Unbonded post-tensioned concrete structures in fire

To achieve thinner and longer floor slabs, rapid construction, and tight control of inservice deflections, modern concrete structures increasingly use high-strength, posttensioned prestressing steel as reinforcement. The resulting structures are called posttensioned (PT) concrete. Post-tensioned concrete slabs are widely believed to benefit from ‘inherent fire endurance.’ This belief is based largely on results from a series of standard fire tests performed on simply-supported specimens some five decades ago. Such tests are of debatable credibility; they do not capture the true structural behaviour of real buildings in real fires, nor do they reflect modern PT concrete construction materials or optimization methods. This thesis seeks to develop a more complete understanding of the structural and thermal response of modern prestressing steel and PT concrete slabs, particularly those with unbonded prestressing steel conditions, to high temperature, in an effort to steer current practice and future research towards the development of defensible, performance-based, safe fire designs. An exhaustive literature review of previous experimentation and real case studies of fire exposed PT concrete structures is presented to address whether current code guidance is adequate. Both bonded and unbonded prestressing steel configurations are considered, and research needs are identified. For unbonded prestressing steel in a localised fire, the review shows that the interaction between thermal relaxation and plastic deformation could result in tendon failure and loss of tensile reinforcement to the concrete, earlier than predicted by available design guidance. Since prestressing steel runs continuously in unbonded PT slabs, local damage to prestressing steel will affect the integrity of adjacent bays in a building. In the event that no bonded steel reinforcement is provided (as permitted by some design codes) a PT slab could lose tensile reinforcement across multiple bays; even those remote from fire. Using existing literature and design guidance, preliminary simplified modelling is presented to illustrate the stress-temperature-time interactions for stressed, unbonded prestressing steel under localised heating. This exercise showed that the observed behaviour cannot be rationally described by the existing design guidance. The high temperature mechanical properties of modern prestressing steel are subsequently considered in detail, both experimentally and analytically. Tests are presented on prestressing steel specimens under constant axial stress at high temperature using a high resolution digital image correlation (DIC) technique to accurately measure deformations. A novel, accurate analytical model of the stresstemperature- time dependent deformation of prestressing steel is developed and validated for both transient and steady-state conditions. Modern prestressing steel behaviour is then compared to its historical prestressing steel counterparts, showing significant differences at high temperature. Attention then turns to other structural actions of a real PT concrete structure (e.g. thermal bowing, restraint, concrete stiffness loss, continuity, spalling, slab splitting etc.) all of which also play inter-related roles influencing a PT slab’s response in fire. A series of three non-standard structural fire experiments on heavily instrumented, continuous, restrained PT concrete slabs under representative sustained service loads were conducted in an effort to better understand the response of PT concrete structures to localised heating. To the author’s knowledge this is the first time a continuous PT slab which includes axial, vertical and rotational restraint has been studied at high temperature, particularly under localised heating. The structural response of all three tests indicates a complex deflection trend in heating and in cooling which differs considerably from the response of a simply supported slab in a standard fire test. Deflection trends in the continuous slab tests were due to a combination of thermal expansion and plastic damage. The test data will enable future efforts to validate computational models which account for the requisite complexities. Overall, the research presented herein shows that some of the design guidance for modern PT concrete slabs is inadequate and should be updated. The high temperature deformation of prestressing steel under localised heating, as would be expected in a real fire, should be considered, since uniform heating of simplysupported elements is both unrealistic and unconservative with respect to tensile rupture of prestressing steel tendons. The most obvious impact of this finding would be to increase the minimum concrete covers required for unbonded PT construction, and to require adequate amounts of bonded steel reinforcement to allow load shedding to the bonded steel at high temperature in the event that the prestressing steel fails or is severely damaged by fire

Microstructural and mechanical characterisation of post-tentioning strands following elevated temperature exposure

Prestressing strands lose strength and become more susceptible to creep deformation when they are heated during a fire. The consequent loss in prestressing force could under certain conditions result in structural collapse, potentially outwith the heated region of the structure. This paper describes a test programme characterising the changes in microstructure of steel prestressing tendons exposed to elevated temperatures. The residual strength tests, hardness testing, and elevated temperature mechanical test were performed to demonstrate how recovery and recrystallisation of the initially work-hardened steel produce changes in its mechanical properties at elevated temperatures. The research results of this paper are beneficial not only in the fire design of post-tensioned structures using modern prestressing steel, but also in the assessment of the tendons’ residual strength after being affected by fire

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

Altres ajuts: Department of Health and Social Care (DHSC); Illumina; LifeArc; Medical Research Council (MRC); UKRI; Sepsis Research (the Fiona Elizabeth Agnew Trust); the Intensive Care Society, Wellcome Trust Senior Research Fellowship (223164/Z/21/Z); BBSRC Institute Program Support Grant to the Roslin Institute (BBS/E/D/20002172, BBS/E/D/10002070, BBS/E/D/30002275); UKRI grants (MC_PC_20004, MC_PC_19025, MC_PC_1905, MRNO2995X/1); UK Research and Innovation (MC_PC_20029); the Wellcome PhD training fellowship for clinicians (204979/Z/16/Z); the Edinburgh Clinical Academic Track (ECAT) programme; the National Institute for Health Research, the Wellcome Trust; the MRC; Cancer Research UK; the DHSC; NHS England; the Smilow family; the National Center for Advancing Translational Sciences of the National Institutes of Health (CTSA award number UL1TR001878); the Perelman School of Medicine at the University of Pennsylvania; National Institute on Aging (NIA U01AG009740); the National Institute on Aging (RC2 AG036495, RC4 AG039029); the Common Fund of the Office of the Director of the National Institutes of Health; NCI; NHGRI; NHLBI; NIDA; NIMH; NINDS.Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care or hospitalization 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