28 research outputs found

    Estudi comparatiu de la composició proximal i anàlisi sensorial del múscul dorsal i el múscul ventral del llobarro

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    El llobarro, és una de les espècies tradicionalment més apreciada en el Mediterrani, conjuntament amb l’orada. La seva alta valoració i la limitada oferta pesquera (actualment de 1.000 tones anuals), van fer que els preus del mercat fossin molt alts (19 €/kg) i com a conseqüència, va incrementar l’activitat aqüícola a partir de l’any 1985. Van haver de passar més de deu anys, perquè l’oferta aqüícola d’Espanya s’igualés amb la pesquera, l’any 1993. A partir d’aquest moment, la progressió va ser espectacular, passant de 370 tones a l’any 1993 a 4.513 l’any 2004. Aquest increment continuat de l’oferta ha modificat els preus, provocant una reducció d’aquests. La situació del sector durant el 2003-2004 va ser de recuperació, amb un relentiment de l’increment de la producció i un augment pausat dels preus, provocat per una supressió de les ajudes a la producció per part de la Unió Europea (Luna Sotorrío, L. et al, 2004)

    De l'aula al front: les memòries de guerra i exili del metge Àngel Latorre Ríos (1936-1939)

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    El metge Àngel Latorre Rios deixà escrites unes Memòries en les que recollí els principals esdeveniments de la seva vida privada i professional. D’aquest text s’hanseleccionat les pàgines dedicades a evocar els seus records dels anys de la guerra civil i l’exili (1936-1939), tot destacant y i analitzant els fets més importants  relacionats amb la seva trajectòria personal i la seva actuació com a metge en mig d’aquell conflicte.El medico Ángel Latorre Rios dejó escritas unas Memorias en las que recogiólos principales acontecimientos de su vida privada y profesional. De este  texto se han seleccionado las pàginas dedicadas a evocar sus recuerdos  correspondientes a los años de la guerra civil y el exilio (1936-1939),  destacando y analizando los hechos más importantes relacionados con el ejercicio de sus deberes profesionales en medio de aquel conflicto

    DNA Methylation at Birth and Fine Motor Ability in Childhood:An Epigenome-wide Association Study with Replication

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    Lower fine motor performance in childhood has been associated with poorer cognitive development and neurodevelopmental conditions such as autism spectrum disorder, yet, biological underpinnings remain unclear. DNA methylation (DNAm), an essential process for healthy neurodevelopment, is a key molecular system of interest. In this study, we conducted the first epigenome-wide association study of neonatal DNAm with childhood fine motor ability and further examined the replicability of epigenetic markers in an independent cohort. The discovery study was embedded in Generation R, a large population-based prospective cohort, including a subsample of 924 ~ 1026 European-ancestry singletons with available data on DNAm in cord blood and fine motor ability at a mean (SD) age of 9.8 (0.4) years. Fine motor ability was measured using a finger-tapping test (3 subtests including left-, right-hand and bimanual), one of the most frequently used neuropsychological instruments of fine motor function. The replication study comprised 326 children with a mean (SD) age of 6.8 (0.4) years from an independent cohort, the INfancia Medio Ambiente (INMA) study. Four CpG sites at birth were prospectively associated with childhood fine motor ability after genome-wide correction. Of these, one CpG (cg07783800 in GNG4) was replicated in INMA, showing that lower levels of methylation at this site were associated with lower fine motor performance in both cohorts. GNG4 is highly expressed in the brain and has been implicated in cognitive decline. Our findings support a prospective, reproducible association between DNAm at birth and fine motor ability in childhood, pointing to GNG4 methylation at birth as a potential biomarker of fine motor ability.The EWAS data was funded by a grant from the Netherlands Genomics Initiative (NGI)/Netherlands Organisation for Scientific Research (NWO) Netherlands Consortium for Healthy Aging (NCHA; project nr. 050-060-810), funds from the Genetic Laboratory of the Department of Internal Medicine, Erasmus MC, and a grant from the National Institute of Child and Human Development (R01HD068437). HT was supported by a grant of the Dutch Ministry of Education, Culture, and Science and the Netherlands Organization for Scientific Research (NWO grant No. 024.001.003, Consortium on Individual Development). FS was supported by a Royal Netherlands Academy of Science and Art (KNAW) Van Leersum fellowship. ML is supported by the scholarship from the China Scholarship Council (201706990036). CC is supported by the European Research Council (ERC) under the European Union’s Horizon 2020 Research and Innovation Programme under grant agreements No 101039672 (TEMPO) and No 848158 (EarlyCause). This project received funding from the European Union’s Horizon 2020 research and innovation programme (733206, LifeCycle).The epigenetic studies in INMA were mainly funded by grants from Instituto de Salud Carlos III (Red INMA G03/176, CB06/02/0041, CP18/00018), Spanish Ministry of Health (FIS-PI04/1436, FIS-PI08/1151 including FEDER funds, FIS-PI11/00610, FIS-FEDER-PI06/0867, FIS-FEDER-PI03-1615) Generalitat de Catalunya-CIRIT 1999SGR 00241, Fundació La marató de TV3 (090430), EU Commission (261357-MeDALL: Mechanisms of the Development of ALLergy), and European Research Council (268479-BREATHE: BRain dEvelopment and Air polluTion ultrafine particles in scHool childrEn)

    Traffic-related air pollution, APOE ∊4 status, and neurodevelopmental outcomes among school children enrolled in the BREATHE project (Catalonia, spain)

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    BACKGROUND: Traffic-related air pollution is emerging as a risk factor for Alzheimer's disease (AD) and impaired brain development. Individual differences in vulnerability to air pollution may involve the e4 allele of Apolipoprotein E (APOE) gene, the primary genetic risk factor for AD. OBJECTIVE: We analyzed whether the association between traffic air pollution and neurodevelopmental outcomes is modified by APOE e4 status in children. METHODS: Data on parent-reported behavior problems (total difficulties scores, Strengths and Difficulties Questionnaire), teacher-reported attention-deficit hyperactivity disorder (ADHD) symptom scores, cognitive performance trajectories (computerized tests of inattentiveness and working memory repeated 2–4 times during January 2012–March 2013), and APOE genotypes were obtained for 1,667 children age 7–11 y attending 39 schools in or near Barcelona. Basal ganglia volume (putamen, caudate, and globus pallidum) was measured in 163 of the children by MRI (October 2012–April 2014.) Average annual outdoor polycyclic aromatic hydrocarbons (PAHs), elemental carbon (EC), and nitrogen dioxide (NO ) concentrations were estimated based on measurements at each school (two 1-wk campaigns conducted 6 months apart in 2012). RESULTS: APOE e4 allele carriers had significantly higher behavior problem scores than noncarriers, and adverse associations with PAHs and NO were stronger or limited to e4 carriers for behavior problem scores (P-interaction 0.03 and 0.04), caudate volume (P-interaction 0.04 and 0.03), and inattentiveness trajectories (P-interaction 0.15 and 0.08, respectively). Patterns of associations with the same outcomes were similar for EC. CONCLUSION: PAHs, EC, and NO were associated with higher behavior problem scores, smaller reductions in inattentiveness over time, and smaller caudate volume in APOE e4 allele carriers in our study population, and corresponding associations were weak or absent among e4 noncarriers. These findings support a potential role of APOE in biological mechanisms that may contribute to associations between air pollution and neurobehavioral outcomes in children

    Neurogenetics of Dynamic Connectivity Patterns Associated With Obsessive-Compulsive Symptoms in Healthy Children

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    Background: Obsessive-compulsive symptoms (OCSs) during childhood predispose to obsessive-compulsive disorder and have been associated with changes in brain circuits altered in obsessive-compulsive disorder samples. OCSs may arise from disturbed glutamatergic neurotransmission, impairing cognitive oscillations and promoting overstable functional states. Methods: A total of 227 healthy children completed the Obsessive Compulsive Inventory-Child Version and underwent a resting-state functional magnetic resonance imaging examination. Genome-wide data were obtained from 149 of them. We used a graph theory-based approach and characterized associations between OCSs and dynamic functional connectivity (dFC). dFC evaluates fluctuations over time in FC between brain regions, which allows characterizing regions with stable connectivity patterns (attractors). We then compared the spatial similarity between OCS-dFC correlation maps and mappings of genetic expression across brain regions to identify genes potentially associated with connectivity changes. In post hoc analyses, we investigated which specific single nucleotide polymorphisms of these genes moderated the association between OCSs and patterns of dFC. Results: OCSs correlated with decreased attractor properties in the left ventral putamen and increased attractor properties in (pre)motor areas and the left hippocampus. At the specific symptom level, increased attractor properties in the right superior parietal cortex correlated with ordering symptoms. In the hippocampus, we identified two single nucleotide polymorphisms in glutamatergic neurotransmission genes (GRM7, GNAQ) that moderated the association between OCSs and attractor features. Conclusions: We provide evidence that in healthy children, the association between dFC changes and OCSs may be mapped onto brain circuits predicted by prevailing neurobiological models of obsessive-compulsive disorder. Moreover, our findings support the involvement of glutamatergic neurotransmission in such brain network changes

    The roses ocean and human health chair: A new way to engage the public in oceans and human health challenges

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    Involving and engaging stakeholders is crucial for studying and managing the complex interactions between marine ecosystems and human health and wellbeing. The Oceans and Human Health Chair was founded in the town of Roses (Catalonia, Spain, NW Mediterranean) in 2018, the fruit of a regional partnership between various stakeholders, and for the purpose of leading the way to better health and wellbeing through ocean research and conservation. The Chair is located in an area of the Mediterranean with a notable fishing, tourist, and seafaring tradition and is close to a marine reserve, providing the opportunity to observe diverse environmental conditions and coastal and maritime activities. The Chair is a case study demonstrating that local, collaborative, transdisciplinary, trans-sector, and bottom-up approaches offer tremendous opportunities for engaging coastal communities to help support long-lasting solutions that benefit everyone, and especially those living by the sea or making their living from the goods and services provided by the sea. Furthermore, the Chair has successfully integrated most of its experts in oceans and human health from the most prestigious institutions in Catalonia. The Chair focuses on three main topics identified by local stakeholders: Fish and Health; Leisure, Health, and Wellbeing; and Medicines from the Sea. Led by stakeholder engagement, the Chair can serve as a novel approach within the oceans and human health field of study to tackle a variety of environmental and public health challenges related to both communicable and non-communicable diseases, within the context of sociocultural issues. Drawing on the example provided by the Chair, four principles are established to encourage improved participatory processes in the oceans and human health field: bottom-up, “think local”, transdisciplinary and trans-sectorial, and “balance the many voices”.info:eu-repo/semantics/publishedVersio

    Genome-wide multi-trait analysis of irritable bowel syndrome and related mental conditions identifies 38 new independent variants

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    Irritable bowel syndrome (IBS) is a chronic disorder of gut-brain interaction frequently accompanied by mental conditions, including depression and anxiety. Despite showing substantial heritability and being partly determined by a genetic component, the genetic underpinnings explaining the high rates of comorbidity remain largely unclear and there are no conclusive data on the temporal relationship between them. Exploring the overlapping genetic architecture between IBS and mental conditions may help to identify novel genetic loci and biological mechanisms underlying IBS and causal relationships between them. We quantified the genetic overlap between IBS, neuroticism, depression and anxiety, conducted a multi-trait genome-wide association study (GWAS) considering these traits and investigated causal relationships between them by using the largest GWAS to date. IBS showed to be a highly polygenic disorder with extensive genetic sharing with mental conditions. Multi-trait analysis of IBS and neuroticism, depression and anxiety identified 42 genome-wide significant variants for IBS, of which 38 are novel. Fine-mapping risk loci highlighted 289 genes enriched in genes upregulated during early embryonic brain development and gene-sets related with psychiatric, digestive and autoimmune disorders. IBS-associated genes were enriched for target genes of anti-inflammatory and antirheumatic drugs, anesthetics and opioid dependence pharmacological treatment. Mendelian-randomization analysis accounting for correlated pleiotropy identified bidirectional causal effects between IBS and neuroticism and depression and causal effects of the genetic liability of IBS on anxiety. These findings provide evidence of the polygenic architecture of IBS, identify novel genome-wide significant variants for IBS and extend previous knowledge on the genetic overlap and relationship between gastrointestinal and mental disorders. The online version contains supplementary material available at 10.1186/s12967-023-04107-5
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