Nivel de inteligencia emocional y estrés laboral en enfermeras de hospitales I - red asistencial La Libertad Essalud

This descriptive correlational investigation, it made since January and December 2019. The purpose was to determine relationship between the level of emotional Intelligence and Work Stress in 94 nurses at hospitals level I La Libertad Healthcare Networkm. The Bar on emotional Intelligence questionnaire and the questionnaire to work Stress based on The Nursing Stress Scale by Pamela Graay Toft y James G were used as instruments. The information so far entered and processed in program IBM SPSS STATISTICS version 25, the results are presente in single and double entry tablets, to determine if there is a relationship between variables, The Pearson correlation test was used considering that there is suficiente evidence of statistical significance if the probability of have a mistake is less than 5 percent (p≤0.05), being 0.001 for what he considers highly significant and also the normality of the data was carried out with the proof of Kolmogorov smirnov. The folowing results are reached as obtained:  64.9 percent of nurses have a highly developed and adequate level of emotional intelligence, 46.8 percent have a high level of Work Stress. There conclution is significant relationship between level of emotional Intelligence and work Stress.La presente investigación descriptiva correlacional, se realizó de enero hasta diciembre 2019, el propósito fué determinar la relación entre el Nivel de Inteligencia emocional y el Estrés laboral en 94 enfermeras de los hospitales I de la Red Asistencial La Libertad. Se utilizaron: el cuestionario de Inteligencia emocional de Bar On adaptado al español y el cuestionario de estrés laboral basado en The Nursing Stress Scale de Pamela Graay Toft y James G. La información se ingresó al programa IBM SPSS STATISTICS Versión 25 y para determinar si hay relación entre las variables se usó la prueba de correlación de Pearson considerando que existen evidencias de significación estadística si la probabilidad de equivocarse es menor o igual al 5 por ciento (p≤0,05), siendo 0,001 por lo que se considera altamente significativa y se realizó la normalidad de los datos con la prueba de kolmogorov smirnov. Se alcanzó los siguientes resultados: el 64,9 por ciento de enfermeras tuvo un nivel de inteligencia emocional muy desarrollada y adecuada y 46,8 por ciento tuvo un alto nivel de Estrés Laboral. Se concluyó que hay correlación altamente significativa (p<0,01) entre el nivel de Inteligencia emocional y el Estrés laboral

Mutation screening of patients with Alzheimer disease identifies APP locus duplication in a Swedish patient

BACKGROUND: Missense mutations in three different genes encoding amyloid-β precursor protein, presenilin 1 and presenilin 2 are recognized to cause familial early-onset Alzheimer disease. Also duplications of the amyloid precursor protein gene have been shown to cause the disease. At the Dept. of Geriatric Medicine, Karolinska University Hospital, Sweden, patients are referred for mutation screening for the identification of nucleotide variations and for determining copy-number of the APP locus. METHODS: We combined the method of microsatellite marker genotyping with a quantitative real-time PCR analysis to detect duplications in patients with Alzheimer disease. RESULTS: In 22 DNA samples from individuals diagnosed with clinical Alzheimer disease, we identified one patient carrying a duplication on chromosome 21 which included the APP locus. Further mapping of the chromosomal region by array-comparative genome hybridization showed that the duplication spanned a maximal region of 1.09 Mb. CONCLUSIONS: This is the first report of an APP duplication in a Swedish Alzheimer patient and describes the use of quantitative real-time PCR as a tool for determining copy-number of the APP locus

Regulation of Amyloid Precursor Protein Processing by the Beclin 1 Complex

Autophagy is an intracellular degradation pathway that functions in protein and organelle turnover in response to starvation and cellular stress. Autophagy is initiated by the formation of a complex containing Beclin 1 (BECN1) and its binding partner Phosphoinositide-3-kinase, class 3 (PIK3C3). Recently, BECN1 deficiency was shown to enhance the pathology of a mouse model of Alzheimer Disease (AD). However, the mechanism by which BECN1 or autophagy mediate these effects are unknown. Here, we report that the levels of Amyloid precursor protein (APP) and its metabolites can be reduced through autophagy activation, indicating that they are a substrate for autophagy. Furthermore, we find that knockdown of Becn1 in cell culture increases the levels of APP and its metabolites. Accumulation of APP and APP C-terminal fragments (APP-CTF) are accompanied by impaired autophagosomal clearance. Pharmacological inhibition of autophagosomal-lysosomal degradation causes a comparable accumulation of APP and APP-metabolites in autophagosomes. Becn1 reduction in cell culture leads to lower levels of its binding partner Pik3c3 and increased presence of Microtubule-associated protein 1, light chain 3 (LC3). Overexpression of Becn1, on the other hand, reduces cellular APP levels. In line with these observations, we detected less BECN1 and PIK3C3 but more LC3 protein in brains of AD patients. We conclude that BECN1 regulates APP processing and turnover. BECN1 is involved in autophagy initiation and autophagosome clearance. Accordingly, BECN1 deficiency disrupts cellular autophagy and autophagosomal-lysosomal degradation and alters APP metabolism. Together, our findings suggest that autophagy and the BECN1-PIK3C3 complex regulate APP processing and play an important role in AD pathology

Molecular Determinants and Genetic Modifiers of Aggregation and Toxicity for the ALS Disease Protein FUS/TLS

A combination of yeast genetics and protein biochemistry define how the fused in sarcoma (FUS) protein might contribute to Lou Gehrig's disease

A genetic cause of Alzheimer disease: mechanistic insights from Down syndrome

Down syndrome, caused by an extra copy of chromosome 21, is associated with a greatly increased risk of early onset Alzheimer disease. It is thought that this risk is conferred by the presence of three copies of the gene encoding amyloid precursor protein (APP), an Alzheimer risk factor, although the possession of extra copies of other chromosome 21 genes may also play a role. Further study of the mechanisms underlying the development of Alzheimer disease in Down syndrome could provide insights into the mechanisms that cause dementia in the general population

Dysregulation of neuronal iron homeostasis as an alternative unifying effect of mutations causing familial Alzheimer's disease

The overwhelming majority of dominant mutations causing early onset familial Alzheimer's disease (EOfAD) occur in only three genes, PSEN1, PSEN2, and APP. An effect-in-common of these mutations is alteration of production of the APP-derived peptide, amyloid ß (Aß). It is this key fact that underlies the authority of the Amyloid Hypothesis that has informed Alzheimer's disease research for over two decades. Any challenge to this authority must offer an alternative explanation for the relationship between the PSEN genes and APP. In this paper, we explore one possible alternative relationship - the dysregulation of cellular iron homeostasis as a common effect of EOfAD mutations in these genes. This idea is attractive since it provides clear connections between EOfAD mutations and major characteristics of Alzheimer's disease such as dysfunctional mitochondria, vascular risk factors/hypoxia, energy metabolism, and inflammation. We combine our ideas with observations by others to describe a "Stress Threshold Change of State" model of Alzheimer's disease that may begin to explain the existence of both EOfAD and late onset sporadic (LOsAD) forms of the disease. Directing research to investigate the role of dysregulation of iron homeostasis in EOfAD may be a profitable way forward in our struggle to understand this form of dementia