Formation of white etching cracks at manganese sulfide (MnS) inclusions in bearing steel due to hammering impact loading

Wind turbine gearbox bearings (WTGBs) are failing prematurely, leading to increased operational costs of wind energy. Bearing failure by white structure flaking (WSF) and axial cracking may both be caused by the propagation of white etching cracks (WECs) and have been observed to cause premature failures; however, their damage mechanism is currently not well understood. Crack initiation has been found to occur at subsurface material defects in bearing steel, which may develop into WECs. One hypothesis for WEC formation at these defects, such as non-metallic inclusions, is that repetitive impact loading of a rolling element on a bearing raceway, due to torque reversals and transient loading during operation, leads to high numbers of stress-concentrating load cycles at defects that exceed the material yield strength. In this study, a number of tests were carried out using a reciprocating hammer-type impact rig. Tests were designed to induce subsurface yielding at stress concentrating manganese sulfide (MnS) inclusions. The effects of increasing surface contact stress and number of impact cycles, with and without surface traction, were investigated. Damage adjacent to MnS inclusions, similar to that observed in a failed WTGB raceway, was recreated on bearing steel test specimens. It has been found that increasing the subsurface equivalent stresses and the number of impact cycles both led to increased damage levels. Damage was observed at subsurface equivalent stresses of above 2.48 GPa after at least 50,000 impact cycles. WECs were recreated during tests that applied surface traction for 1,000,000 impacts

Population structure of the rice sheath blight pathogen Rhizoctonia solani AG-1 IA from India

The population structure of Rhizoctonia solani AG-1 IA causing rice sheath blight from India was evaluated for 96 isolates using seven RFLP loci. Nineteen of the isolates did not hybridise to R. solani AG-1 IA RFLP probes and rDNA analyses subsequently confirmed that they were either Ceratobasidium oryzae-sativae isolates or another Rhizoctonia sp. The population structure of the remaining 77 R. solani AG-1 IA Indian isolates was similar to that of a previously characterized Texas population. Clonal dispersal of R. solani AG-1 IA in India was moderate within fields and no clones were shared among field populations. Low levels of population subdivision and small genetic distances among populations were consistent with high levels of gene flow. Frequent sexual reproduction was indicated by the fact that most populations were in Hardy-Weinberg equilibrium (HWE). The two loci (R68 and R111) that deviated significantly from HWE showed an excess of heterozygosity. Although Texas and Indian populations were geographically very distant, they exhibited only moderate population subdivision, with an FST value of 0.19

Inhibitory Effect of Gamma Interferon on Cultured Human Keratinocyte Thrombospondin Production, Distribution, and Biologic Activities

Rapidly proliferating keratinocytes (KCs) maintained in low calcium, serum-free medium produce and utilize thrombospondin (TSP) as an attachment and spreading factor. To begin to understand the modulation of KC TSP metabolism, gamma interferon (IFN-γ), a product of activated T lymphocytes, was added to KC cultures. IFN-γ; was chosen because activated T cells appear at sites of cutaneous injury. Two additional cytokines including tumor necrosis factor (TNF) and IFN-β were also examined. IFN-γ (600 U/ml), but not TNF (500 U/ml) or IFN-β (103 U/ml), as single agents decreased KC TSP biosynthesis, secretion, and utilization as an attachment factor. IFN-γ alone did not detectably decrease TSP mRNA levels suggesting a post-transcriptional effect in KCs. However, the combination of IFN-γ (600 U/ml) and TNF (500 U/ml) inhibited TSP mRNA production. These results demonstrate the modulation of KC TSP metabolism and biologic activity

Threshold Maps for Inclusion-Initiated Micro-Cracks and White Etching Areas in Bearing Steel: The Role of Impact Loading and Surface Sliding

Wind turbine gearbox (WTG) bearings can fail prematurely, significantly affecting wind turbine operational availability and the cost of energy production. The current most commonly accepted theory of failure mechanism is that the bearing subsurface is weakened by white etching crack (WEC) networks that eventually lead to the flaking away of material from the bearing surface. Subsurface damage due to rolling contact fatigue (RCF) is thought to be the main cause of premature failure, resulting from the initiation of micro-cracks, often at non-metallic inclusions or other material defects, which then propagate to the bearing surface. This study proposes a hypothesis that impact loading together with high levels of surface traction and contact pressure are important factors contributing to the initiation of micro-cracks and white etching areas (WEAs) at non-metallic inclusions which may lead to the formation of WEC networks. Both repeated impact and twin-disc RCF tests were designed to investigate inclusion-initiated micro-cracks and WEAs at subsurface in order to test this hypothesis. This led to the recreation of inclusion-initiated micro-cracks and WEAs in tested specimens, similar to the subsurface damage observed at inclusions in failed WTG bearing raceways. Tests were carried out to determine threshold levels of contact pressure, surface traction, and impact loading required for the formation of inclusion-initiated micro-cracks and WEAs

Initiation of sub-surface micro-cracks and white etching areas from debonding at non-metallic inclusions in wind turbine gearbox bearing

In this study, a failed planetary bearing from a wind turbine gearbox was destructively examined to investigate the initiation of micro-cracks and butterflies at non-metallic inclusions, and the effect of debonding between these inclusions and the steel matrix. The butterflies were scanned using Atomic Force Microscopy (AFM) to show the topography that could not be assessed by using other microscopy techniques. Nano-indentation was conducted across a butterfly wing and a non-metallic inclusion to measure the hardness at the interface with the steel matrix. It was found that the White Etching Areas (WEA) in the region of the butterfly wing was a damaged material that showed tearing at the debonding gap between the inclusion and steel matrix. This study highlighted the effect of debonding on the initiation of micro-cracks, WEA and inclusion cracking. A direct relationship was found between the size of inclusions and the total length of inclusions and micro-cracks or butterfly wings. The depth of the observed sub-surface damage was correlated with the sub-surface stress distribution and these results suggested that surface traction could be an important contributing factor to the subsurface damage initiation

Introduction: Shakespeare's public spheres

Habermas’ sense of a “cultural Public Sphere” is a notoriously complex term and, when applied to Early Modern cultures, needs careful definition. This essay both introduces the variety of methods by which we might approach playtexts with a view to their public – auditory – impact and contributes to a debate about an audience's understanding of Shakespeare's plays. By selecting two words and their spread of use in one play, Twelfth Night, we might appreciate the potential for meaningful ambiguity latent in how we hear the language of live performance. If we search for how certain terms (in this case, the cluster of semes derived from repetitions of “fancy” and “play”), we might find at times incompatible senses, yet we get near to appreciating the range of Early Modern dramatic language

Drug-gene interactions of antihypertensive medications and risk of incident cardiovascular disease: A pharmacogenomics study from the CHARGE consortium

Background Hypertension is a major risk factor for a spectrum of cardiovascular diseases (CVD), including myocardial infarction, sudden death, and stroke. In the US, over 65 million people have high blood pressure and a large proportion of these individuals are prescribed antihypertensive medications. Although large long-term clinical trials conducted in the last several decades have identified a number of effective antihypertensive treatments that reduce the risk of future clinical complications, responses to therapy and protection from cardiovascular events vary among individuals. Methods Using a genome-wide association study among 21,267 participants with pharmaceutically treated hypertension, we explored the hypothesis that genetic variants might influence or modify the effectiveness of common antihypertensive therapies on the risk ofmajor cardiovascular outcomes. The classes of drug treatments included angiotensin-converting enzyme inhibitors, beta-blockers, calcium channel blockers, and diuretics. In the setting of the Cohorts for Heart and Aging Research in Genomic Epidemiology (CHARGE) consortium, each study performed array-based genome-wide genotyping, imputed to HapMap Phase II reference panels, and used additive genetic models in proportional hazards or logistic regressionmodels to evaluate drug-gene interactions for each of four therapeutic drug classes. We used meta-analysis to combine study-specific interaction estimates for approximately 2 million single nucleotide polymorphisms (SNPs) in a discovery analysis among 15,375 European Ancestry participants (3,527 CVD cases) with targeted follow-up in a case-only study of 1,751 European Ancestry GenHAT participants as well as among 4,141 African-Americans (1,267 CVD cases). Results Although drug-SNP interactions were biologically plausible, exposures and outcomes were well measured, and power was sufficient to detect modest interactions, we did not identify any statistically significant interactions from the four antihypertensive therapy meta-analyses (Pinteraction > 5.0×10-8). Similarly, findings were null for meta-analyses restricted to 66 SNPs with significant main effects on coronary artery disease or blood pressure from large published genom

Discovery of Genetic Variation on Chromosome 5q22 Associated with Mortality in Heart Failure

Failure of the human heart to maintain sufficient output of blood for the demands of the body, heart failure, is a common condition with high mortality even with modern therapeutic alternatives. To identify molecular determinant

Genome-Wide Association Study for Incident Myocardial Infarction and Coronary Heart Disease in Prospective Cohort Studies: The CHARGE Consortium

Background Data are limited on genome-wide association studies (GWAS) for incident coronary heart disease (CHD). Moreover, it is not known whether genetic variants identified to date also associate with risk of CHD in a prospective setting. Methods We performed a two-stageGWAS analysis of incident myocardial infarction (MI) and CHD in a total of 64,297 individuals (including 3898MI cases, 5465 CHD cases). SNPs that passed an arbitrary threshold of 5×10-6 in Stage I were taken to Stage II for further discovery. Furthermore, in an analysis of prognosis, we studied whether known SNPs from former GWAS were associated with totalmortality in individuals who experienced MI during follow-up. Results In Stage I 15 loci passed the threshold of 5×10-6; 8 loci for MI and 8 loci for CHD, for which one locus overlapped and none were reported in previous GWAS meta-analyses. We took 60 SNPs representing these 15 loci to Stage II of discovery. Four SNPs near QKI showed nominally significant association with MI (p-value<8.8×10-3) and three exceeded the genome-wide significance threshold when Stage I and Stage II results were combined (top SNP rs6941513: p = 6.2×10-9). Despite excellent power, the 9p21 locus SNP (rs1333049) was only modestly associated with MI (HR = 1.09, p-value = 0.02) and marginally with CHD (HR = 1.06, p-value = 0.08). Among an inception cohort of those who experienced MI during follow-up, the risk allele of rs1333049 was associated with a decreased risk of subsequent mortality (HR = 0.90, p-value = 3.2×10-3). Conclusions QKI represents a novel locus that may serve as a predictor of incident CHD in prospective studies. The association of the 9p21 locus both with increased risk of first myocardial infarction and longer survival after MI highlights the importance of study design in investigating genetic determinants of complex disorders

Genomewide meta-analysis identifies loci associated with IGF-I and IGFBP-3 levels with impact on age-related traits

The growth hormone/insulin-like growth factor (IGF) axis can be manipulated in animal models to promote longevity, and IGF-related proteins including IGF-I and IGF-binding protein-3 (IGFBP-3) have also been implicated in risk of human diseases including cardiovascular diseases, diabetes, and cancer. Throug