¿HAY INCONMENSURABILIDAD TECNOLÓGICA?

Mediante la noción matemática de inconmensurabilidad, Kuhn indicó la falta de un lenguaje común que hiciese posible la traducción de los términos que se emplean de ordinario en las teorías científicas. Sin embargo, Kuhn no extendió el alcance de la relación de inconmensurabilidad al dominio de la tecnología, aunque recurrió a él para ilustrar este fenómeno semántico. Pese a lo controversial que pueda resultar, en este trabajo mostraré que la historia de la tecnología proporciona la evidencia necesaria a favor de la tesis de que hay inconmensurabilidad tecnológica. Para ello, examinaré dicha tesis y explicaré cómo operaría en el dominio de la tecnología. También analizaré dos casos históricos a su favor. El primero proviene de la sustitución de la teoría del contacto de la pila voltaica por la teoría química de la batería. El segundo caso se da a partir deltránsito de la teoría material del calor a la termodinámica. &nbsp

Verifying Policy Enforcers

Policy enforcers are sophisticated runtime components that can prevent failures by enforcing the correct behavior of the software. While a single enforcer can be easily designed focusing only on the behavior of the application that must be monitored, the effect of multiple enforcers that enforce different policies might be hard to predict. So far, mechanisms to resolve interferences between enforcers have been based on priority mechanisms and heuristics. Although these methods provide a mechanism to take decisions when multiple enforcers try to affect the execution at a same time, they do not guarantee the lack of interference on the global behavior of the system. In this paper we present a verification strategy that can be exploited to discover interferences between sets of enforcers and thus safely identify a-priori the enforcers that can co-exist at run-time. In our evaluation, we experimented our verification method with several policy enforcers for Android and discovered some incompatibilities.Comment: Oliviero Riganelli, Daniela Micucci, Leonardo Mariani, and Yli\`es Falcone. Verifying Policy Enforcers. Proceedings of 17th International Conference on Runtime Verification (RV), 2017. (to appear

Expected Constant Round Byzantine Broadcast under Dishonest Majority

Byzantine Broadcast (BB) is a central question in distributed systems, and an important challenge is to understand its round complexity. Under the honest majority setting, it is long known that there exist randomized protocols that can achieve BB in expected constant rounds, regardless of the number of nodes $n$. However, whether we can match the expected constant round complexity in the corrupt majority setting --- or more precisely, when $f \geq n/2 + \omega(1)$ --- remains unknown, where $f$ denotes the number of corrupt nodes. In this paper, we are the first to resolve this long-standing question. We show how to achieve BB in expected $O((n/(n-f))^2)$ rounds. Our results hold under both a static adversary and a weakly adaptive adversary who cannot perform ``after-the-fact removal\u27\u27 of messages already sent by a node before it becomes corrupt

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

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

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