Challenges for Model-Driven Development of Strategically Aligned Information Systems

[EN] Model-Driven Development (MDD) has been proposed as an alternative to the traditional development of information systems, given its ability to integrate different stakeholders into the information system engineering process. Currently, longtime researched MDD methods and modern no-code and low-code platforms support the generation of the working code of the information system and services. However, in today's continuously changing environment, organisations need to align the information systems and services with the business structure, strategy, and processes they support. This article shows the design challenges for integrating business strategy information into a model-driven development method. We applied a set of mechanism experiments on an MDD method composed of three modelling frameworks with demonstrated semantic consistency, that covers the organisational, business process, and information system levels to identify information loss and transformation coverage issues that prevent the generation of information systems and services that are strategically aligned. The challenges were discussed with experts, confirming the relevance of avoiding the overlapping between the strategic and business process concepts, providing organisational-level constructs to express strategic ends and means, and considering the organisational structure in the modular design of business process and information systems and services.This work was supported in part by the Spanish State Research Agency and the Generalitat Valenciana under Project MICIN/AEI/10.13039/501100011033, Project GV/2021/072, and Project INNEST/2021/57 by Agencia Valenciana de Innovacion (AVI); in part by the European Regional Development Fund (ERDF), the European Union Next Generation, and Plan de Recuperacion, Transformacion y Resiliencia (PRTR); and in part by the National Agency for Research and Development (ANID)/Scholarship Program/Doctorado Becas Chile under Grant 2020-72210494.Noel-Lopez, R.; Panach, JI.; Pastor López, O. (2022). Challenges for Model-Driven Development of Strategically Aligned Information Systems. IEEE Access. 10:38237-38253. https://doi.org/10.1109/ACCESS.2022.316222538237382531

Generación de Modelos de Requisitos a partir de Modelos Organizacionales: Un enfoque basado en patrones

RESUMENActualmente, la fase temprana de la Ingeniería de Requisitos, en la cual se aborda el estudio de la organización en la cual seimplantará el sistema de software, es un área incipiente de investigación para múltiples grupos de investigación en el mundo. Enesta área se utilizan modelos que permiten describir una organización utilizando actores, metas, procesos organizacionales yrelaciones entre actores. Por otra parte, la fase tardía de la Ingeniería de Requisitos (Requisitos tardíos), donde se analiza lafuncionalidad esperada del sistema de información, cuenta actualmente con un nivel mayor de madurez, ya que existen múltiplestécnicas y herramientas para describir el sistema de software que se va a desarrollar, dentro de su ambiente operacional, junto consus funciones y cualidades relevantes. Sin embargo, a pesar de que existen metodologías que dan soporte en forma separada aestas dos fases de la Ingeniería de Requisitos, se ha descuidado el desarrollo de técnicas que permitan derivar, en formametodológica un modelo de requisitos tardíos a partir de los requisitos tempranos. Esto es debido, en gran medida a la grandiferencia entre los niveles de abstracción que existen entre estas dos especificaciones. Por lo tanto el objetivo de este trabajo esproporcionar reglas sistemáticas para generar requisitos de sistemas de información a partir de la información relevante de unmodelo organizacional. PALABRAS CLAVESModelado organizacional,Modelo de requisitos, Casos de uso,Lenguajes de patrones

Integrating the goal and business process perspectives in information system analysis

There are several motivations to promote investment and scientific effort in the integration of intentional and operational perspectives: organisational reengineering, continuous improvement of business processes, alignment among complementary analysis perspectives, information traceability, etc. In this paper we propose the integration of two modelling languages that support the creation of goal and business process models: the i* goal-oriented modelling method and Communication Analysis, a communication-oriented business process modelling method. We describe the methodological integration of the two modelling methods with the aim of fulfilling several criteria: i) to rely on appropriate theories; ii) to provide abstract and concrete syntaxes; iii) to provide scenarios of application; and iv) to develop tool support. We provide guidelines for using the two modelling methods in a top-down analysis scenario. We also present an illustrative case that demonstrates the feasibility of the approach.Peer ReviewedPostprint (author's final draft

Liver-specific insulin receptor isoform A expression enhances hepatic glucose uptake and ameliorates liver steatosis in a mouse model of diet-induced obesity

Among the main complications associated with obesity are insulin resistance and altered glucose and lipid metabolism within the liver. It has previously been described that insulin receptor isoform A (IRA) favors glucose uptake and glycogen storage in hepatocytes compared with isoform B (IRB), improving glucose homeostasis in mice lacking liver insulin receptor. Thus, we hypothesized that IRA could also improve glucose and lipid metabolism in a mouse model of high-fatdiet-induced obesity. We addressed the role of insulin receptor isoforms in glucose and lipid metabolism in vivo. We expressed IRA or IRB specifically in the liver by using adeno-associated viruses (AAVs) in a mouse model of diet-induced insulin resistance and obesity. IRA, but not IRB, expression induced increased glucose uptake in the liver and muscle, improving insulin tolerance. Regarding lipid metabolism, we found that AAV-mediated IRA expression also ameliorated hepatic steatosis by decreasing the expression of Fasn, Pgc1a, Acaca and Dgat2 and increasing Scd-1 expression. Taken together, our results further unravel the role of insulin receptor isoforms in hepatic glucose and lipid metabolism in an insulin-resistant scenario. Our data strongly suggest that IRA is more efficient than IRB at favoring hepatic glucose uptake, improving insulin tolerance and ameliorating hepatic steatosis. Therefore, we conclude that a gene therapy approach for hepatic IRA expression could be a safe and promising tool for the regulation of hepatic glucose consumption and lipid metabolism, two key processes in the development of non-alcoholic fatty liver disease associated with obesity

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

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

Search for dark matter produced in association with bottom or top quarks in √s = 13 TeV pp collisions with the ATLAS detector

A search for weakly interacting massive particle dark matter produced in association with bottom or top quarks is presented. Final states containing third-generation quarks and miss- ing transverse momentum are considered. The analysis uses 36.1 fb−1 of proton–proton collision data recorded by the ATLAS experiment at √s = 13 TeV in 2015 and 2016. No significant excess of events above the estimated backgrounds is observed. The results are in- terpreted in the framework of simplified models of spin-0 dark-matter mediators. For colour- neutral spin-0 mediators produced in association with top quarks and decaying into a pair of dark-matter particles, mediator masses below 50 GeV are excluded assuming a dark-matter candidate mass of 1 GeV and unitary couplings. For scalar and pseudoscalar mediators produced in association with bottom quarks, the search sets limits on the production cross- section of 300 times the predicted rate for mediators with masses between 10 and 50 GeV and assuming a dark-matter mass of 1 GeV and unitary coupling. Constraints on colour- charged scalar simplified models are also presented. Assuming a dark-matter particle mass of 35 GeV, mediator particles with mass below 1.1 TeV are excluded for couplings yielding a dark-matter relic density consistent with measurements

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