2015
- Full Text
- View/download PDF
46. White shark (Carcharodon carcharias) microsatellite genotypes (six loci) from regions along Australia's southern and eastern coastline.
- Author
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Blower, D.C., Pandolfi, J.M., Gomez-Cabrera, M. del C., Bruce, B.D., Ovenden, J.R., Blower, D.C., Pandolfi, J.M., Gomez-Cabrera, M. del C., Bruce, B.D., and Ovenden, J.R.
- Abstract
Despite international protection of white sharks (Carcharodon carcharias), important conservation parameters such as abundance, population structure and genetic diversity are largely unknown. The tissue of 97 predominately juvenile white sharks sampled from spatially distant eastern and southwestern Australian coastlines was sequenced for the mitochondrial DNA (mtDNA) control region and genotyped with six nuclear-encoded microsatellite loci. MtDNA population structure was found between the eastern and southwestern coasts (FST = 0.142, p < 0.001), implying female natal philopatry. This concords with recent satellite and acoustic tracking findings which suggest the sustained presence of discrete east coast nursery areas. Furthermore, population subdivision was found between the same regions with biparentally inherited microsatellite markers (FST = 0.009, p <0.05), suggesting that males may also exhibit some degree of reproductive philopatry. Five sharks captured along the east coast had mtDNA haplotypes that resembled western Indian Ocean sharks more closely than Australian/New Zealand sharks, suggesting that transoceanic dispersal or migration resulting in breeding may occur sporadically. Our most robust estimate of contemporary genetic effective population size was low and below the threshold at which adaptive potential may be lost. For a variety of reasons, these contemporary estimates were at least one, possibly two orders of magnitude below our historical effective size estimates. Further population decline could expose these genetically isolated populations to detrimental genetic effects. Regional Australian white shark conservation management units should be implemented until genetic population structure, size and diversity can be investigated in more detail. Reference: Blower, D. C., Pandolfi, J. M., Gomez-Cabrera, M. del C., Bruce, B. D. & Ovenden, J. R. (2012). Population genetics of Australian white sharks reveals fine-scale spatial structure, transoceanic
- Published
- 2012
47. Growth Hormone Replacement Therapy Prevents Sarcopenia by a Dual Mechanism: Improvement of Protein Balance and of Antioxidant Defenses
- Author
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Brioche, T., primary, Kireev, R. A., additional, Cuesta, S., additional, Gratas-Delamarche, A., additional, Tresguerres, J. A., additional, Gomez-Cabrera, M. C., additional, and Vina, J., additional
- Published
- 2013
- Full Text
- View/download PDF
48. FORUM ISSUE: “Free Radicals and Physical Exercise”
- Author
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Vina, J., primary and Gomez-Cabrera, M. C., additional
- Published
- 2013
- Full Text
- View/download PDF
49. Increased Average Longevity among the “Tour de France” Cyclists
- Author
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Sanchis-Gomar, F., primary, Olaso-Gonzalez, G., additional, Corella, D., additional, Gomez-Cabrera, M. C., additional, and Vina, J., additional
- Published
- 2011
- Full Text
- View/download PDF
50. Effect of xanthine oxidase-generated extracellular superoxide on skeletal muscle force generation
- Author
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Gomez-Cabrera, M. C., primary, Close, G. L., additional, Kayani, A., additional, McArdle, A., additional, Viña, J., additional, and Jackson, M. J., additional
- Published
- 2010
- Full Text
- View/download PDF
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