Mortality and pulmonary complications in patients undergoing surgery with perioperative SARS-CoV-2 infection: an international cohort study

Background: The impact of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) on postoperative recovery needs to be understood to inform clinical decision making during and after the COVID-19 pandemic. This study reports 30-day mortality and pulmonary complication rates in patients with perioperative SARS-CoV-2 infection. Methods: This international, multicentre, cohort study at 235 hospitals in 24 countries included all patients undergoing surgery who had SARS-CoV-2 infection confirmed within 7 days before or 30 days after surgery. The primary outcome measure was 30-day postoperative mortality and was assessed in all enrolled patients. The main secondary outcome measure was pulmonary complications, defined as pneumonia, acute respiratory distress syndrome, or unexpected postoperative ventilation. Findings: This analysis includes 1128 patients who had surgery between Jan 1 and March 31, 2020, of whom 835 (74·0%) had emergency surgery and 280 (24·8%) had elective surgery. SARS-CoV-2 infection was confirmed preoperatively in 294 (26·1%) patients. 30-day mortality was 23·8% (268 of 1128). Pulmonary complications occurred in 577 (51·2%) of 1128 patients; 30-day mortality in these patients was 38·0% (219 of 577), accounting for 81·7% (219 of 268) of all deaths. In adjusted analyses, 30-day mortality was associated with male sex (odds ratio 1·75 [95% CI 1·28–2·40], p\textless0·0001), age 70 years or older versus younger than 70 years (2·30 [1·65–3·22], p\textless0·0001), American Society of Anesthesiologists grades 3–5 versus grades 1–2 (2·35 [1·57–3·53], p\textless0·0001), malignant versus benign or obstetric diagnosis (1·55 [1·01–2·39], p=0·046), emergency versus elective surgery (1·67 [1·06–2·63], p=0·026), and major versus minor surgery (1·52 [1·01–2·31], p=0·047). Interpretation: Postoperative pulmonary complications occur in half of patients with perioperative SARS-CoV-2 infection and are associated with high mortality. Thresholds for surgery during the COVID-19 pandemic should be higher than during normal practice, particularly in men aged 70 years and older. Consideration should be given for postponing non-urgent procedures and promoting non-operative treatment to delay or avoid the need for surgery. Funding: National Institute for Health Research (NIHR), Association of Coloproctology of Great Britain and Ireland, Bowel and Cancer Research, Bowel Disease Research Foundation, Association of Upper Gastrointestinal Surgeons, British Association of Surgical Oncology, British Gynaecological Cancer Society, European Society of Coloproctology, NIHR Academy, Sarcoma UK, Vascular Society for Great Britain and Ireland, and Yorkshire Cancer Research

A new comprehensive model of damage for flexural subassemblies prone to fatigue

Fatigue resistance is a key performance for the life-cycle sustainability of materials and structures. Structural members subjected to flexural forces such as spring hinges in origami structures are one of the most commonly existing in nature and engineering practice but predicting their fatigue resistance is a challenge because of complex mechanisms of crack localization, nonstationary amplitudes in the time domain, and the influence of stress gradient due to bending moment. We developed a general lumped damage simulation model for predicting the fatigue life and the associated crack propagation in the full range of elastic and plastic amplitudes. It is found that the developed comprehensive damage model demonstrates a new perspective for fatigue-induced remaining life quantification for engineering structures. (c) 2021 Elsevier Ltd. All rights reserved

Damage Evolution Modeling for Steel Structures Subjected to Combined High Cycle Fatigue and High-Intensity Dynamic Loadings

This paper presents a method for modeling the initiation and propagation of the damage in steel structures under combined fatigue loading. An existing model in the literature is used as the main key to the development of the new formulation herein proposed, where a significant computational improvement for the cracking incubation phase under high cycle fatigue (HCF) is achieved. The results show a satisfactory comparison with experimental data available in the literature and the carried parametric simulations demonstrate the effectiveness of the model once strength reduction could be estimated after 0, 20, 40, and 60 years of HCF. The reduction of the structural capacity was evaluated by the consideration of the final damage due to a high-intensity dynamic loading at the end of the HCF phase

Modeling of localization using Nash variational formulations: The extended damage mechanics

It is assumed in this paper that energy dissipation is a two-phase phenomenon. During the prelocalization stage, dissipation is a continuous process. After localization, it is lumped in surfaces of zero volume. To describe this process, it is proposed a new formulation called extended damage mechanics. The new framework incorporates the additional terms of lumped energy dissipation into a weak form of the damage evolution law. The variational formulation allowing for this approach characterizes the solution as a non-cooperative equilibrium point. This concept is also named after its inventor, the mathematician John Forbes Nash, as Nash point. Finally, numerical implementation of the extended damage mechanics is performed to describe the objectivity of the numerical simulations with respect to the finite element meshes in some practical cases of solids and structures

Modeling of localization using Nash variational formulations: The extended damage mechanics

It is assumed in this paper that energy dissipation is a two-phase phenomenon. During the prelocalization stage, dissipation is a continuous process. After localization, it is lumped in surfaces of zero volume. To describe this process, it is proposed a new formulation called extended damage mechanics. The new framework incorporates the additional terms of lumped energy dissipation into a weak form of the damage evolution law. The variational formulation allowing for this approach characterizes the solution as a non-cooperative equilibrium point. This concept is also named after its inventor, the mathematician John Forbes Nash, as Nash point. Finally, numerical implementation of the extended damage mechanics is performed to describe the objectivity of the numerical simulations with respect to the finite element meshes in some practical cases of solids and structures

An MRI-based morphometric and structural covariance network study of Brazilian adolescents stratified by depression risk

OBJECTIVE: To explore differences in regional cortical morphometric structure between adolescents at risk for depression or with current depression. METHODS: We analyzed cross-sectional structural neuroimaging data from a sample of 150 Brazilian adolescents classified as low-risk (n=50) or high-risk for depression (n=50) or with current depression (n=50) through a vertex-based approach with measurements of cortical volume, surface area and thickness. Differences between groups in subcortical volumes and in the organization of networks of structural covariance were also explored. RESULTS: No significant differences in brain structure between groups were observed in whole-brain vertex-wise cortical volume, surface area or thickness. Also, no significant differences in subcortical volume were observed between risk groups. In relation to the structural covariance network, there was an indication of an increase in the hippocampus betweenness centrality index in the high-risk group network compared to the low-risk and current depression group networks. However, this result was only statistically significant when applying false discovery rate correction for nodes within the affective network. CONCLUSION: In an adolescent sample recruited using an empirically based composite risk score, no major differences in brain structure were detected according to the risk and presence of depression

Effects of the brain-derived neurotropic factor variant Val66Met on cortical structure in late childhood and early adolescence

Background: The brain-derived neurotrophic factor (BDNF) Val66Met polymorphism (rs6265) has been associated with several neuropsychiatric disorders and regional structural brain changes in adults, but little is known about Val66Met's effect on brain morphology during typical or atypical neurodevelopment. Windows of vulnerability to psychopathology may be associated with the different alleles of the Val66Met polymorphism during childhood and adolescence. Methodology: We investigated the effect of Val66Met on cortical thickness in MRI scans of 718 children and adolescents (6-12 years old) with typical development, and in those meeting DSM criteria for a psychiatric disorder. Results: Val66Met had a significant effect on cortical thickness. Considering the typically developing group, Met carriers presented thicker parietal and occipital lobes and prefrontal cortices compared to Val homozygotes. Met carriers with psychiatric disorders presented thicker medial and lateral temporal cortices than Val homozygotes. Furthermore, a significant genotype x psychiatric diagnosis interaction was found: Met-carriers with a psychiatric diagnosis presented thinner bilateral prefrontal cortices than Val homozygotes. Conclusion: This study provides evidence that Val66Met is associated with cortical maturation in children and adolescents with and without psychiatric disorders.National Institute of Developmental Psychiatry for Children and Adolescent (INPD) [CNPq 465550/2014-2, FAPESP 2014/50917-0]Sunnybrook Health Sciences CentreSunnybrook Research InstituteCentre for Collaborative Drug ResearchCanadian Partnership for Stroke RecoverySao Paulo Research Foundation (FAPESP) [2013/08531-5]Brazilian National Council for Scientific and Technological Development (CNPq) [312984/2014-6, 442026/2014-5]FAPESP [2014/07280-1]Natl Inst Dev Psychiat Children & Adolescents INC, Sao Paulo, Brazil|Univ Fed Sao Paulo, Dept Psychiat, Sao Paulo, BrazilUniv Toronto, Dept Pharmacol & Toxicol, Toronto, ON, CanadaSunnybrook Res Inst, Hurvitz Brain Sci Program, Toronto, ON, CanadaUniv Fed Sao Paulo, Dept Morphol & Genet, Sao Paulo, BrazilChildrens Hosp Philadelphia, Ctr Appl Genom, Philadelphia, PA 19104 USAUniv Fed Rio Grande do Sul, Hosp Clin Porto Alegre, Dept Psychiat, Porto Alegre, RS, BrazilUniv Fed ABC, Math & Stat Inst, Santo Andre, BrazilUniv Sao Paulo, Dept & Inst Psychiat IPq, Sao Paulo, BrazilUniv Sao Paulo, Inst Radiol INRAD, Sao Paulo, BrazilPontificia Univ Catolica Rio Grande do Sul, DCNL, Porto Alegre, RS, BrazilUniv Fed Sao Paulo, Dept Psychiat, Sao Paulo, BrazilUniv Fed Sao Paulo, Dept Morphol & Genet, Sao Paulo, Brazil|CNPq 465550/2014-2FAPESP 2014/50917-0FAPESP: 2013/08531-5CNPq: [312984/2014-6, 442026/2014-5FAPESP: 2014/07280-1Web of Scienc