Hindered thermal warping triggers tensile cracking in the cores of compressed columns of a fire-loaded tunnel segment structure: Efficiency and accuracy of beam theory prediction, compared to FEM

The nonlinear Finite Element Method (FEM) is the current gold standard for the thermo-mechanical analysis of reinforced concrete structures. As an alternative, this paper is devoted to a model reduction strategy which reduces the CPU time by a factor of 500. This strategy combines Fourier series-based solutions for the thermal conduction problem, and thermo-elastic Timoshenko beam theory. Temperature histories known to be relevant for fire accidents enter series solutions quantifying the conduction of heat into a closed cell frame consisting of slabs, walls, and columns. Corresponding temperature profiles are translated into thermal eigenstrains. The latter are represented as the sum of three portions: (i) their cross-sectional averages (called thermal eigenstretches); (ii) their cross-sectional moments (called thermal eigencurvatures); and (iii) the remaining eigenstrain distributions (called eigenwarping). The latter portion is hindered at the cross-sectional scale, giving rise to non-linearly distributed self-equilibrated thermal stresses. The eigenstretches and eigencurvatures, in turn, are constrained at the scale of the frame structure. Together with external mechanical loads, they enter the exact solutions of thermo-elastic Timoshenko beam theory with equivalent cross-sections accounting for the different material properties of concrete and steel. Axial normal stresses, quantified from beam-theory-related normal forces and bending moments, are superimposed with the hindered-warping-induced stresses. These stresses agree well with corresponding results obtained by the nonlinear FEM. As regards the load carrying behavior of the columns, excessive thermal tensile strains at the periphery of the columns trigger, in the core of the columns, large tensile stresses which even exceed the strength of concrete. Respective cracking events are considered through reduced effective columnar cross-sections. Right after initiation of cracking, around 12min after the start of the heating process, the cracks propagate for some 30sec quite rapidly, and very much slower thereafter. If the initial cross-sections of the columns are increased, more pronounced hindered thermal warping, together with less quickly evolving compressive forces, results in earlier cracking. Overall, it is concluded that tensile cracking is the key material non-linearity, at least during the first 30min of the fire test, with maximum temperatures up to 300°C

High-dynamic compressive and tensile strength of specimens made of cementitious materials

The strength of specimens made of cementitious materials increases with increasing loading rate. Herein, themodel of Fischer et al. (CCR 58, 2014, 186–200) is revisited in the context of high-dynamic compression andextended to high-dynamic tension. The model is based on the assumptions (i) that cracking will start if the quasistaticmaterial strength is reached, and (ii) that the high-dynamic strength gain refers to the increase of the stressduring the failure process of the tested specimen. The model explains the behavior of cylindrical specimens madeof dry cement paste, mortar, and concrete, subjected to high-dynamic compression. It also elucidates the performanceof cylindrical specimens made of dry mortar and concrete, subjected to high-dynamic tension. It isconcluded that the high-dynamic strength gain is a structural effect and that structures will be damaged if thedynamic stress exceeds the quasi-static strength, no matter how fast the stress is increased and how short thestress pulse lasts.Austrian Science Fund (FWF

Novel loci for adiponectin levels and their influence on type 2 diabetes and metabolic traits: A multi-ethnic meta-analysis of 45,891 individuals

Circulating levels of adiponectin, a hormone produced predominantly by adipocytes, are highly heritable and are inversely associated with type 2 diabetes mellitus (T2D) and other metabolic traits. We conducted a meta-analysis of genome-wide association studies in 39,883 individuals of European ancestry to identify genes associated with metabolic disease. We identified 8 novel loci associated with adiponectin levels and confirmed 2 previously reported loci (P = 4.5×10−8- 1.2 ×10−43). Using a novel method to combine data across ethnicities (N = 4,232 African Americans, N = 1,776 Asians, and N = 29,347 Europeans), we identified two additional novel loci. Expression analyses of 436 human adipocyte samples revealed that mRNA levels of 18 genes at candidate regions were associated with adiponectin concentrations after accounting for multiple testing (p<3×10−4). We next developed a multi-SNP genotypic risk score to test the association of adiponectin decreasing risk alleles on metabolic traits and diseases using consortia-level meta-analytic data. This risk score was associated with increased risk of T2D (p = 4.3×10−3, n = 22,044), increased triglycerides (p = 2.6×10−14, n = 93,440), increased waist-to-hip ratio (p = 1.8×10−5, n = 77,167), increased glucose two hours post oral glucose tolerance testing (p = 4.4×10−3, n = 15,234), increased fasting insulin (p = 0.015, n = 48,238), but with lower in HDL- cholesterol concentrations (p = 4.5×10−13, n = 96,748) and decreased BMI (p = 1.4×10−4, n = 121,335). These findings identify novel genetic determinants of adiponectin levels, which, taken together, influence risk of T2D and markers of insulin resistance

Genome-wide association identifies nine common variants associated with fasting proinsulin levels and provides new insights into the pathophysiology of type 2 diabetes

OBJECTIVE - Proinsulin is a precursor of mature insulin and C-peptide. Higher circulating proinsulin levels are associated with impaired b-cell function, raised glucose levels, insulin resistance, and type 2 diabetes (T2D). Studies of the insulin processing pathway could provide new insights about T2D pathophysiology. RESEARCH DESIGN AND METHODS - We have conducted a meta-analysis of genome-wide association tests of ;2.5 million genotyped or imputed single nucleotide polymorphisms (SNPs) and fasting proinsulin levels in 10,701 nondiabetic adults of European ancestry, with follow-up of 23 loci in up to 16,378 individuals, using additive genetic models adjusted for age, sex, fasting insulin, and study-specific covariates. RESULTS - Nine SNPs at eight loci were associated with proinsulin levels (P < 5 × 10-8). Two loci (LARP6 and SGSM2) have not been previously related to metabolic traits, one (MADD) has been associated with fasting glucose, one (PCSK1) has been implicated in obesity, and four (TCF7L2, SLC30A8, VPS13C/ C2CD4A/B, and ARAP1, formerly CENTD2) increase T2D risk. The proinsulin-raising allele of ARAP1 was associated with a lower fasting glucose (P = 1.7 3 10-4), improved b-cell function (P = 1.1 × 10-5), and lower risk of T2D (odds ratio 0.88; P = 7.8 × 10-6). Notably, PCSK1 encodes the protein prohormone convertase 1/3, the first enzyme in the insulin processing pathway. A genotype score composed of the nine proinsulin-raising alleles was not associated with coronary disease in two large case-control datasets. CONCLUSIONS - We have identified nine genetic variants associated with fasting proinsulin. Our findings illuminate the biology underlying glucose homeostasis and T2D development in humans and argue against a direct role of proinsulin in coronary artery disease pathogenesis