Microstructure-guided numerical simulations to predict the thermal performance of a hierarchical cement-based composite material

This paper presents a microstructure-guided numerical homogenization technique to predict the effective thermal conductivity of a hierarchical cement-based material containing phase change material (PCM)-impregnated lightweight aggregates (LWA). Porous inclusions such as LWAs embedded in a cementitious matrix are filled with multiple fluid phases including PCM to obtain desirable thermal properties for building and infrastructure applications. Simulations are carried out on realistic three-dimensional microstructures generated using pore structure information. An inverse analysis procedure is used to extract the intrinsic thermal properties of those microstructural components for which data is not available. The homogenized heat flux is predicted for an imposed temperature gradient from which the effective composite thermal conductivity is computed. The simulated effective composite thermal conductivities are found to correlate very well with experimental measurements for a family of LWA-PCM composites considered in the paper. Comparisons with commonly used analytical homogenization models show that the microstructure-guided simulation approach provides superior results for composites exhibiting large property contrast between phases. By linking the microstructure and thermal properties of hierarchical materials, an efficient framework is available for optimizing the material design to improve thermal efficiency of a wide variety of heterogeneous materials

First Principles-Based Design of Economical Ultra-High Performance Concrete

This paper presents a novel strategy to design the binder phase of ultra-high performance concrete (UHPC) from commonly available cement replacement (fly ash, slag, microsilica, metakaolin) and fine filler (limestone) materials. A packing algorithm is used to extract the number density, mean centroidal distance, and coordination number of the microstructure. Similarly, rheological studies on the pastes provide yield stress, plastic viscosity, and mini-slump spread. The selection criteria involves using the three microstructural and three rheological parameters individually or in combination to define packing and flow coefficients. The selection criteria is flexible enough to allow users modify the constraints depending on the application. The binder with the desired packing and rheological features is combined with aggregate sizes and amounts chosen from a compressible packing model based on maximum packing density. A fiber volume fraction of 1% is also used, along with accommodations for wall and loosening effects. The model is programmed in a userfriendly environment to enable engineers select aggregates from locally available materials. Compressive strengths greater than 150 MPa are obtained for the selected UHPC mixtures after 28 days of moist curing. The strength-normalized cost of such mixtures is only a fraction of that of proprietary UHPCs

Concert recording 2022-04-28

[Track 1]. Por una cabeza / Carlos Gardel ; arr. Dominic Na ; [Track 2]. Concerto in G minor for two cellos, RV. 531. I. Allegro / Antonio Vivaldi ; arr. Dominic Na ; [Track 3]. Sonata in G major. I. Allegro non troppo / Giovanni Battista Sammartini ; arr. Dominic Na ; [Track 4]. Salut d\u27amour, op. 12 / Edward Elgar ; arr. Dominic Na ; [Track 5]. Adoration / Florence Price ; arr. Dominic Na ; [Track 6]. Kol Nidrei, op. 47 / Max Bruch ; arr. Dominic Na ; [Track 7]. Concerto in G minor for two cellos, RV. 531. I. Adagio-moderato, Allegro molto / Antonio Vivaldi ; arr. Dominic Na ; [Track 8]. Liebesfreud from Three old Viennese dances. I. Allegro / Fritz Kreisler ; arr. Dominic Na

Concert recording 2022-04-28

[Track 1]. Por una cabeza / Carlos Gardel ; arr. Dominic Na ; [Track 2]. Concerto in G minor for two cellos, RV. 531. I. Allegro / Antonio Vivaldi ; arr. Dominic Na ; [Track 3]. Sonata in G major. I. Allegro non troppo / Giovanni Battista Sammartini ; arr. Dominic Na ; [Track 4]. Salut d\u27amour, op. 12 / Edward Elgar ; arr. Dominic Na ; [Track 5]. Adoration / Florence Price ; arr. Dominic Na ; [Track 6]. Kol Nidrei, op. 47 / Max Bruch ; arr. Dominic Na ; [Track 7]. Concerto in G minor for two cellos, RV. 531. I. Adagio-moderato, Allegro molto / Antonio Vivaldi ; arr. Dominic Na ; [Track 8]. Liebesfreud from Three old Viennese dances. I. Allegro / Fritz Kreisler ; arr. Dominic Na

Anti–miR-93-5p therapy prolongs sepsis survival by restoring the peripheral immune response

Sepsis remains a leading cause of death for humans and currently has no pathogenesis-specific therapy. Hampered progress is partly due to a lack of insight into deep mechanistic processes. In the past decade, deciphering the functions of small noncoding miRNAs in sepsis pathogenesis became a dynamic research topic. To screen for new miRNA targets for sepsis therapeutics, we used samples for miRNA array analysis of PBMCs from patients with sepsis and control individuals, blood samples from 2 cohorts of patients with sepsis, and multiple animal models: mouse cecum ligation puncture–induced (CLP-induced) sepsis, mouse viral miRNA challenge, and baboon Gram+ and Gram– sepsis models. miR-93-5p met the criteria for a therapeutic target, as it was overexpressed in baboons that died early after induction of sepsis, was downregulated in patients who survived after sepsis, and correlated with negative clinical prognosticators for sepsis. Therapeutically, inhibition of miR-93-5p prolonged the overall survival of mice with CLP-induced sepsis, with a stronger effect in older mice. Mechanistically, anti–miR-93-5p therapy reduced inflammatory monocytes and increased circulating effector memory T cells, especially the CD4+ subset. AGO2 IP in miR-93–KO T cells identified important regulatory receptors, such as CD28, as direct miR-93-5p target genes. In conclusion, miR-93-5p is a potential therapeutic target in sepsis through the regulation of both innate and adaptive immunity, with possibly a greater benefit for elderly patients than for young patients

Dissecting the Shared Genetic Architecture of Suicide Attempt, Psychiatric Disorders, and Known Risk Factors

Background Suicide is a leading cause of death worldwide, and nonfatal suicide attempts, which occur far more frequently, are a major source of disability and social and economic burden. Both have substantial genetic etiology, which is partially shared and partially distinct from that of related psychiatric disorders. Methods We conducted a genome-wide association study (GWAS) of 29,782 suicide attempt (SA) cases and 519,961 controls in the International Suicide Genetics Consortium (ISGC). The GWAS of SA was conditioned on psychiatric disorders using GWAS summary statistics via multitrait-based conditional and joint analysis, to remove genetic effects on SA mediated by psychiatric disorders. We investigated the shared and divergent genetic architectures of SA, psychiatric disorders, and other known risk factors. Results Two loci reached genome-wide significance for SA: the major histocompatibility complex and an intergenic locus on chromosome 7, the latter of which remained associated with SA after conditioning on psychiatric disorders and replicated in an independent cohort from the Million Veteran Program. This locus has been implicated in risk-taking behavior, smoking, and insomnia. SA showed strong genetic correlation with psychiatric disorders, particularly major depression, and also with smoking, pain, risk-taking behavior, sleep disturbances, lower educational attainment, reproductive traits, lower socioeconomic status, and poorer general health. After conditioning on psychiatric disorders, the genetic correlations between SA and psychiatric disorders decreased, whereas those with nonpsychiatric traits remained largely unchanged. Conclusions Our results identify a risk locus that contributes more strongly to SA than other phenotypes and suggest a shared underlying biology between SA and known risk factors that is not mediated by psychiatric disorders.Peer reviewe

Elucidating the influences of compliant microscale inclusions on the fracture behavior of cementitious composites

The fracture response of cementitious composites containing compliant microencapsulated inclusions and its influence on the fracture process zone (FPZ) are reported. The incorporation of small amounts of phase change material (PCM) microcapsules (replacing up to 10% by volume of sand) is found to slightly improve the strength, fracture toughness, critical crack tip opening displacement (CTODc), and the strain energy release rates. Digital image correlation is used to examine the FPZ at the tip of the advancing crack, to better explain the influences of compliant microscale inclusions on energy dissipation. The FPZ widths are found to slightly increase with PCM dosage but its lengths remain unchanged. The increase in FPZ width is linearly related to the CTODc, showing that inelastic deformations of the crack-tip in the direction of crack opening are indeed influenced by microscale inclusions. It is shown that cementitious systems containing microencapsulated PCMs can be designed to demonstrate mechanical performance (including fracture) equivalent to or even better than their PCM-free counterparts, in addition to the well-described thermal performance

HIF-2α Preserves Mitochondrial Activity and Glucose Sensing in Compensating β-Cells in Obesity.

In obesity, increased mitochondrial metabolism with the accumulation of oxidative stress leads to mitochondrial damage and β-cell dysfunction. In particular, β-cells express antioxidant enzymes at relatively low levels and are highly vulnerable to oxidative stress. Early in the development of obesity, β-cells exhibit increased glucose-stimulated insulin secretion in order to compensate for insulin resistance. This increase in β-cell function under the condition of enhanced metabolic stress suggests that β-cells possess a defense mechanism against increased oxidative damage, which may become insufficient or decline at the onset of type 2 diabetes. Here, we show that metabolic stress induces β-cell hypoxia inducible factor 2α (HIF-2α), which stimulates antioxidant gene expression (e.g., Sod2 and Cat) and protects against mitochondrial reactive oxygen species (ROS) and subsequent mitochondrial damage. Knockdown of HIF-2α in Min6 cells exaggerated chronic high glucose-induced mitochondrial damage and β-cell dysfunction by increasing mitochondrial ROS levels. Moreover, inducible β-cell HIF-2α knockout mice developed more severe β-cell dysfunction and glucose intolerance on a high-fat diet, along with increased ROS levels and decreased islet mitochondrial mass. Our results provide a previously unknown mechanism through which β-cells defend against increased metabolic stress to promote β-cell compensation in obesity