Methods for structural design at elevated temperatures

A procedure which can be used to design elevated temperature structures is discussed. The desired goal is to have the same confidence in the structural integrity at elevated temperature as the factor of safety gives on mechanical loads at room temperature. Methods of design and analysis for creep, creep rupture, and creep buckling are presented. Example problems are included to illustrate the analytical methods. Creep data for some common structural materials are presented. Appendix B is description, user's manual, and listing for the creep analysis program. The program predicts time to a given creep or to creep rupture for a material subjected to a specified stress-temperature-time spectrum. Fatigue at elevated temperature is discussed. Methods of analysis for high stress-low cycle fatigue, fatigue below the creep range, and fatigue in the creep range are included. The interaction of thermal fatigue and mechanical loads is considered, and a detailed approach to fatigue analysis is given for structures operating below the creep range

Exploring the possibility space: taking stock of the diverse capabilities and gaps in integrated assessment models

Integrated assessment models (IAMs) have emerged as key tools for building and assessing long term climate mitigation scenarios. Due to their central role in the recent IPCC assessments, and international climate policy analyses more generally, and the high uncertainties related to future projections, IAMs have been critically assessed by scholars from different fields receiving various critiques ranging from adequacy of their methods to how their results are used and communicated. Although IAMs are conceptually diverse and evolved in very different directions, they tend to be criticised under the umbrella of 'IAMs'. Here we first briefly summarise the IAM landscape and how models differ from each other. We then proceed to discuss six prominent critiques emerging from the recent literature, reflect and respond to them in the light of IAM diversity and ongoing work and suggest ways forward. The six critiques relate to (a) representation of heterogeneous actors in the models, (b) modelling of technology diffusion and dynamics, (c) representation of capital markets, (d) energy-economy feedbacks, (e) policy scenarios, and (f) interpretation and use of model results

Producing policy-relevant science by enhancing robustness and model integration for the assessment of global environmental change

We use the flexible model coupling technology known as the bespoke framework generator to link established existing modules representing dynamics in the global economy (GEMINI_E3), the energy system (TIAM-WORLD), the global and regional climate system (MAGICC6, PLASIM-ENTS and ClimGEN), the agricultural system, the hydrological system and ecosystems (LPJmL), together in a single integrated assessment modelling (IAM) framework, building on the pre-existing framework of the Community Integrated Assessment System. Next, we demonstrate the application of the framework to produce policy-relevant scientific information. We use it to show that when using carbon price mechanisms to induce a transition from a high-carbon to a low-carbon economy, prices can be minimised if policy action is taken early, if burden sharing regimes are used, and if agriculture is intensified. Some of the coupled models have been made available for use at a secure and user-friendly web portal

Electromagnetic Properties of Indium Isotopes Elucidate the Doubly Magic Character of ¹⁰⁰Sn

Understanding the nuclear properties in the vicinity of 100Sn – suggested to be the heaviest doubly magic nucleus with equal proton number Z and neutron number N – has been a long-standing challenge for experimental and theoretical nuclear physics. In particular, contradictory experimental evidence exists regarding the role of nuclear collectivity in this region of the nuclear chart. Here, we provide additional evidence for the doubly-magic character of 100Sn by measuring the ground-state electromagnetic moments and nuclear charge radii of indium (Z = 49) isotopes as N approaches 50 from above using precision laser spectroscopy. Our results span almost the complete range between the two major neutron closed shells at N = 50 and N = 82 and reveal parabolic trends as a function of the neutron number, with a clear reduction toward these two neutron closed-shells. A detailed comparison between our experimental and numerical results from two complementary nuclear many-body frameworks, density functional theory and ab initio methods, exposes deficiencies in nuclear models and establishes a benchmark for future theoretical developments.<br/

Serum Potassium and Risk of Death or Kidney Replacement Therapy in Older People With CKD Stages 4-5: Eight-Year Follow-up

Rationale &amp; Objective: Hypokalemia may accelerate kidney function decline. Both hypo- and hyperkalemia can cause sudden cardiac death. However, little is known about the relationship between serum potassium and death or the occurrence of kidney failure requiring replacement therapy (KRT). We investigated this relationship in older people with chronic kidney disease (CKD) stage 4-5. Study Design: Prospective observational cohort study. Setting &amp; Participants: We followed 1,714 patients (≥65 years old) from the European Quality (EQUAL) study for 8 years from their first estimated glomerular filtration rate (eGFR) &lt; 20 mL/min/1.73 m2 measurement. Exposure: Serum potassium was measured every 3 to 6 months and categorized as ≤3.5, &gt;3.5-≤4.0, &gt;4.0-≤4.5, &gt;4.5-≤5.0 (reference), &gt;5.0-≤5.5, &gt;5.5-≤6.0, and &gt;6.0 mmol/L. Outcome: The combined outcome death before KRT or start of KRT. Analytical Approach: The association between categorical and continuous time-varying potassium and death or KRT start was examined using Cox proportional hazards and restricted cubic spline analyses, adjusted for age, sex, diabetes, cardiovascular disease, renin-angiotensin-aldosterone system (RAAS) inhibition, eGFR, and subjective global assessment (SGA). Results: At baseline, 66% of participants were men, 42% had diabetes, 47% cardiovascular disease, and 54% used RAAS inhibitors. Their mean age was 76 ± 7 (SD) years, mean eGFR was 17 ± 5 (SD) mL/min/1.73 m2, and mean SGA was 6.0 ± 1.0 (SD). Over 8 years, 414 (24%) died before starting KRT, and 595 (35%) started KRT. Adjusted hazard ratios for death or KRT according to the potassium categories were 1.6 (95% CI, 1.1-2.3), 1.4 (95% CI, 1.1-1.7), 1.1 (95% CI, 1.0-1.4), 1 (reference), 1.1 (95% CI, 0.9-1.4), 1.8 (95% CI, 1.4-2.3), and 2.2 (95% CI, 1.5-3.3). Hazard ratios were lowest at a potassium of about 4.9 mmol/L. Limitations: Shorter intervals between potassium measurements would have allowed for more precise estimations. Conclusions: We observed a U-shaped relationship between serum potassium and death or KRT start among patients with incident CKD 4-5, with a nadir risk at a potassium level of 4.9 mmol/L. These findings underscore the potential importance of preventing both high and low potassium in patients with CKD 4-5. Plain-Language Summary: Abnormal potassium blood levels may increase the risk of death or kidney function decline, especially in older people with chronic kidney disease (CKD). We studied 1,714 patients aged ≥65 years with advanced CKD from the European Quality (EQUAL) study and followed them for 8 years. We found that both low and high levels of potassium were associated with an increased risk of death or start of kidney replacement therapy, with the lowest risk observed at a potassium level of 4.9 mmol/L. In patients with CKD, the focus is often on preventing high blood potassium. However, this relatively high optimum potassium level stresses the potential importance of also preventing low potassium levels in older patients with advanced CKD

Associations between depressive symptoms and disease progression in older patients with chronic kidney disease: results of the EQUAL study

Background Depressive symptoms are associated with adverse clinical outcomes in patients with end-stage kidney disease; however, few small studies have examined this association in patients with earlier phases of chronic kidney disease (CKD). We studied associations between baseline depressive symptoms and clinical outcomes in older patients with advanced CKD and examined whether these associations differed depending on sex. Methods CKD patients (&gt;= 65 years; estimated glomerular filtration rate &lt;= 20 mL/min/1.73 m(2)) were included from a European multicentre prospective cohort between 2012 and 2019. Depressive symptoms were measured by the five-item Mental Health Inventory (cut-off &lt;= 70; 0-100 scale). Cox proportional hazard analysis was used to study associations between depressive symptoms and time to dialysis initiation, all-cause mortality and these outcomes combined. A joint model was used to study the association between depressive symptoms and kidney function over time. Analyses were adjusted for potential baseline confounders. Results Overall kidney function decline in 1326 patients was -0.12 mL/min/1.73 m(2)/month. A total of 515 patients showed depressive symptoms. No significant association was found between depressive symptoms and kidney function over time (P = 0.08). Unlike women, men with depressive symptoms had an increased mortality rate compared with those without symptoms [adjusted hazard ratio 1.41 (95% confidence interval 1.03-1.93)]. Depressive symptoms were not significantly associated with a higher hazard of dialysis initiation, or with the combined outcome (i.e. dialysis initiation and all-cause mortality). Conclusions There was no significant association between depressive symptoms at baseline and decline in kidney function over time in older patients with advanced CKD. Depressive symptoms at baseline were associated with a higher mortality rate in men

Antiinflammatory Therapy with Canakinumab for Atherosclerotic Disease

Background: Experimental and clinical data suggest that reducing inflammation without affecting lipid levels may reduce the risk of cardiovascular disease. Yet, the inflammatory hypothesis of atherothrombosis has remained unproved. Methods: We conducted a randomized, double-blind trial of canakinumab, a therapeutic monoclonal antibody targeting interleukin-1β, involving 10,061 patients with previous myocardial infarction and a high-sensitivity C-reactive protein level of 2 mg or more per liter. The trial compared three doses of canakinumab (50 mg, 150 mg, and 300 mg, administered subcutaneously every 3 months) with placebo. The primary efficacy end point was nonfatal myocardial infarction, nonfatal stroke, or cardiovascular death. RESULTS: At 48 months, the median reduction from baseline in the high-sensitivity C-reactive protein level was 26 percentage points greater in the group that received the 50-mg dose of canakinumab, 37 percentage points greater in the 150-mg group, and 41 percentage points greater in the 300-mg group than in the placebo group. Canakinumab did not reduce lipid levels from baseline. At a median follow-up of 3.7 years, the incidence rate for the primary end point was 4.50 events per 100 person-years in the placebo group, 4.11 events per 100 person-years in the 50-mg group, 3.86 events per 100 person-years in the 150-mg group, and 3.90 events per 100 person-years in the 300-mg group. The hazard ratios as compared with placebo were as follows: in the 50-mg group, 0.93 (95% confidence interval [CI], 0.80 to 1.07; P = 0.30); in the 150-mg group, 0.85 (95% CI, 0.74 to 0.98; P = 0.021); and in the 300-mg group, 0.86 (95% CI, 0.75 to 0.99; P = 0.031). The 150-mg dose, but not the other doses, met the prespecified multiplicity-adjusted threshold for statistical significance for the primary end point and the secondary end point that additionally included hospitalization for unstable angina that led to urgent revascularization (hazard ratio vs. placebo, 0.83; 95% CI, 0.73 to 0.95; P = 0.005). Canakinumab was associated with a higher incidence of fatal infection than was placebo. There was no significant difference in all-cause mortality (hazard ratio for all canakinumab doses vs. placebo, 0.94; 95% CI, 0.83 to 1.06; P = 0.31). Conclusions: Antiinflammatory therapy targeting the interleukin-1β innate immunity pathway with canakinumab at a dose of 150 mg every 3 months led to a significantly lower rate of recurrent cardiovascular events than placebo, independent of lipid-level lowering. (Funded by Novartis; CANTOS ClinicalTrials.gov number, NCT01327846.