Síndrome de «burnout» y apoyo social en maestros de Educación Primaria

This paper examines the relationship between burnout and perceived social support in a sample of 801 Primary School teachers. The Maslach Burnout Inventory (MBI) and the Duke-UNC-11 questionnaire were used. The statistical method used was canonical correspondence analysis, where the linear combination of the social support factors that maximises the dispersion of values of the three dimensions of the MBI was selected. The results of the study show that perceived social support relates to each of the dimensions of burnout syndrome in a different way and that is key to restore psychosocial balance.Este trabajo examina la relación entre burnout y apoyo social percibido en una muestra de 801 maestros de Educación Primaria. Para ello se usa el Maslach Burnout Inventory (MBI) y el cuestionario Duke-UNC-11. El método estadístico empleado fue el análisis canónico de correspondencias, donde se seleccionó la combinación lineal de los factores del apoyo social que maximiza la dispersión de valores de las tres dimensiones del MBI. Los resultados muestran que un 20,8% de los maestros sufre burnout. El apoyo social percibido, en su carácter restaurador del equilibrio psicosocial, se relaciona de distinto modo con las tres dimensiones del burnout.</em

Prognostic stratification of adult primary glioblastoma multiforme patients based on their tumor gene amplification profiles

Several classification systems have been proposed to address genomic heterogeneity of glioblastoma multiforme, but they either showed limited prognostic value and/or are difficult to implement in routine diagnostics. Here we propose a prognostic stratification model for these primary tumors based on tumor gene amplification profiles, that might be easily implemented in routine diagnostics, and potentially improve the patients management. Gene amplification profiles were prospectively evaluated in 80 primary glioblastoma multiforme tumors using singlenucleotide polymorphism arrays and the results obtained validated in publicly available data from 267/347 cases. Gene amplification was detected in 45% of pati

Identification of genetic variants associated with Huntington's disease progression: a genome-wide association study

Background Huntington's disease is caused by a CAG repeat expansion in the huntingtin gene, HTT. Age at onset has been used as a quantitative phenotype in genetic analysis looking for Huntington's disease modifiers, but is hard to define and not always available. Therefore, we aimed to generate a novel measure of disease progression and to identify genetic markers associated with this progression measure. Methods We generated a progression score on the basis of principal component analysis of prospectively acquired longitudinal changes in motor, cognitive, and imaging measures in the 218 indivduals in the TRACK-HD cohort of Huntington's disease gene mutation carriers (data collected 2008–11). We generated a parallel progression score using data from 1773 previously genotyped participants from the European Huntington's Disease Network REGISTRY study of Huntington's disease mutation carriers (data collected 2003–13). We did a genome-wide association analyses in terms of progression for 216 TRACK-HD participants and 1773 REGISTRY participants, then a meta-analysis of these results was undertaken. Findings Longitudinal motor, cognitive, and imaging scores were correlated with each other in TRACK-HD participants, justifying use of a single, cross-domain measure of disease progression in both studies. The TRACK-HD and REGISTRY progression measures were correlated with each other (r=0·674), and with age at onset (TRACK-HD, r=0·315; REGISTRY, r=0·234). The meta-analysis of progression in TRACK-HD and REGISTRY gave a genome-wide significant signal (p=1·12 × 10−10) on chromosome 5 spanning three genes: MSH3, DHFR, and MTRNR2L2. The genes in this locus were associated with progression in TRACK-HD (MSH3 p=2·94 × 10−8 DHFR p=8·37 × 10−7 MTRNR2L2 p=2·15 × 10−9) and to a lesser extent in REGISTRY (MSH3 p=9·36 × 10−4 DHFR p=8·45 × 10−4 MTRNR2L2 p=1·20 × 10−3). The lead single nucleotide polymorphism (SNP) in TRACK-HD (rs557874766) was genome-wide significant in the meta-analysis (p=1·58 × 10−8), and encodes an aminoacid change (Pro67Ala) in MSH3. In TRACK-HD, each copy of the minor allele at this SNP was associated with a 0·4 units per year (95% CI 0·16–0·66) reduction in the rate of change of the Unified Huntington's Disease Rating Scale (UHDRS) Total Motor Score, and a reduction of 0·12 units per year (95% CI 0·06–0·18) in the rate of change of UHDRS Total Functional Capacity score. These associations remained significant after adjusting for age of onset. Interpretation The multidomain progression measure in TRACK-HD was associated with a functional variant that was genome-wide significant in our meta-analysis. The association in only 216 participants implies that the progression measure is a sensitive reflection of disease burden, that the effect size at this locus is large, or both. Knockout of Msh3 reduces somatic expansion in Huntington's disease mouse models, suggesting this mechanism as an area for future therapeutic investigation

Vascular and Cardiac Target Organ Damage in Type 2 Diabetics With and Without Diabetic Retinopathy

Objective: In this study, we sought to assess the differences in cardiac and vascular end-organ damage in type 2 diabetics, with and without diabetic retinopathy. Methods: A cross-sectional study of 131 diabetic patients (44 with diabetic retinopathy and 87 without diabetic retinopathy). Retinography was performed with a Topcon TRC NW 200 non-mydriatic retinal camera. Using the Early Treatment of Diabetic Retinopathy Study Severity Scale, two independent observers graded the retinopathy. Pulse-wave velocity, ambulatory arterial stiffness indices, ambulatory arterial stiffness indices to blood pressure variability ratio, carotid intima and ndash;media thickness, and ankle/brachial index were used as markers of vascular damage. Left ventricular hypertrophy was evaluated by the Cornell voltage and ndash;duration product and Lewis Index. Results: A total of 33.60% of the subjects had diabetic retinopathy. The patients with diabetic retinopathy were more likely to be women (p=0.031), be insulin users (p=0.001), have a longer duration of disease (p=0.033), and have poorer blood glucose control (HbA1c 6.98 in patients with diabetic retinopathy versus 6.40 in patients without diabetic retinopathy) (p=0.012). Patients with diabetic retinopathy did not statistically differ from diabetics without retinopathy with regards to cardiac or vascular target organ damage. However, patients with diabetic retinopathy showed a trend (defined as a p-value ranging from 0.051 to 0.15) toward a higher resting heart rate, higher ratio of night/day SBP, higher ratio of night/day DBP, higher resting ambulatory systolic blood pressure measure (mmHg), higher resting ambulatory diastolic blood pressure measure (mmHg), higher ASSI-BPVR, and higher Lewis Index. Conclusions: Although the sample size limited the conclusions that could be drawn between diabetic retinopathy and levels of vascular and cardiac target organ damage, trends were observed in a number of indices for these conditions and measures thereof. [Arch Clin Exp Surg 2013; 2(4.000): 212-218

Identification of genetic and molecular determinants associated with cardiotoxicity by anthracyclines and taxanes according to age

Resumen del trabajo presentado al 5th Symposium on Biomedical Research: "Advances and Perspectives In Pharmacology, Drug Toxicity and Pharmacogenetics", celebrado en Madrid del 15 al 16 de marzo de 2018.[Introduction]: Cardiotoxicity due to anthracyclines (CDA) is a very common problem in cancer patients, with great repercussion on their quality of life, which limits chemotherapy treatment and has consequences in the final prognosis of the oncologic disease itself. The susceptibility and degree of cardiotoxicity by anthracyclines is very heterogeneous among patients, and who will suffer this complication is unknown. CDA is a complex trait, thus follows a model of quantitative genetics, whose polygenic component is mostly unidentified. In addition, as a complex trait, CDA heterogeneity is explained by the variability among subphenotypes that would participate in its pathogenesis. Thus, anthracyclines exert their toxicity through DNA damage, so that among these subphenotypes would be the molecular pathways involved in the response to it, and a series of signaling pathways that promote and others that protect from that heart damage anthracyclines have a pro-genotoxicity effect. Differences in these pathways with the genetic variants linked with them could contribute to different susceptibility to CDA among individuals.[Material and Methods]: we identified the genetic and molecular determinants of cardiotoxicity in a simplified model of controlled genetic and phenotypic heterogeneity, generated by a backcross of two mouse strains of divergent phenotypic behavior, FVB and C57BL/6. We evaluated cardiac damage at histopathological level and also quantified different subphenotypes such as signaling pathways associated with cardiac damage and protection, genotoxicity pathways, TGFβ levels, telomere length, and expression of miRNAs in the myocardium.[Results]: We quantified anthracycline cardiotoxicity in a heterogeneous cohort of mice with breast cancer generated by a backcross. Cardiotoxicity was higher in old mice, was higher in the combined treatment with taxanes, was higher in the subendocardial zone and was influenced by the genetic background. We have identified multiple QTL associated with CDA in these different conditions studied. Differences in the grade of anthracycline cardiotoxicity at the histopathological level were accompanied by differences in the molecular levels in the myocardium of different molecular components of the pathways of response to damage at DNA, signaling pathways, miRNAs and telomere length. QTLs associated with these subphenotypes help to define CDA variability. Lastly, we have also defined CDA by multivariate models.[Conclusion]: The identification of genetic and molecular factors responsible for the increased risk of CDA will contribute to a better understanding of their pathophysiology, which could lead to new approaches to predict, prevent and treat this serious complication of chemotherapy.JPL was partially supported by FEDER and the MICINN (SAF2014-56989-R, SAF2017-88854R), the Instituto de Salud Carlos III (PIE14/00066), “Proyectos Integrados IBSAL 2015” (IBY15/00003), the Sandra Ibarra Foundation “de Solidaridad Frente al Cáncer” Foundation and “We can be heroes” Foundation.Peer reviewe