Introducing Low Cycle Fatigue in IEC Standard Range Pair Spectra

The effect of low cycle fatigue (LCF) on the damage accumulation is still a matter of discussion. For this purpose the effect of LCF is investigated using different damage accumulation methods and measured wind turbine fatigue loads

NEW WISPER - Creating a New Load Sequence From Modern Wind Turbine Data

The well established WISPER load spectrum, a commonly used load spectrum in wind turbine design, was developped for significantly smaller wind turbine as built today. Therefore a NEW WISPER load spectrum was developped within the EU-project "OPTIMAT BLADES". This paper presents the new load spectrum and the major issues which were important for the creation. Additionally a comparison between the "old" and NEW WISPER is given using different damage accumulation methods

Experimental investigation and numerical description of the damage evolution in a duplex stainless steel subjected to VHCF-loading

The present study documents how the irreversible fraction of cyclic plastic strain, induced by loading amplitudes close to the durability limit, causes fatigue damage such as (i) slip band development, (ii) fatigue crack initiation and (iii) short fatigue crack propagation. The damage evolution of the austenitic-ferritic duplex stainless steel X2CrNiMoN22-5-3 (318 LN) was investigated up to one billion load cycles by means of high resolution electron microscopy (HR-SEM, TEM), focused ion beam (FIB) cutting, confocal laser scanning microscopy (CLSM), in-situ far field microscopy and high-energy (87.1 keV) X-ray diffraction (XRD) experiments. The experimentally identified damage mechanisms were implemented into three-dimensional finite element simulations, which consider crystal plasticity. These simulations enable fatigue life predictions of real microstructures obtained for instance by means of, e.g. automated electron back scatter diffraction (EBSD) analysis. The simulations allow for determining whether microcracks (i) initiate in a microstructure, (ii) arrest in the midst of the first grain, (iii) are permanently, (iv) temporary or (v) not at all blocked by grain or phase boundaries. Moreover, this concept is capable to contribute to the concept of tailored microstructures for improved cyclic-loading behaviour

A new Fgf10 mutation in the mouse leads to atrophy of the harderian gland and slit-eye phenotype in heterozygotes: A novel model for dry-eye disease?

PURPOSE. The purpose of the present study was to characterize a new slit-eye phenotype in the mouse. METHODS. Genomewide linkage analysis was performed, and a candidate gene was sequenced. Eyes of the mutants were described morphologically, histologically, and by in situ hybridization. To allow morphologic and functional studies of the retina, mutants were outcrossed to C57BL/6. RESULTS. Within an ongoing ethyl-nitrosourea mutagenesis screen with C3HeB/FeJ mice, the authors identified a new mutant (referred to as Aey17) showing a slit-eye phenotype in heterozygotes; homozygous mutants are not viable because of major developmental defects. This mutation was mapped to the distal end of mouse chromosome 13, suggesting Fgf10 (encoding the fibroblast growth factor 10) as a candidate gene. An A -> G transition in the penultimate base of the first intron of Fgf10 leading to aberrant splicing with an additional 49 bp in exon 2 and to a frameshift with a premature stop codon after 54 new amino acids was identified. Histologic analysis of the major ocular tissues (cornea, lens, retina) did not reveal major alterations compared with the wild type, but the size of the Harderian gland was remarkably reduced in heterozygotes. Although Fgf10 was expressed in the developing retina, neither electroretinography nor the virtual drum indicated any abnormalities in heterozygous mutants; overall eye size was identical in wild types and heterozygotes. CONCLUSIONS. The mutation in the Fgf10 gene leads to a dominant slit-eye phenotype caused by atrophy of the Harderian gland

The 2020 motile active matter roadmap

Activity and autonomous motion are fundamental in living and engineering systems. This has stimulated the new field of 'active matter' in recent years, which focuses on the physical aspects of propulsion mechanisms, and on motility-induced emergent collective behavior of a larger number of identical agents. The scale of agents ranges from nanomotors and microswimmers, to cells, fish, birds, and people. Inspired by biological microswimmers, various designs of autonomous synthetic nano- and micromachines have been proposed. Such machines provide the basis for multifunctional, highly responsive, intelligent (artificial) active materials, which exhibit emergent behavior and the ability to perform tasks in response to external stimuli. A major challenge for understanding and designing active matter is their inherent nonequilibrium nature due to persistent energy consumption, which invalidates equilibrium concepts such as free energy, detailed balance, and time-reversal symmetry. Unraveling, predicting, and controlling the behavior of active matter is a truly interdisciplinary endeavor at the interface of biology, chemistry, ecology, engineering, mathematics, and physics. The vast complexity of phenomena and mechanisms involved in the self-organization and dynamics of motile active matter comprises a major challenge. Hence, to advance, and eventually reach a comprehensive understanding, this important research area requires a concerted, synergetic approach of the various disciplines. The 2020 motile active matter roadmap of Journal of Physics: Condensed Matter addresses the current state of the art of the field and provides guidance for both students as well as established scientists in their efforts to advance this fascinating area

Deferasirox in children with transfusion-dependent thalassemia or sickle cell anemia: A large cohort real-life experience from Turkey (REACH-THEM).

OBJECTIVES: To evaluate the long-term efficacy and safety of deferasirox therapy in a large observational cohort of children with transfusion-dependent thalassemia (TDT) and sickle cell anemia (SCA) in Turkey. METHODS: This was a multicenter, prospective cohort study including TDT and SCA patients aged 2-18 years with iron overload (≥100 mL/kg of pRBC or a serum ferritin [SF] level >1000 μg/L) receiving deferasirox. Patients were followed for up to 3 years according to standard practice. RESULTS: A total of 439 patients were evaluated (415 [94.5%] TDT, 143 [32.6%] between 2 and 6 years). Serum ferritin levels consistently and significantly decreased across 3 years of deferasirox therapy from a median of 1775.5 to 1250.5 μg/L (P < 0.001). Serum ferritin decreases were noted in TDT (1804.9 to 1241 μg/L), SCA (1655.5 to 1260 μg/L), and across age groups of 2-6 years (1971.5 to 1499 μg/L), 7-12 years (1688.5 to 1159.8 μg/L), and 13-18 years (1496.5 to 1107 μg/L). Serum ferritin decreases were also noted for all deferasirox dose groups but only significant in patients with doses ≥30 mg/kg/d (n = 120, -579.6 median reduction, P < 0.001). Only 9 (2%) patients had adverse events suspected to be related to deferasirox. Serum creatinine slightly increased but remained within the normal range. CONCLUSIONS: Deferasirox has long-term efficacy and safety in children with TDT and SCA, although higher doses (≥30 mg/kg/d) may be required to achieve iron balance