Efectividad de las fajinas en el control de la erosión edáfica post-incendio en los montes de Castejón de Valdejasa

Una de las consecuencias de los incendios forestales es el aumento de la escorrentía y erosión de las zonas quemadas. Entre los múltiples tratamientos post-incendio, el presente estudio se ocupa de comprobar la efectividad de las fajinas instaladas en los montes de Castejón de Valdejasa tras el incendio acaecido en el verano del 2009. Para ello se seleccionaron cuatro zonas de estudio diferenciando dos tipos de suelo (calizo y yesoso) y dos orientaciones de las laderas (norte y sur), con tres réplicas por zona. En dichas zonas se cuantificó la cantidad de sedimentos y escorrentía producidos durante los años 2012 y 2013, inmediatamente después de la instalación de las fajinas que fueron colocadas a finales del 2011. También se realizaron análisis de las propiedades del suelo de las distintas zonas así como de la calidad del agua de escorrentía. Durante el 2012 las fajinas presentaron un rendimiento del 91,1% al disminuir la erosión de 8,51 Mg ha-1 año-1 en las parcelas control a 0,76 Mg ha-1 año-1 en las parcelas tratadas y siendo su actuación significativa en tres de las cuatro zonas de estudio. Se observaron mayores rendimientos de las mismas en las zonas orientadas al sur. Así mismo también produjeron una reducción significativa de la escorrentía cuyos valores variaron de 6,88 mm año-1 en las parcelas control a 3,30 mm año-1 en las parcelas fajinadas, lo que supuso un 52% de rendimiento. Tanto los valores de sedimentos como de escorrentía disminuyeron en el año 2013 debido a un crecimiento de la vegetación que se produjo en todas las zonas a excepción de Yesos Sur. La cantidad de suelo desnudo al final del estudio fue inferior al 50% en todas las zonas menos en la indicada, por lo que solamente en esta última se observaron diferencias significativas en erosión y en escorrentía. Aunque el primer año después del incendio es cuando mayores cantidades de erosión se producen, el presente estudio demuestra que las medidas de tratamiento post-incendio, en zonas semiáridas, son efectivas aún en el tercer y cuarto año después del siniestro, sobre todo en laderas orientadas al sur con suelos pobres al producirse una lenta regeneración de la vegetación existente

NTMC2T5.1 is involved in chloroplast clustering around nucleus in Nicotiana benthamiana.

Plants have developed mechanisms to protect themselves from pathogens and resist their attacks. Among these, clustering of chloroplasts around the nuclear envelope is a phenomenon that has been proposed as a general response to the perception of pathogens, such as viruses and bacteria [1]. Additionally, it has been hypothesized that chloroplast clustering could serve as an efficient way of transferring signals —such as lipids and reactive oxygen species— between these two organelles in order to induce changes in the expression of pathogen defence-related genes. Synaptotagmin-like mitochondrial-lipid-binding (SMP) domain proteins are evolutionarily conserved in eukaryotes and participate in the formation of membrane contact sites between organelles. In particular, their SMP domains allow the lipid transport between the membranes of different organelles [2]. Our group is focus on studying NTMC2T5 proteins, a group of SMP proteins, with two homologs in Arabidopsis thaliana. By transiently overexpressing AtNTMC2T5.1 and some truncated versions in Nicotiana benthamiana leaf cells, and using confocal microscopy, we have determined the subcellular localization of the encoded protein. This protein is anchored to the chloroplast outer envelope and interacts with the membranes of other organelles, like the ER and the nuclear envelope membrane [3]. Additionally, we have detected that overexpression of NTMC2T5 proteins causes a significant chloroplast clustering around nucleus, that it was not observed when overexpressing other proteins. Thus, we have estimated the contribution of its functional domains in the clustering. Our results suggest that the C-terminal hydrophobic region (HR) of AtNTMC2T5.1 is essential for this process. Moreover, our Arabidopsis ntmc2t5.1/t5.2 knock down plants showed slower growth when treated with flagelin22 and reduced chloroplast clustering when treated with H2O2.Universidad de Málaga. Campus de Excelencia Internacional Andalucía Tech

NTMC2T5: a newly identified lipid transfer proteins at ER-chloroplast contact sites involved in development and stress response.

In plants, fatty acid synthesis takes place at chloroplasts, and they are assembled into glycerolipids and sphingolipids at the endoplasmic reticulum (ER). Then, the newly ER synthetized lipids are sent back to the chloroplast to form part of their membranes. Since, no vesicular transport has been described between these two organelles, lipid transport might be mediated by lipid transport proteins (LTP) via a non-vesicular pathway.Universidad de Málaga. Campus de Excelencia Internacional Andalucía Tech

Salida internacional a México: la academia, la cultura y la empresa

Visita Técnica InternacionalEl siguiente informe muestra como por medio de la interculturalidad se caracteriza una población, se identifica y se conoce su realidad, integrándose de este modo con la academia bajo lineamientos como ubicación, idioma, riesgos, oportunidades, entre otros, y al final como se materializa la puesta en marcha de un proyecto, que al principio en un momento fue solamente una idea.RESUMEN INTRODUCCIÓN OBJETIVOS INFORME CULTURAL INFORME ACADEMICO INFORME EMPRESARIAL CONCLUSIONES Y RECOMENDACIONES BIBLIOGRAFÍAEspecializaciónEspecialista en Formulación y Evaluación Social y Económica de Proyecto

Common variants in Alzheimer’s disease and risk stratification by polygenic risk scores

Funder: Funder: Fundación bancaria ‘La Caixa’ Number: LCF/PR/PR16/51110003 Funder: Grifols SA Number: LCF/PR/PR16/51110003 Funder: European Union/EFPIA Innovative Medicines Initiative Joint Number: 115975 Funder: JPco-fuND FP-829-029 Number: 733051061Genetic discoveries of Alzheimer's disease are the drivers of our understanding, and together with polygenetic risk stratification can contribute towards planning of feasible and efficient preventive and curative clinical trials. We first perform a large genetic association study by merging all available case-control datasets and by-proxy study results (discovery n = 409,435 and validation size n = 58,190). Here, we add six variants associated with Alzheimer's disease risk (near APP, CHRNE, PRKD3/NDUFAF7, PLCG2 and two exonic variants in the SHARPIN gene). Assessment of the polygenic risk score and stratifying by APOE reveal a 4 to 5.5 years difference in median age at onset of Alzheimer's disease patients in APOE ɛ4 carriers. Because of this study, the underlying mechanisms of APP can be studied to refine the amyloid cascade and the polygenic risk score provides a tool to select individuals at high risk of Alzheimer's disease

New insights into the genetic etiology of Alzheimer's disease and related dementias

Characterization of the genetic landscape of Alzheimer's disease (AD) and related dementias (ADD) provides a unique opportunity for a better understanding of the associated pathophysiological processes. We performed a two-stage genome-wide association study totaling 111,326 clinically diagnosed/'proxy' AD cases and 677,663 controls. We found 75 risk loci, of which 42 were new at the time of analysis. Pathway enrichment analyses confirmed the involvement of amyloid/tau pathways and highlighted microglia implication. Gene prioritization in the new loci identified 31 genes that were suggestive of new genetically associated processes, including the tumor necrosis factor alpha pathway through the linear ubiquitin chain assembly complex. We also built a new genetic risk score associated with the risk of future AD/dementia or progression from mild cognitive impairment to AD/dementia. The improvement in prediction led to a 1.6- to 1.9-fold increase in AD risk from the lowest to the highest decile, in addition to effects of age and the APOE ε4 allele

Hyperoxemia and excess oxygen use in early acute respiratory distress syndrome : Insights from the LUNG SAFE study

Publisher Copyright: © 2020 The Author(s). Copyright: Copyright 2020 Elsevier B.V., All rights reserved.Background: Concerns exist regarding the prevalence and impact of unnecessary oxygen use in patients with acute respiratory distress syndrome (ARDS). We examined this issue in patients with ARDS enrolled in the Large observational study to UNderstand the Global impact of Severe Acute respiratory FailurE (LUNG SAFE) study. Methods: In this secondary analysis of the LUNG SAFE study, we wished to determine the prevalence and the outcomes associated with hyperoxemia on day 1, sustained hyperoxemia, and excessive oxygen use in patients with early ARDS. Patients who fulfilled criteria of ARDS on day 1 and day 2 of acute hypoxemic respiratory failure were categorized based on the presence of hyperoxemia (PaO2 > 100 mmHg) on day 1, sustained (i.e., present on day 1 and day 2) hyperoxemia, or excessive oxygen use (FIO2 ≥ 0.60 during hyperoxemia). Results: Of 2005 patients that met the inclusion criteria, 131 (6.5%) were hypoxemic (PaO2 < 55 mmHg), 607 (30%) had hyperoxemia on day 1, and 250 (12%) had sustained hyperoxemia. Excess FIO2 use occurred in 400 (66%) out of 607 patients with hyperoxemia. Excess FIO2 use decreased from day 1 to day 2 of ARDS, with most hyperoxemic patients on day 2 receiving relatively low FIO2. Multivariate analyses found no independent relationship between day 1 hyperoxemia, sustained hyperoxemia, or excess FIO2 use and adverse clinical outcomes. Mortality was 42% in patients with excess FIO2 use, compared to 39% in a propensity-matched sample of normoxemic (PaO2 55-100 mmHg) patients (P = 0.47). Conclusions: Hyperoxemia and excess oxygen use are both prevalent in early ARDS but are most often non-sustained. No relationship was found between hyperoxemia or excessive oxygen use and patient outcome in this cohort. Trial registration: LUNG-SAFE is registered with ClinicalTrials.gov, NCT02010073publishersversionPeer reviewe

Analysis of shared heritability in common disorders of the brain

ience, this issue p. eaap8757 Structured Abstract INTRODUCTION Brain disorders may exhibit shared symptoms and substantial epidemiological comorbidity, inciting debate about their etiologic overlap. However, detailed study of phenotypes with different ages of onset, severity, and presentation poses a considerable challenge. Recently developed heritability methods allow us to accurately measure correlation of genome-wide common variant risk between two phenotypes from pools of different individuals and assess how connected they, or at least their genetic risks, are on the genomic level. We used genome-wide association data for 265,218 patients and 784,643 control participants, as well as 17 phenotypes from a total of 1,191,588 individuals, to quantify the degree of overlap for genetic risk factors of 25 common brain disorders. RATIONALE Over the past century, the classification of brain disorders has evolved to reflect the medical and scientific communities' assessments of the presumed root causes of clinical phenomena such as behavioral change, loss of motor function, or alterations of consciousness. Directly observable phenomena (such as the presence of emboli, protein tangles, or unusual electrical activity patterns) generally define and separate neurological disorders from psychiatric disorders. Understanding the genetic underpinnings and categorical distinctions for brain disorders and related phenotypes may inform the search for their biological mechanisms. RESULTS Common variant risk for psychiatric disorders was shown to correlate significantly, especially among attention deficit hyperactivity disorder (ADHD), bipolar disorder, major depressive disorder (MDD), and schizophrenia. By contrast, neurological disorders appear more distinct from one another and from the psychiatric disorders, except for migraine, which was significantly correlated to ADHD, MDD, and Tourette syndrome. We demonstrate that, in the general population, the personality trait neuroticism is significantly correlated with almost every psychiatric disorder and migraine. We also identify significant genetic sharing between disorders and early life cognitive measures (e.g., years of education and college attainment) in the general population, demonstrating positive correlation with several psychiatric disorders (e.g., anorexia nervosa and bipolar disorder) and negative correlation with several neurological phenotypes (e.g., Alzheimer's disease and ischemic stroke), even though the latter are considered to result from specific processes that occur later in life. Extensive simulations were also performed to inform how statistical power, diagnostic misclassification, and phenotypic heterogeneity influence genetic correlations. CONCLUSION The high degree of genetic correlation among many of the psychiatric disorders adds further evidence that their current clinical boundaries do not reflect distinct underlying pathogenic processes, at least on the genetic level. This suggests a deeply interconnected nature for psychiatric disorders, in contrast to neurological disorders, and underscores the need to refine psychiatric diagnostics. Genetically informed analyses may provide important "scaffolding" to support such restructuring of psychiatric nosology, which likely requires incorporating many levels of information. By contrast, we find limited evidence for widespread common genetic risk sharing among neurological disorders or across neurological and psychiatric disorders. We show that both psychiatric and neurological disorders have robust correlations with cognitive and personality measures. Further study is needed to evaluate whether overlapping genetic contributions to psychiatric pathology may influence treatment choices. Ultimately, such developments may pave the way toward reduced heterogeneity and improved diagnosis and treatment of psychiatric disorders

Rare coding variants in PLCG2, ABI3, and TREM2 implicate microglial-mediated innate immunity in Alzheimer's disease

We identified rare coding variants associated with Alzheimer’s disease (AD) in a 3-stage case-control study of 85,133 subjects. In stage 1, 34,174 samples were genotyped using a whole-exome microarray. In stage 2, we tested associated variants (P<1×10-4) in 35,962 independent samples using de novo genotyping and imputed genotypes. In stage 3, an additional 14,997 samples were used to test the most significant stage 2 associations (P<5×10-8) using imputed genotypes. We observed 3 novel genome-wide significant (GWS) AD associated non-synonymous variants; a protective variant in PLCG2 (rs72824905/p.P522R, P=5.38×10-10, OR=0.68, MAFcases=0.0059, MAFcontrols=0.0093), a risk variant in ABI3 (rs616338/p.S209F, P=4.56×10-10, OR=1.43, MAFcases=0.011, MAFcontrols=0.008), and a novel GWS variant in TREM2 (rs143332484/p.R62H, P=1.55×10-14, OR=1.67, MAFcases=0.0143, MAFcontrols=0.0089), a known AD susceptibility gene. These protein-coding changes are in genes highly expressed in microglia and highlight an immune-related protein-protein interaction network enriched for previously identified AD risk genes. These genetic findings provide additional evidence that the microglia-mediated innate immune response contributes directly to AD development

CARB-ES-19 Multicenter Study of Carbapenemase-Producing Klebsiella pneumoniae and Escherichia coli From All Spanish Provinces Reveals Interregional Spread of High-Risk Clones Such as ST307/OXA-48 and ST512/KPC-3

ObjectivesCARB-ES-19 is a comprehensive, multicenter, nationwide study integrating whole-genome sequencing (WGS) in the surveillance of carbapenemase-producing K. pneumoniae (CP-Kpn) and E. coli (CP-Eco) to determine their incidence, geographical distribution, phylogeny, and resistance mechanisms in Spain.MethodsIn total, 71 hospitals, representing all 50 Spanish provinces, collected the first 10 isolates per hospital (February to May 2019); CPE isolates were first identified according to EUCAST (meropenem MIC &gt; 0.12 mg/L with immunochromatography, colorimetric tests, carbapenem inactivation, or carbapenem hydrolysis with MALDI-TOF). Prevalence and incidence were calculated according to population denominators. Antibiotic susceptibility testing was performed using the microdilution method (EUCAST). All 403 isolates collected were sequenced for high-resolution single-nucleotide polymorphism (SNP) typing, core genome multilocus sequence typing (cgMLST), and resistome analysis.ResultsIn total, 377 (93.5%) CP-Kpn and 26 (6.5%) CP-Eco isolates were collected from 62 (87.3%) hospitals in 46 (92%) provinces. CP-Kpn was more prevalent in the blood (5.8%, 50/853) than in the urine (1.4%, 201/14,464). The cumulative incidence for both CP-Kpn and CP-Eco was 0.05 per 100 admitted patients. The main carbapenemase genes identified in CP-Kpn were blaOXA–48 (263/377), blaKPC–3 (62/377), blaVIM–1 (28/377), and blaNDM–1 (12/377). All isolates were susceptible to at least two antibiotics. Interregional dissemination of eight high-risk CP-Kpn clones was detected, mainly ST307/OXA-48 (16.4%), ST11/OXA-48 (16.4%), and ST512-ST258/KPC (13.8%). ST512/KPC and ST15/OXA-48 were the most frequent bacteremia-causative clones. The average number of acquired resistance genes was higher in CP-Kpn (7.9) than in CP-Eco (5.5).ConclusionThis study serves as a first step toward WGS integration in the surveillance of carbapenemase-producing Enterobacterales in Spain. We detected important epidemiological changes, including increased CP-Kpn and CP-Eco prevalence and incidence compared to previous studies, wide interregional dissemination, and increased dissemination of high-risk clones, such as ST307/OXA-48 and ST512/KPC-3