On the Performance of video quality assessment metrics under different compression and packet llss scenariov

[EN] When comparing the performance of video coding approaches, evaluating different commercial video encoders, or measuring the perceived video quality in a wireless environment, Rate/distortion analysis is commonly used, where distortion is usually measured in terms of PSNR values. However, PSNR does not always capture the distortion perceived by a human being. As a consequence, significant efforts have focused on defining an objective video quality metric that is able to assess quality in the same way as a human does. We perform a study of some available objective quality assessment metrics in order to evaluate their behavior in two different scenarios. First, we deal with video sequences compressed by different encoders at different bitrates in order to properly measure the video quality degradation associated with the encoding system. In addition, we evaluate the behavior of the quality metrics when measuring video distortions produced by packet losses in mobile ad hoc network scenarios with variable degrees of network congestion and node mobility. Our purpose is to determine if the analyzed metrics can replace the PSNR while comparing, designing, and evaluating video codec proposals, and, in particular, under video delivery scenarios characterized by bursty and frequent packet losses, such as wireless multihop environments.This research was supported by the Spanish Ministry of Education and Science under Grant no. TIN2011-27543-C0303.S.Martinez-Rach, MO.; Pinol, P.; Lopez, OM.; Perez Malumbres, M.; Oliver Gil, JS.; Tavares De Araujo Cesariny Calafate, CM. (2014). On the Performance of video quality assessment metrics under different compression and packet llss scenariov. Scientific World Journal. 2014:1-18. doi:10.1155/2014/743604S118201

Multiancestry analysis of the HLA locus in Alzheimer's and Parkinson's diseases uncovers a shared adaptive immune response mediated by HLA-DRB1*04 subtypes

11 páginas, 4 figuras, 2 tablas. Datasets en su material suplementario. This article contains supporting information online at https://www.pnas.org/lookup/suppl/doi:10.1073/pnas.2302720120/-/DCSupplemental.Across multiancestry groups, we analyzed Human Leukocyte Antigen (HLA) associations in over 176,000 individuals with Parkinson's disease (PD) and Alzheimer's disease (AD) versus controls. We demonstrate that the two diseases share the same protective association at the HLA locus. HLA-specific fine-mapping showed that hierarchical protective effects of HLA-DRB1*04 subtypes best accounted for the association, strongest with HLA-DRB1*04:04 and HLA-DRB1*04:07, and intermediary with HLA-DRB1*04:01 and HLA-DRB1*04:03. The same signal was associated with decreased neurofibrillary tangles in postmortem brains and was associated with reduced tau levels in cerebrospinal fluid and to a lower extent with increased Aβ42. Protective HLA-DRB1*04 subtypes strongly bound the aggregation-prone tau PHF6 sequence, however only when acetylated at a lysine (K311), a common posttranslational modification central to tau aggregation. An HLA-DRB1*04-mediated adaptive immune response decreases PD and AD risks, potentially by acting against tau, offering the possibility of therapeutic avenues.This work was supported by the Michael J. Fox Foundation grant MJFF-020161 (E.M., Z.G.-O.), NIH and National Institute of Aging grants AG060747 (M.D.G.), AG066206 (Z.H.), AG066515 (Z.H., M.D.G.), the European Union’s Horizon 2020 research and innovation program under the Marie Skłodowska-Curie (grant agreement No. 890650, Y.L.G.), the Alzheimer’s Association (AARF-20-683984, M.E.B.), and the Iqbal Farrukh and Asad Jamal Fund, a grant from the EU Joint Programme—Neurodegenerative Disease Research (European Alzheimer DNA BioBank, EADB; JPND), the Japan Agency for Medical Research and Development JP21dk0207045 (T.I.), JP21dk020704 (K.O., S.N.), JP21km040550 (K.O.), the Einstein Center for Neurosciences in Berlin (S.M.Y.), the Swedish Research Council (#2018-02532, H.Z.), the European Research Council (#681712, H.Z.), and the Swedish State Support for Clinical Research (#ALFGBG-720931, H.Z.). Inserm UMR1167 is also funded by the Inserm, Institut Pasteur de Lille, Lille Métropole Communauté Urbaine, and the French government’s LABEX DISTALZ program (development of innovative strategies for a transdisciplinary approach to AD). Additional funders of individual investigators and institutions who contributed to data collection and genotyping are provided in SI Appendix.Peer reviewe

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

Saltar la barrera : crisis socio-ambiental, resistencias populares y construcción de alternativas latinoamericanas al neoliberalismo

La sociedad contemporánea se encuentra en un proceso de crisis, de transformación y ajustes, pero también de construcción de alternativas al orden neoliberal consolidado durante los últimos cuarenta años, tanto en América Latina como en el mundo, por acción de gobiernos civiles y/o militares. Las consecuencias de la implementación de este modelo plantean importantes desafíos para los movimientos populares y especialmente para los trabajadores y trabajadoras, retos derivados de las profundas y rápidas transformaciones ocurridas en el mundo del trabajo, en las relaciones entre desarrollo y naturaleza, pero también en las estrategias de participación política de los sectores progresistas. En el centro de esta publicación, se encuentra la pregunta por un futuro posible, pensado desde las distintas realidades Latinoamericanas

Democracia versus neoliberalismo : 25 años de neoliberalismo en Chile

El diagnóstico crítico sobre las consecuencias del sistema político económico instalado en Chile durante la dictadura militar de Pinochet parece consolidarse después de varias décadas de funcionamiento del modelo. Comienza a tomar fuerza a partir de las movilizaciones sociales ocurridas entre el 2006 y el 2011, y hoy muchos afirman la inauguración de un nuevo ciclo político, uno auspicioso para las demandas de millones de chilenos y chilenas que vieron cómo las conquistas sociales alcanzadas durante el siglo veinte por amplios sectores de la sociedad chilena, fueron abolidas y los derechos de las nuevas generaciones, conculcados. Hoy se abre la posibilidad de construir una nueva carta constitucional y de avanzar hacia una democracia efectiva que incluya a todos los sectores de la sociedad chilena. Sin embargo, el diagnóstico también es claro en afirmar que la inauguración de este ciclo no depende únicamente del sistema político que cree la nueva constitución, sino que principalmente del tránsito hacia un nuevo modelo de desarrollo. Este tránsito será demandante para todos los actores de la sociedad y especialmente para las organizaciones y los movimientos sociales, puesto que frente a la posibilidad también se abre un espacio de enorme disputa entre las clases que se han beneficiado del modelo por décadas, concentrando grandes cuotas de poder político y económico, y la gran mayoría de los chilenos y chilenas que han sufrido la desigualdad y la injusticia, asumiendo la mayor parte del riesgo por el crecimiento económico del país

Genetic Associations between Modifiable Risk Factors and Alzheimer Disease

Importance: An estimated 40% of dementia is potentially preventable by modifying 12 risk factors throughout the life course. However, robust evidence for most of these risk factors is lacking. Effective interventions should target risk factors in the causal pathway to dementia. Objective: To comprehensively disentangle potentially causal aspects of modifiable risk factors for Alzheimer disease (AD) to inspire new drug targeting and improved prevention. Design, Setting, and Participants: This genetic association study was conducted using 2-sample univariable and multivariable mendelian randomization. Independent genetic variants associated with modifiable risk factors were selected as instrumental variables from genomic consortia. Outcome data for AD were obtained from the European Alzheimer & Dementia Biobank (EADB), generated on August 31, 2021. Main analyses were conducted using the EADB clinically diagnosed end point data. All analyses were performed between April 12 and October 27, 2022. Exposures: Genetically determined modifiable risk factors. Main Outcomes and Measures: Odds ratios (ORs) and 95% CIs for AD were calculated per 1-unit change of genetically determined risk factors. Results: The EADB-diagnosed cohort included 39106 participants with clinically diagnosed AD and 401577 control participants without AD. The mean age ranged from 72 to 83 years for participants with AD and 51 to 80 years for control participants. Among participants with AD, 54% to 75% were female, and among control participants, 48% to 60% were female. Genetically determined high-density lipoprotein (HDL) cholesterol concentrations were associated with increased odds of AD (OR per 1-SD increase, 1.10 [95% CI, 1.05-1.16]). Genetically determined high systolic blood pressure was associated with increased risk of AD after adjusting for diastolic blood pressure (OR per 10-mm Hg increase, 1.22 [95% CI, 1.02-1.46]). In a second analysis to minimize bias due to sample overlap, the entire UK Biobank was excluded from the EADB consortium; odds for AD were similar for HDL cholesterol (OR per 1-SD unit increase, 1.08 [95% CI, 1.02-1.15]) and systolic blood pressure after adjusting for diastolic blood pressure (OR per 10-mm Hg increase, 1.23 [95% CI, 1.01-1.50]). Conclusions and Relevance: This genetic association study found novel genetic associations between high HDL cholesterol concentrations and high systolic blood pressure with higher risk of AD. These findings may inspire new drug targeting and improved prevention implementation

Multiancestry analysis of the HLA locus in Alzheimer's and Parkinson's diseases uncovers a shared adaptive immune response mediated by HLA-DRB1*04 subtypes

Abstract: Across multiancestry groups, we analyzed Human Leukocyte Antigen (HLA) associations in over 176,000 individuals with Parkinson's disease (PD) and Alzheimer's disease (AD) versus controls. We demonstrate that the two diseases share the same protective association at the HLA locus. HLA-specific fine-mapping showed that hierarchical protective effects of HLA-DRB1*04 subtypes best accounted for the association, strongest with HLA-DRB1*04:04 and HLA-DRB1* 04:07, and intermediary with HLA-DRB1* 04:01 and HLA- DRB1*04:03. The same signal was associated with decreased neurofibrillary tangles in postmortem brains and was associated with reduced tau levels in cerebrospinal fluid and to a lower extent with increased A beta 42. Protective HLA-DRB1*04 subtypes strongly bound the aggregation-prone tau PHF6 sequence, however only when acetylated at a lysine (K311), a common posttranslational modification central to tau aggregation. An HLA-DRB1*04-mediated adaptive immune response decreases PD and AD risks, potentially by acting against tau, offering the possibility of therapeutic avenues