Finite-element analysis of contact between elastic self-affine surfaces

Finite element methods are used to study non-adhesive, frictionless contact between elastic solids with self-affine surfaces. We find that the total contact area rises linearly with load at small loads. The mean pressure in the contact regions is independent of load and proportional to the rms slope of the surface. The constant of proportionality is nearly independent of Poisson ratio and roughness exponent and lies between previous analytic predictions. The contact morphology is also analyzed. Connected contact regions have a fractal area and perimeter. The probability of finding a cluster of area $a_c$ drops as $a_c^{-\tau}$ where $\tau$ increases with decreasing roughness exponent. The distribution of pressures shows an exponential tail that is also found in many jammed systems. These results are contrasted to simpler models and experiment.Comment: 13 pages, 15 figures. Replaced after changed in response to referee comments. Final two figures change

Contact mechanics: contact area and interfacial separation from small contact to full contact

We present a molecular dynamics study of the contact between a rigid solid with a randomly rough surface and an elastic block with a flat surface. The numerical calculations mainly focus on the contact area and the interfacial separation from small contact (low load) to full contact (high load). For small load the contact area varies linearly with the load and the interfacial separation depends logarithmically on the load. For high load the contact area approaches the nominal contact area (i.e., complete contact), and the interfacial separation approaches zero. The numerical results have been compared with analytical theory and experimental results. They are in good agreement with each other. The present findings may be very important for soft solids, e.g., rubber, or for very smooth surfaces, where complete contact can be reached at moderate high loads without plastic deformation of the solids.Comment: 15 pages, 23 figure

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.

New genetic loci link adipose and insulin biology to body fat distribution.

Body fat distribution is a heritable trait and a well-established predictor of adverse metabolic outcomes, independent of overall adiposity. To increase our understanding of the genetic basis of body fat distribution and its molecular links to cardiometabolic traits, here we conduct genome-wide association meta-analyses of traits related to waist and hip circumferences in up to 224,459 individuals. We identify 49 loci (33 new) associated with waist-to-hip ratio adjusted for body mass index (BMI), and an additional 19 loci newly associated with related waist and hip circumference measures (P < 5 × 10(-8)). In total, 20 of the 49 waist-to-hip ratio adjusted for BMI loci show significant sexual dimorphism, 19 of which display a stronger effect in women. The identified loci were enriched for genes expressed in adipose tissue and for putative regulatory elements in adipocytes. Pathway analyses implicated adipogenesis, angiogenesis, transcriptional regulation and insulin resistance as processes affecting fat distribution, providing insight into potential pathophysiological mechanisms

Multiscale modeling of two-dimensional contacts

A hybrid simulation method is introduced and used to study two-dimensional single-asperity and multi-asperity contacts both quasistatically and dynamically. The method combines an atomistic treatment of the interfacial region with a finite-element method description of subsurface deformations. The dynamics in the two regions are coupled through displacement boundary conditions applied at the outer edges of an overlap region. The two solutions are followed concurrently but with different time resolution. The method is benchmarked against full atomistic simulations. Accurate results are obtained for contact areas, pressures, and static and dynamic friction forces. The time saving depends on the fraction of the system treated atomistically and is already more than a factor of 20 for the relatively small systems considered here