VIII Encuentro de Docentes e Investigadores en Historia del Diseño, la Arquitectura y la Ciudad

Acta de congresoLa conmemoración de los cien años de la Reforma Universitaria de 1918 se presentó como una ocasión propicia para debatir el rol de la historia, la teoría y la crítica en la formación y en la práctica profesional de diseñadores, arquitectos y urbanistas. En ese marco el VIII Encuentro de Docentes e Investigadores en Historia del Diseño, la Arquitectura y la Ciudad constituyó un espacio de intercambio y reflexión cuya realización ha sido posible gracias a la colaboración entre Facultades de Arquitectura, Urbanismo y Diseño de la Universidad Nacional y la Facultad de Arquitectura de la Universidad Católica de Córdoba, contando además con la activa participación de mayoría de las Facultades, Centros e Institutos de Historia de la Arquitectura del país y la región. Orientado en su convocatoria tanto a docentes como a estudiantes de Arquitectura y Diseño Industrial de todos los niveles de la FAUD-UNC promovió el debate de ideas a partir de experiencias concretas en instancias tales como mesas temáticas de carácter interdisciplinario, que adoptaron la modalidad de presentación de ponencias, entre otras actividades. En el ámbito de VIII Encuentro, desarrollado en la sede Ciudad Universitaria de Córdoba, se desplegaron numerosas posiciones sobre la enseñanza, la investigación y la formación en historia, teoría y crítica del diseño, la arquitectura y la ciudad; sumándose el aporte realizado a través de sus respectivas conferencias de Ana Clarisa Agüero, Bibiana Cicutti, Fernando Aliata y Alberto Petrina. El conjunto de ponencias que se publican en este Repositorio de la UNC son el resultado de dos intensas jornadas de exposiciones, cuyos contenidos han posibilitado actualizar viejos dilemas y promover nuevos debates. El evento recibió el apoyo de las autoridades de la FAUD-UNC, en especial de la Secretaría de Investigación y de la Biblioteca de nuestra casa, como así también de la Facultad de Arquitectura de la UCC; va para todos ellos un especial agradecimiento

Time-resolved, single-ended laser absorption thermometry and H 2 O, CO 2 , and CO speciation in a H 2 /C 2 H 4 -fueled rotating detonation engine

The article of record as published may be found at http://dx.doi.org/10.1016/j.proci.2020.06.125Proceedings of the Combustion Institute 38Rotating detonation engines (RDEs) require novel diagnostic tools to better understand complex detonation behavior and improve performance. To this end, a single-ended laser absorption sensor for in situ , time-resolved measurements of temperature, H 2 O, CO 2 , and CO concentrations has been developed and deployed within the annulus of a hydrogen/ethylene/air-fed RDE. With a measurement rate of 44 kS/s, the sensor delivers four co-aligned, mid-infrared laser beams into the annular detonation chamber and captures the back-reflected radiation through a single optical port. A ray-tracing optimization algorithm, designed to maximize signal-to-noise ratio and beam-perturbation tolerance, was used to determine the optimal sensor optical configuration. Wavelength-modulation spectroscopy (WMS) further compensated for interference sources in the harsh detonation environment. Time-resolved and time-averaged sensor measurements of gas temperature and species at equivalence ratios of 0.74, 0.87, and 1.03 are presented.Office of Naval ResearchInnovative Scientific Solution, Inc.Department of Defense through the National Defense Science and Engineering Graduate (NDSEG)N00014-15-P-112

Stabilized methods for high-speed compressible flows: toward hypersonic simulations

A stabilized finite element framework for high-speed compressible flows is presented. The Streamline-Upwind/Petrov–Galerkin formulation augmented with discontinuity-capturing (DC) are the main constituents of the framework that enable accurate, efficient, and stable simulations in this flow regime. Full- and reduced-energy formulations are employed for this class of flow problems and their relative accuracy is assessed. In addition, a recently developed DC formulation is presented and is shown to be particularly well suited for hypersonic flows. Several verification and validation cases, ranging from 1D to 3D flows and supersonic to the hypersonic regimes, show the excellent performance of the proposed framework and set the stage for its deployment on more advanced applications.This is a post-peer-review, pre-copyedit version of an article published in Computational Mechanics. The final authenticated version is available online at DOI: 10.1007/s00466-020-01963-6. Posted with permission.</p

Finite element methodology for modeling aircraft aerodynamics: development, simulation, and validation

In this work, we propose and validate a new stabilized compressible flow finite element framework for the simulation of aerospace applications. The framework is comprised of the streamline upwind/Petrov–Galerkin (SUPG)-based Navier–Stokes equations for compressible flows, the weakly enforced essential boundary conditions that act as a wall function, and the entropy-based discontinuity-capturing equation that acts as a shock-capturing operator. The accuracy and robustness of the framework is tested for various Mach numbers ranging from low-subsonic to transonic flow regimes. The aerodynamic simulations are carried out for 2D and 3D validation cases of flow around the NACA 0012 airfoil, RAE 2822 airfoil, ONERA M6 wing, and NASA Common Research Model (CRM) aircraft. The pressure coefficients obtained from the simulations of all cases are compared with experimental data. The computational results show good agreement with the experimental findings and demonstrate the accuracy and effectiveness of the finite element framework presented in this work for the simulation of aircraft aerodynamics.This article is published as Rajanna, Manoj R., Emily L. Johnson, David Codoni, Artem Korobenko, Yuri Bazilevs, Ning Liu, Jim Lua, Nam Phan, and Ming-Chen Hsu. "Finite element methodology for modeling aircraft aerodynamics: development, simulation, and validation." Computational Mechanics 70, no. 3 (2022): 549-563. DOI: 10.1007/s00466-022-02178-7. Works produced by employees of the U.S. Government as part of their official duties are not copyrighted within the U.S. The content of this document is not copyrighted

Finite Element Simulation and Validation for Aerospace Applications: Stabilized Methods, Weak Dirichlet Boundary Conditions, and Discontinuity Capturing for Compressible Flows

The objective of this work is to investigate and validate a new stabilized compressible flow finite element framework for the simulation of aerospace applications. The framework is comprised of the streamline upwind/Petrov–Galerkin (SUPG)-based Navier–Stokes equations for compressible flows, the weakly enforced essential boundary conditions that act as a wall function, and the entropy-based discontinuity-capturing equation that act as a shock-capturing operator. The accuracy and robustness of the framework is tested for various Mach numbers ranging from low-subsonic to transonic flow regimes. The aerodynamic simulations are carried out for 2D and 3D validation cases of flow around the NACA 0012 airfoil, RAE 2822 airfoil, ONERA M6 wing, and NASA Common Research Model (CRM) aircraft. The pressure coefficients obtained from the simulations of all cases are compared with experimental data. The computational results show good agreement with the experimental findings and demonstrate the accuracy and effectiveness of the finite element framework presented in this work for the simulation of aircraft aerodynamics.This proceeding is published as Rajanna, Manoj R., Emily L. Johnson, David Codoni, Artem Korobenko, Yuri Bazilevs, Ning Liu, Jim Lua, Nam D. Phan, and Ming-Chen Hsu. "Finite Element Simulation and Validation for Aerospace Applications: Stabilized Methods, Weak Dirichlet Boundary Conditions, and Discontinuity Capturing for Compressible Flows." In AIAA SCITECH 2022 Forum, p. 1077. 2022. DOI: 10.2514/6.2022-1077. Works produced by employees of the U.S. Government as part of their official duties are not copyrighted within the U.S. The content of this document is not copyrighted

miR-322 regulates insulin signaling pathway and protects against metabolic syndrome-induced cardiac dysfunction in mice.

We identified murine miR-322, orthologous to human miR-424, as a new regulator of insulin receptor, IGF-1 receptor and sirtuin 4 mRNA in vitro and in vivo in the heart and found that miR-322/424 is highly expressed in the heart of mice. C57Bl/6N mice fed 10weeks of high fat diet (HFD) presented signs of cardiomyopathy and a stable miR-322 cardiac level while cardiac function was slightly affected in 11week-old ob/ob which overexpressed miR-322. We thus hypothesized that mmu-miR-322 could be protective against cardiac consequences of hyperinsulinemia and hyperlipidemia. We overexpressed or knocked-down mmu-miR-322 using AAV9 and monitored cardiac function in wild-type C57Bl/6N mice fed a control diet (CD) or a HFD and in ob/ob mice. The fractional shortening progressively declined while the left ventricle systolic diameter increased in HFD mice infected with an AAVcontrol or with an AAVsponge (decreasing miR-322 bioavailability) but also in ob/ob mice infected with AAVsponge. Similar observations were also found in CD-fed mice infected with AAVsponge. On the contrary over-expressing miR-322 with AAVmiR-322 was efficient in protecting the heart from HFD effects in C57Bl/6N mice. This cardioprotection could be associated with the regulation of identified targets IGF1R, INSR and CD1, a decrease in insulin signaling pathway and an enrichment of genes involved in mitochondrial function and fatty acid oxidation as demonstrated by transcriptome analysis. Altogether, these results emphasize miR-322 as a new potential therapeutic target against cardiac consequences of metabolic syndrome, which represents an increasing burden in the western countries

Preservation Analysis of Macrophage Gene Coexpression Between Human and Mouse Identifies PARK2 as a Genetically Controlled Master Regulator of Oxidative Phosphorylation in Humans

Macrophages are key players involved in numerous pathophysiological pathways and an in-depth characterization of their gene regulatory networks can help in better understanding how their dysfunction may impact on human diseases. We here conducted a cross-species network analysis of macrophage gene expression data between human and mouse to identify conserved networks across both species, and assessed whether such networks could reveal new disease-associated regulatory mechanisms. From a sample of 684 individuals processed for genome-wide macrophage gene expression profiling, we identified 27 groups of coexpressed genes (modules). Six modules were found preserved (P < 10−4) in macrophages from 86 mice of the Hybrid Mouse Diversity Panel. One of these modules was significantly [false discovery rate (FDR) = 8.9 × 10−11] enriched for genes belonging to the oxidative phosphorylation (OXPHOS) pathway. This pathway was also found significantly (FDR < 10−4) enriched in susceptibility genes for Alzheimer, Parkinson, and Huntington diseases. We further conducted an expression quantitative trait loci analysis to identify SNP that could regulate macrophage OXPHOS gene expression in humans. This analysis identified the PARK2 rs192804963 as a trans-acting variant influencing (minimal P-value = 4.3 × 10−8) the expression of most OXPHOS genes in humans. Further experimental work demonstrated that PARK2 knockdown expression was associated with increased OXPHOS gene expression in THP1 human macrophages. This work provided strong new evidence that PARK2 participates to the regulatory networks associated with oxidative phosphorylation and suggested that PARK2 genetic variations could act as a trans regulator of OXPHOS gene macrophage expression in humans

Shared genetic regulatory networks for cardiovascular disease and type 2 diabetes in multiple populations of diverse ethnicities in the United States

Cardiogenics ConsortiumInternational audienceCardiovascular diseases (CVD) and type 2 diabetes (T2D) are closely interrelated complex diseases likely sharing overlapping pathogenesis driven by aberrant activities in gene networks. However, the molecular circuitries underlying the pathogenic commonalities remain poorly understood. We sought to identify the shared gene networks and their key intervening drivers for both CVD and T2D by conducting a comprehensive integrative analysis driven by five multi-ethnic genome-wide association studies (GWAS) for CVD and T2D, expression quantitative trait loci (eQTLs), ENCODE, and tissue-specific gene network models (both co-expression and graphical models) from CVD and T2D relevant tissues. We identified pathways regulating the metabolism of lipids, glucose, and branched-chain amino acids, along with those governing oxidation, extracellular matrix, immune response, and neuronal system as shared pathogenic processes for both diseases. Further, we uncovered 15 key drivers including HMGCR, CAV1, IGF1 and PCOLCE, whose network neighbors collectively account for approximately 35% of known GWAS hits for CVD and 22% for T2D. Finally, we cross-validated the regulatory role of the top key drivers using in vitro siRNA knockdown, in vivo gene knockout, and two Hybrid Mouse Diversity Panels each comprised of >100 strains. Findings from this in-depth assessment of genetic and functional data from multiple human cohorts provide strong support that common sets of tissue-specific molecular networks drive the pathogenesis of both CVD and T2D across ethnicities and help prioritize new therapeutic avenues for both CVD and T2D

Computational analysis of 10,860 phenotypic annotations in individuals with SCN2A-related disorders.

PURPOSE: Pathogenic variants in SCN2A cause a wide range of neurodevelopmental phenotypes. Reports of genotype-phenotype correlations are often anecdotal, and the available phenotypic data have not been systematically analyzed. METHODS: We extracted phenotypic information from primary descriptions of SCN2A-related disorders in the literature between 2001 and 2019, which we coded in Human Phenotype Ontology (HPO) terms. With higher-level phenotype terms inferred by the HPO structure, we assessed the frequencies of clinical features and investigated the association of these features with variant classes and locations within the Na(V)1.2 protein. RESULTS: We identified 413 unrelated individuals and derived a total of 10,860 HPO terms with 562 unique terms. Protein-truncating variants were associated with autism and behavioral abnormalities. Missense variants were associated with neonatal onset, epileptic spasms, and seizures, regardless of type. Phenotypic similarity was identified in 8/62 recurrent SCN2A variants. Three independent principal components accounted for 33% of the phenotypic variance, allowing for separation of gain-of-function versus loss-of-function variants with good performance. CONCLUSION: Our work shows that translating clinical features into a computable format using a standardized language allows for quantitative phenotype analysis, mapping the phenotypic landscape of SCN2A-related disorders in unprecedented detail and revealing genotype-phenotype correlations along a multidimensional spectrum