Stress-strain properties of ferritic steels using automated ball-indentation testing - pile-up effects included

The automated Ball-Indentation (Bl) testing is based cm repeated indentation of a spherical indenter at a single location on a metallic sample. The indentation loads and the corresponding depths in an indentation are used to extract the key mechanical flow properties using well established mathematical relationships. The technique is almost nondestructive and an excellent substitute for the conventional tensile test especially when there is very little volume of specimen available for testing. The distortion at the original plane of surface caused by the material displaced by the indentation is referred to as the pile-up or sink-in effect. The pile-up behaviour alters the actual contact area and hence the indentation diameter which is used for calculating tire stress-strain parameters. It is well established that the extent of pile-up is related to the strain hardening coefficient of the material. This paper describes the methodology for deriving the plastic stress-strain properties by automated ball-indentation technique taking into account the usually ignored pile-up effects. Flow properties derived from ball-indentation tests using die proposed methodology were found to be in good agreement with those of tensile test results for various ferritic steels like AISI 1025 carbon steel, 2.25C:r-lMo steel, Mod 9Cr-lMo steel with different work hardening characteristics

Genetic mechanisms of critical illness in COVID-19.

Host-mediated lung inflammation is present1, and drives mortality2, in the critical illness caused by coronavirus disease 2019 (COVID-19). Host genetic variants associated with critical illness may identify mechanistic targets for therapeutic development3. Here we report the results of the GenOMICC (Genetics Of Mortality In Critical Care) genome-wide association study in 2,244 critically ill patients with COVID-19 from 208 UK intensive care units. We have identified and replicated the following new genome-wide significant associations: on chromosome 12q24.13 (rs10735079, P = 1.65 × 10-8) in a gene cluster that encodes antiviral restriction enzyme activators (OAS1, OAS2 and OAS3); on chromosome 19p13.2 (rs74956615, P = 2.3 × 10-8) near the gene that encodes tyrosine kinase 2 (TYK2); on chromosome 19p13.3 (rs2109069, P = 3.98 ×  10-12) within the gene that encodes dipeptidyl peptidase 9 (DPP9); and on chromosome 21q22.1 (rs2236757, P = 4.99 × 10-8) in the interferon receptor gene IFNAR2. We identified potential targets for repurposing of licensed medications: using Mendelian randomization, we found evidence that low expression of IFNAR2, or high expression of TYK2, are associated with life-threatening disease; and transcriptome-wide association in lung tissue revealed that high expression of the monocyte-macrophage chemotactic receptor CCR2 is associated with severe COVID-19. Our results identify robust genetic signals relating to key host antiviral defence mechanisms and mediators of inflammatory organ damage in COVID-19. Both mechanisms may be amenable to targeted treatment with existing drugs. However, large-scale randomized clinical trials will be essential before any change to clinical practice

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2–4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

Miniaturized Testing of Engineering Materials

This book is a comprehensive overview of methods of characterizing the mechanical properties of engineering materials using specimen sizes in the micro-scale regime (0.3-5.0 mm). A range of issues associated with miniature specimen testing like correlation methodologies for data transferability between different specimen sizes, use of numerical simulation/analysis for data inversion, application to actual structures using scooped out samples or by in-situ testing, and more importantly developing a common code of practice are discussed and presented in a concise manner

Karthik---12/02

ABSTRACT. The heat-affected zone (HAZ) of 2.25Cr-1Mo steel weldments consists of coarse-grained bainite, finegrained bainite, and intercritical structures. Mechanical properties of the individual regions of the HAZ are difficult to determine by conventional methods because of the difficulty in making mechanical test pieces of adequate dimensions from the individual microstructures of very small regions in the HAZ. This paper describes the use of shear punch tests to determine the mechanical properties of the individual regions in the HAZ. A linear correlation established between the tensile properties and the corresponding properties obtained from the shear punch test of various heat-treated structures was used to characterize the mechanical properties for individual regions in the HAZ of actual weldments

Small specimen test techniques for estimating the tensile property degradation of modqa 9Cr-1Mo steel on thermal aging

The degradation in mechanical properties of modified (mod) 9Cr-1Mo steel on thermal aging at 923 K has been studied using the small specimen test techniques-shear-punch and ball-indentation tests. Small volumes of material required for these test techniques make them unique tools for the assessment of service related degradation and failure analysis of structural components. A variety of heat treated microstructural conditions of mod 9Cr-1Mo steel is generated on which both conventional tensile test and shear-punch/ball-indentation tests are carried out. The relationship between conventional tensile properties and small specimen test results is established from these standardization experiments. Small specimens of Mod 9Cr-1Mo steel in the thermally aged conditions are tested using both shear punch and ball-indentation techniques and the tensile property changes are determined. Both these tests identically reflect and quantify the changes in the tensile properties with aging time which correlates well with the microstructural changes observed using optical and electron microscopic studies

Tensile-shear correlations obtained from shear punch test technique using a modified experimental approach

Shear punch testing has been a very useful technique for evaluating mechanical properties of irradiated alloys using a very small volume of material. The load-displacement data is influenced by the compliance of the fixture components. This paper describes a modified experimental approach where the compliances of the punch and die components are eliminated. The analysis of the load-displacement data using the modified setup for various alloys like low carbon steel, SS316, modified 9Cr-1Mo, 2.25Cr-1Mo indicate that the shear yield strength evaluated at 0.2% offset of normalized displacement relates to the tensile YS as per the Von Mises yield relation (σ<SUB>ys</SUB> = 1.73Τ<SUB>ys</SUB>). A universal correlation of type UTS = mΤ<SUB>max</SUB> where m is a function of strain hardening exponent, is seen to be obeyed for all the materials in this study. The use of analytical models developed for blanking process are explored for evaluating strain hardening exponent from the load-displacement data. This study is directed towards rationalizing the tensile-shear empirical correlations for a more reliable prediction of tensile properties from shear punch tests

Finite element analysis of shear punch testing and experimental validation

In this work, finite element analysis (FEA) of the shear punch testing is carried out to study the specimen deformation up to yielding and the results are compared and validated with experimental data for four different materials. The elastic portion of the FEA generated load-displacement curve overlaps with the corresponding experimental curve only when the fixture compliances are eliminated in experiments. Based on through thickness plasticity in the FEA study, the shear yield stress estimated at an offset of 0.15% of normalized displacement compares well with the experimentally determined shear yield strength and satisfies the von Mises yield relation &#963;ys=1.73&#964;ys. The effects of die-punch clearance and specimen thickness on shear yield strength studied using FEA are also discussed