Effects of MAR-M247 substrate (modified) composition on coating oxidation coating/substrate interdiffusion

The effects of gamma+gamma' Mar-M247 substrate composition on gamma+beta Ni-Cr-Al-Zr coating oxidation and coating/substrate interdiffusion were evaluated. These results were also compared to a prior study for a Ni-Cr-Al-Zr coated gamma Ni-Cr-Al substrate with equivalent Al and Cr atomic percentages. Cyclic oxidation behavior at 1130 C was investigated using change in weight curves. Concentration/distance profiles were measured for Al, Cr, Co, W, and Ta. The surface oxides were examined by X-ray diffraction and scanning electron microscopy. The results indicate that variations of Ta and C concentrations in the substrate do not affect oxidation resistance, while additions of grain boundary strengthening elements (Zr, Hf, B) increase oxidation resistance. In addition, the results indicate that oxidation phenomena in gamma+beta/gamma+gamma' Mar-M247 systems have similar characteristics to the l gamma+beta/gamma Ni-Cr-Al system

Thermal barrier coating life prediction model development

The objectives are to determine the predominant modes of degradation of a plasma sprayed thermal barrier coating system, and then to develop and verify life prediction models accounting for these degradation modes. Two possible predominant failure mechanisms being evaluated are bond coat oxidation and bond coat creep

Thermal barrier coating life prediction model

This is the first report of the first phase of a 3-year program. Its objectives are to determine the predominant modes of degradation of a plasma sprayed thermal barrier coating system, then to develop and verify life prediction models accounting for these degradation modes. The first task (Task I) is to determine the major failure mechanisms. Presently, bond coat oxidation and bond coat creep are being evaluated as potential TBC failure mechanisms. The baseline TBC system consists of an air plasma sprayed ZrO2-Y2O3 top coat, a low pressure plasma sprayed NiCrAlY bond coat, and a Rene'80 substrate. Pre-exposures in air and argon combined with thermal cycle tests in air and argon are being utilized to evaluate bond coat oxidation as a failure mechanism. Unexpectedly, the specimens pre-exposed in argon failed before the specimens pre-exposed in air in subsequent thermal cycles testing in air. Four bond coats with different creep strengths are being utilized to evaluate the effect of bond coat creep on TBC degradation. These bond coats received an aluminide overcoat prior to application of the top coat to reduce the differences in bond coat oxidation behavior. Thermal cycle testing has been initiated. Methods have been selected for measuring tensile strength, Poisson's ratio, dynamic modulus and coefficient of thermal expansion both of the bond coat and top coat layers

Effect of bond coat creep and oxidation on TBC integrity

The potential of thermal barrier coatings (TBCs) on high-pressure turbine (HPT) nozzles and blades is limited at present by the inability to quantitatively predict TBC life for these components. The goal is to isolate the major TBC failure mechanisms, which is part of the larger program aimed at developing TBC life prediction models. Based on the results of experiments to isolate TBC failure mechanisms, the effects of bond coat oxidation and bond coat creep on TBC integrity is discussed. In bond coat oxidation experiments, Rene prime 80 specimens coated with a NiCrAlY/ZrO2-8 percent Y2O3 TBC received isothermal pre-exposures at 2000 F in static argon, static air, or received no pre-exposure. The effects of oxidation due to the pre-exposures were determined by thermal cycle tests in both static air and static argon at 2000 F. To study the effect of bond coat creep on TBS behavior, four bond coats with different creep properties were evaluated by thermal cycle tests in air at 2000 F. The test results, the relative importance of these two failure mechanisms, and how their effects may be quantified will also be discussed

Thermal barrier coating life prediction model development

This report describes work performed to determine the predominat modes of degradation of a plasma sprayed thermal barrier coating system and to develop and verify life prediction models accounting for these degradation modes. The primary TBC system consisted of a low pressure plasma sprayed NiCrAlY bond coat, an air plasma sprayed ZrO2-Y2O3 top coat, and a Rene' 80 substrate. The work was divided into 3 technical tasks. The primary failure mode to be addressed was loss of the zirconia layer through spalling. Experiments showed that oxidation of the bond coat is a significant contributor to coating failure. It was evident from the test results that the species of oxide scale initially formed on the bond coat plays a role in coating degradation and failure. It was also shown that elevated temperature creep of the bond coat plays a role in coating failure. An empirical model was developed for predicting the test life of specimens with selected coating, specimen, and test condition variations. In the second task, a coating life prediction model was developed based on the data from Task 1 experiments, results from thermomechanical experiments performed as part of Task 2, and finite element analyses of the TBC system during thermal cycles. The third and final task attempted to verify the validity of the model developed in Task 2. This was done by using the model to predict the test lives of several coating variations and specimen geometries, then comparing these predicted lives to experimentally determined test lives. It was found that the model correctly predicts trends, but that additional refinement is needed to accurately predict coating life

Thermal barrier coating life prediction model

The objectives of this program are to determine the predominant modes of degradation of a plasma sprayed thermal barrier coating system, and then to develop and verify life prediction models accounting for these degradation modes. The program is divided into two phases, each consisting of several tasks. The work in Phase 1 is aimed at identifying the relative importance of the various failure modes, and developing and verifying life prediction model(s) for the predominant model for a thermal barrier coating system. Two possible predominant failure mechanisms being evaluated are bond coat oxidation and bond coat creep. The work in Phase 2 will develop design-capable, causal, life prediction models for thermomechanical and thermochemical failure modes, and for the exceptional conditions of foreign object damage and erosion

Thermal barrier coating life prediction model

This is the second annual report of the first 3-year phase of a 2-phase, 5-year program. The objectives of the first phase are to determine the predominant modes of degradation of a plasma sprayed thermal barrier coating system and to develop and verify life prediction models accounting for these degradation modes. The primary TBC system consists of an air plasma sprayed ZrO-Y2O3 top coat, a low pressure plasma sprayed NiCrAlY bond coat, and a Rene' 80 substrate. Task I was to evaluate TBC failure mechanisms. Both bond coat oxidation and bond coat creep have been identified as contributors to TBC failure. Key property determinations have also been made for the bond coat and the top coat, including tensile strength, Poisson's ratio, dynamic modulus, and coefficient of thermal expansion. Task II is to develop TBC life prediction models for the predominant failure modes. These models will be developed based on the results of thermmechanical experiments and finite element analysis. The thermomechanical experiments have been defined and testing initiated. Finite element models have also been developed to handle TBCs and are being utilized to evaluate different TBC failure regimes

Environmental chemical stressors as epigenome modifiers:a new horizon in assessment of toxicological effects

In eukaryotic cells, chromatin transformation from euchromatin into heterochromatin as a means of controlling gene expression and replication has been known as the ?accessibility hypothesis?. The interplay of epigenetic changes including histone modifications, DNA methylation, RNA interference (RNAi) and other functional epigenetic components are intricate. It is believed that these changes are well-programmed, inherited and can be modified by environmental contaminant stressors. Environmentally-driven epigenetic alterations during development, e.g. embryonic, foetal or neonatal stage, may influence disease susceptibility in adulthood. Therefore, understanding how epigenome modifications develop in response to environmental chemicals and, how epigenetic-xenobiotic interactions influence human health will shed new insights into gene-environment interactions in the epidemiology of several diseases including cancer. In this review, we consider studies of chemical modifiers including nutritional and xenobiotic effects on epigenetic components in vitro or in vivo. By examining the most-studied epigenome modifications and how their respective roles are interlinked, we highlight the central role of xenbiotic-modified epigenetic mechanisms. A major requirement will be to study and understand effects following environmentally-relevant exposures. We suggest that the study of epigenetic toxicology will open up new opportunities to devise strategies for the prevention or treatment of at-risk populations

The role of epigenetic dysregulation in the epidemic of allergic disease

The epidemic of allergic disease in early life is one of the clearest indicators that the developing immune system is vulnerable to modern environmental changes. A range of environmental exposures epidemiologically associated with allergic disease have been shown to have effects on the foetal immune function in pregnancy, including microbial burden, dietary changes and environmental pollutants. Preliminary studies now suggest that these early effects on immune development may be mediated epigenetically through a variety of processes that collectively modify gene expression and allergic susceptibility and that these effects are potentially heritable across generations. It is also possible that rising rates of maternal allergy, a recognised direct risk factor for infant allergic disease, may be further amplifying the effects of environmental changes. Whilst effective prevention strategies are the ultimate goal in reversing the allergy epidemic, the specific environmental drivers, target genes, and intracellular pathways and mechanisms of early life immune programming are still unclear. It is hoped that identifying genes that are differentially regulated in association with subsequent allergic disease will assist in identifying causal pathways and upstream contributing environmental factors. In this way, epigenetic paradigms are likely to provide valuable insights into how the early environment can be modified to more favourably drive immune development and reverse the allergic epidemic