Regímenes laborales en la productividad de los trabajadores administrativos de una universidad pública, Apurímac, 2021

La presente investigación tuvo como propósito principal determinar la influencia de los regímenes laborales en la productividad de los trabajadores administrativos de una universidad pública de la región Apurímac, 2021; para lograr ese propósito la investigación tomó como tipo de investigación a la básica, además se afianzó en el diseño no experimental, de corte transeccional, la muestra estuvo compuesta por 103 trabajadores administrativos de una universidad pública, a los que se les aplicó una encuesta cuyo instrumento fueron dos cuestionarios con 20 ítems medidos a través de una escala tipo Likert, instrumento que fue validad por juicio de expertos además de la determinación de la confiablidad utilizando Alfa de Cronbach; los resultados muestran un 58.25% de los encuestados consideran como regular al régimen laboral en el que se encuentran y un 38.83% consideran que la productividad laboral es alta; la influencia de los regímenes laborales en la productividad laboral se ha determinado que es baja, utilizando una prueba de Nagelkerke que presenta un valor de 0.104, por lo que se puede afirmar que la productividad laboral es explicada en un 10.4% por los regímenes laborales, lo que es bastante bajo

Active Design – How the built environment matters to mobile games for health

Mobile games for health aim to provide both for an attractive gaming experience and for a positive effect on their users’ wellbeing. Most of these games are context-sensitive, as they take note of the state of the player’s environment and use this information to adapt the game experience. This article points to the limited research available that validates either the physiological effects of playing context-sensitive games for health regularly, or research that focuses on the complex relationship between mobile games, a players’ health and wellbeing, and the (urban) environment in which many of these games are being played. It reviews aspects of health-oriented urban design that has been shown to influence people’s everyday activity patterns including running and cycling. It speculates how “active design” context can also have an impact on how we play mobile games for health and explains how this knowledge can be used to improve such games

Genetic forms of primary progressive aphasia within the GENetic Frontotemporal dementia Initiative (GENFI) cohort: comparison with sporadic primary progressive aphasia

Samra et al. report that progranulin mutations are the commonest genetic cause of primary progressive aphasia. Two subtypes are seen: a nonfluent variant (similar in phenotype to its sporadic counterpart) and a 'not otherwise specified' variant (with unique linguistic features). Revised criteria for primary progressive aphasia should consider genetic phenotypes. Primary progressive aphasia is most commonly a sporadic disorder, but in some cases, it can be genetic. This study aimed to understand the clinical, cognitive and imaging phenotype of the genetic forms of primary progressive aphasia in comparison to the canonical nonfluent, semantic and logopenic subtypes seen in sporadic disease. Participants with genetic primary progressive aphasia were recruited from the international multicentre GENetic Frontotemporal dementia Initiative study and compared with healthy controls as well as a cohort of people with sporadic primary progressive aphasia. Symptoms were assessed using the GENetic Frontotemporal dementia Initiative language, behavioural, neuropsychiatric and motor scales. Participants also underwent a cognitive assessment and 3 T volumetric T1-weighted MRI. One C9orf72 (2%), 1 MAPT (6%) and 17 GRN (44%) symptomatic mutation carriers had a diagnosis of primary progressive aphasia. In the GRN cohort, 47% had a diagnosis of nonfluent variant primary progressive aphasia, and 53% had a primary progressive aphasia syndrome that did not fit diagnostic criteria for any of the three subtypes, called primary progressive aphasia-not otherwise specified here. The phenotype of the genetic nonfluent variant primary progressive aphasia group largely overlapped with that of sporadic nonfluent variant primary progressive aphasia, although the presence of an associated atypical parkinsonian syndrome was characteristic of sporadic and not genetic disease. The primary progressive aphasia -not otherwise specified group however was distinct from the sporadic subtypes with impaired grammar/syntax in the presence of relatively intact articulation, alongside other linguistic deficits. The pattern of atrophy seen on MRI in the genetic nonfluent variant primary progressive aphasia group overlapped with that of the sporadic nonfluent variant primary progressive aphasia cohort, although with more posterior cortical involvement, whilst the primary progressive aphasia-not otherwise specified group was strikingly asymmetrical with involvement particularly of the insula and dorsolateral prefrontal cortex but also atrophy of the orbitofrontal cortex and the medial temporal lobes. Whilst there are overlapping symptoms between genetic and sporadic primary progressive aphasia syndromes, there are also distinct features. Future iterations of the primary progressive aphasia consensus criteria should encompass such information with further research needed to understand the earliest features of these disorders, particularly during the prodromal period of genetic disease

Affect Recognition using Psychophysiological Correlates in High Intensity VR Exergaming

User experience estimation of VR exergame players by recognising their affective state could enable us to personalise and optimise their experience. Affect recognition based on psychophysiological measurements has been successful for moderate intensity activities. High intensity VR exergames pose challenges as the effects of exercise and VR headsets interfere with those measurements. We present two experiments that investigate the use of different sensors for affect recognition in a VR exergame. The first experiment compares the impact of physical exertion and gamification on psychophysiological measurements during rest, conventional exercise, VR exergaming, and sedentary VR gaming. The second experiment compares underwhelming, overwhelming and optimal VR exergaming scenarios. We identify gaze fixations, eye blinks, pupil diameter and skin conductivity as psychophysiological measures suitable for affect recognition in VR exergaming and analyse their utility in determining affective valence and arousal. Our findings provide guidelines for researchers of affective VR exergames.This project has received funding from the European Union’s Horizon 2020 research and innovation programme under the Marie Skłodowska-Curie grant agreement No 665992 </p

L’Image railleuse

La fonction critique des images s’incarne de manière privilégiée dans la satire. Si la satire s’est constituée en genre littéraire dès l’Antiquité, avant de gagner les beaux-arts et les arts graphiques à l’âge classique, ce sont les médias modernes – édition, presse, expositions, télévision, internet – qui, en élargissant progressivement sa sphère d’influence, ont renouvelé ses formes et ses objectifs tout en augmentant leur efficacité. Autorisant une diffusion planétaire et presque instantanée des images satiriques, internet et les technologies numériques n’ont pas seulement transformé la matérialité et les moyens d’action de cette imagerie et leurs effets sociopolitiques, ils ont aussi affecté les formes de la recherche sur le satirique en donnant accès de plus en plus rapidement à des corpus extrêmement vastes. La satire est aujourd’hui partout, sans qu’aucun acteur ni canal de diffusion ne puisse prétendre en contrôler ses usages généralisés ni son effectivité. Cette publication regroupe les actes du colloque qui s’est tenu du 25 au 27 juin 2015 à l’Institut national d’histoire de l’art, à Paris, organisé par l’Institut national d’histoire de l’art, l’université du Québec à Montréal et le LARHRA-UMR 5190 du CNRS, avec le soutien de l’Agence universitaire de la Francophonie et le Conseil de recherches en sciences humaines du Canada

Convergent genetic and expression data implicate immunity in Alzheimer's disease

Background Late–onset Alzheimer's disease (AD) is heritable with 20 genes showing genome wide association in the International Genomics of Alzheimer's Project (IGAP). To identify the biology underlying the disease we extended these genetic data in a pathway analysis. Methods The ALIGATOR and GSEA algorithms were used in the IGAP data to identify associated functional pathways and correlated gene expression networks in human brain. Results ALIGATOR identified an excess of curated biological pathways showing enrichment of association. Enriched areas of biology included the immune response (p = 3.27×10-12 after multiple testing correction for pathways), regulation of endocytosis (p = 1.31×10-11), cholesterol transport (p = 2.96 × 10-9) and proteasome-ubiquitin activity (p = 1.34×10-6). Correlated gene expression analysis identified four significant network modules, all related to the immune response (corrected p 0.002 – 0.05). Conclusions The immune response, regulation of endocytosis, cholesterol transport and protein ubiquitination represent prime targets for AD therapeutics

Genome-wide analyses reveal a potential role for the MAPT, MOBP, and APOE loci in sporadic frontotemporal dementia

Frontotemporal dementia (FTD) is the second most common cause of early-onset dementia after Alzheimer disease (AD). Efforts in the field mainly focus on familial forms of disease (fFTDs), while studies of the genetic etiology of sporadic FTD (sFTD) have been less common. In the current work, we analyzed 4,685 sFTD cases and 15,308 controls looking for common genetic determinants for sFTD. We found a cluster of variants at the MAPT (rs199443; p = 2.5 × 10−12, OR = 1.27) and APOE (rs6857; p = 1.31 × 10−12, OR = 1.27) loci and a candidate locus on chromosome 3 (rs1009966; p = 2.41 × 10−8, OR = 1.16) in the intergenic region between RPSA and MOBP, contributing to increased risk for sFTD through effects on expression and/or splicing in brain cortex of functionally relevant in-cis genes at the MAPT and RPSA-MOBP loci. The association with the MAPT (H1c clade) and RPSA-MOBP loci may suggest common genetic pleiotropy across FTD and progressive supranuclear palsy (PSP) (MAPT and RPSA-MOBP loci) and across FTD, AD, Parkinson disease (PD), and cortico-basal degeneration (CBD) (MAPT locus). Our data also suggest population specificity of the risk signals, with MAPT and APOE loci associations mainly driven by Central/Nordic and Mediterranean Europeans, respectively. This study lays the foundations for future work aimed at further characterizing population-specific features of potential FTD-discriminant APOE haplotype(s) and the functional involvement and contribution of the MAPT H1c haplotype and RPSA-MOBP loci to pathogenesis of sporadic forms of FTD in brain cortex

Common variants at ABCA7, MS4A6A/MS4A4E, EPHA1, CD33 and CD2AP are associated with Alzheimer's disease

We sought to identify new susceptibility loci for Alzheimer's disease through a staged association study (GERAD+) and by testing suggestive loci reported by the Alzheimer's Disease Genetic Consortium (ADGC) in a companion paper. We undertook a combined analysis of four genome-wide association datasets (stage 1) and identified ten newly associated variants with P ≤ 1 × 10−5. We tested these variants for association in an independent sample (stage 2). Three SNPs at two loci replicated and showed evidence for association in a further sample (stage 3). Meta-analyses of all data provided compelling evidence that ABCA7 (rs3764650, meta P = 4.5 × 10−17; including ADGC data, meta P = 5.0 × 10−21) and the MS4A gene cluster (rs610932, meta P = 1.8 × 10−14; including ADGC data, meta P = 1.2 × 10−16) are new Alzheimer's disease susceptibility loci. We also found independent evidence for association for three loci reported by the ADGC, which, when combined, showed genome-wide significance: CD2AP (GERAD+, P = 8.0 × 10−4; including ADGC data, meta P = 8.6 × 10−9), CD33 (GERAD+, P = 2.2 × 10−4; including ADGC data, meta P = 1.6 × 10−9) and EPHA1 (GERAD+, P = 3.4 × 10−4; including ADGC data, meta P = 6.0 × 10−10)

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

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