Non-destructive detection of machining-induced white layers in ferromagnetic alloys

Machining-induced white layers are an undesirable surface integrity feature which, due to their physical properties, can have a direct effect on the in-service performance of aero-engine components. Typically, destructive methods such as cross-sectional microscopy are used during inspection to identify white layers. This is costly, both in terms of parts sacrificed and time-consumed. A non-destructive evaluation method could speed-up inspection and allow all parts to be inspected before entering service as well as throughout the component life cycle. The present work covers the quantitative characterization of machining-induced white layers in super chrome molybdenum vanadium steel through destructive methods in addition to Barkhausen noise non-destructive testing of the same surfaces. White layers formed by machining with severely worn inserts were measured to be up to 50% harder than the bulk material, possess nano-scale grains and can have an associated compressive residual stress state of up to -1800 MPa. Barkhausen noise testing was used to show that surfaces with a white layer formed by SPD could be detected by measuring shifts in the peak frequency of the Barkhausen noise signal, caused by the compressive near-surface residual stress state associated with the formation of white layers of this type

On deformation characterisation of machined surfaces and machining-induced white layers in a milled titanium alloy

Machining-induced white layers and severely deformed layers are undesirable surface integrity features which can be formed when machining high-strength aerospace alloys. An orthogonal milling process has been designed and performed to assess the impact of cutting speeds, tool wear, cutting edge radius and climb vs conventional milling on white layer formation and plastic strain distribution. The plastic deformation in the machined surface associated with the formation of white layers in Ti-6Al-4V has been quantified using micro-grids of different length scales printed using the electron beam lithography technique. It was found that white layers formed via the severe plastic deformation mechanism, at equivalent plastic strain values in excess of 1.2 and in regions of the cutting arc with the instantaneous chip thickness of less than the cutting-edge radius and ploughing and rubbing being the dominant mechanisms. The results indicated that the magnitude of the measured strains and the depth of plastically deformed material was greater at lower cutting speeds, during climb milling and when machining with a larger cutting edge radius and tool flank wear land

Destructive and non-destructive testing methods for characterization and detection of machining induced white layer: A review paper

The presence of machining-induced white layer in the near-surface of critical aeroengine alloys has a detrimental effect on the lifetime of a component. Present techniques for identifying and characterizing white layer, such as optical microscopy and hardness testing, whilst effective, are destructive, costly and time-consuming. Non-destructive testing methods may, therefore, offer improvements to the process of white layer detection. This paper discusses the formation mechanisms and the defining physical properties of machining-induced white layers before offering a comprehensive review of the current state-of-the-art in both destructive and non-destructive testing methods for detecting this anomalous surface feature

Specific heat and heat conductivity of the BaTiO3 polycrystalline films with the thickness in the range 20 - 1100 nm

Thermal properties - specific heat and heat conductivity coefficient - of polycrystalline BaTiO3 films on massive substrates were studied as a function of the temperature and the film thickness by ac-hot probe method. The anomalies of specific heat with decreasing of the film thickness from 1100 to 20 nm revealed the reducing of critical temperature (Tc) and excess entropy of the ferroelectric phase transition, which becomes diffused. The critical thickness of the film at which Tc = 0 estimated as 2.5 nm.Comment: 12 pages, 7 figures, 2 tables, 450kb; submitted to J.Phys.:Cond.Mat

Fatigue life of machined components

A correlation between machining process and fatigue strength of machined components clearly exists. However, a complete picture of the knowledge on this is not readily available for practical applications. This study addresses this issue by investigating the effects of machining methods on fatigue life of commonly used materials, such as titanium alloys, steel, aluminium alloys and nickel alloys from previous literature. Effects of turning, milling, grinding and different non-conventional machining processes on fatigue strength of above-mentioned materials have been investigated in detail with correlated information. It is found that the effect of materials is not significant except steel in which phase change causes volume expansion, resulting in compressive/tensile residual stresses based on the amounts of white layers. It is very complex to identify the influence of surface roughness on the fatigue strength of machined components in the presence of residual stresses. The polishing process improves the surface roughness, but removes the surface layers that contain compressive residual stresses to decrease the fatigue strength of polished specimens. The compressive and tensile residual stresses improve and reduce fatigue strength, respectively. Grinding process induces tensile residual stresses on the machined surfaces due to high temperature generation. On the other hand, milling and turning processes induce compressive residual stresses. High temperature non-conventional machining generates a network of micro-cracks on the surfaces in addition to tensile residual stresses to subsequently reduce fatigue strength of machined components. Embedded grits of abrasive water jet machining degrade the fatigue performance of components machined by this method

Up-Regulation of MUC2 and IL-1β Expression in Human Colonic Epithelial Cells by Shigella and Its Interaction with Mucins

BACKGROUND: The entire gastrointestinal tract is protected by a mucous layer, which contains complex glycoproteins called mucins. MUC2 is one such mucin that protects the colonic mucosa from invading microbes. The initial interaction between microbes and mucins is an important step for microbial pathogenesis. Hence, it was of interest to investigate the relationship between host (mucin) and pathogen interaction, including Shigella induced expression of MUC2 and IL-1β during shigellosis. METHODS: The mucin-Shigella interaction was revealed by an in vitro mucin-binding assay. Invasion of Shigella dysenteriae into HT-29 cells was analyzed by Transmission electron microscopy. Shigella induced mucin and IL-1β expression were analyzed by RT-PCR and Immunofluorescence. RESULTS: The clinical isolates of Shigella were found to be virulent by a congo-red binding assay. The in vitro mucin-binding assay revealed both Shigella dysenteriae and Shigella flexneri have binding affinity in the increasing order of: guinea pig small intestinal mucin<guinea pig colonic mucin< Human colonic mucin. Invasion of Shigella dysenteriae into HT-29 cells occurs within 2 hours. Interestingly, in Shigella dysenteriae infected conditions, significant increases in mRNA expression of MUC2 and IL-1β were observed in a time dependent manner. Further, immunofluorescence analysis of MUC2 shows more positive cells in Shigella dysenteriae treated cells than untreated cells. CONCLUSIONS: Our study concludes that the Shigella species specifically binds to guinea pig colonic mucin, but not to guinea pig small intestinal mucin. The guinea pig colonic mucin showed a greater binding parameter (R), and more saturable binding, suggesting the presence of a finite number of receptor binding sites in the colonic mucin of the host. In addition, modification of mucins with TFMS and sodium metaperiodate significantly reduced mucin-bacterial binding; suggesting that the mucin-Shigella interaction occurs through carbohydrate epitopes on the mucin backbones. Overproduction of MUC2 may alter adherence and invasion of Shigella dysenteriae into human colonic epithelial cells

A multi-model intercomparison of halogenated very short-lived substances (TransCom-VSLS): Linking oceanic emissions and tropospheric transport for a reconciled estimate of the stratospheric source gas injection of bromine

Abstract. The first concerted multi-model intercomparison of halogenated very short-lived substances (VSLS) has been performed, within the framework of the ongoing Atmospheric Tracer Transport Model Intercomparison Project (TransCom). Eleven global models or model variants participated (nine chemical transport models and two chemistry–climate models) by simulating the major natural bromine VSLS, bromoform (CHBr3) and dibromomethane (CH2Br2), over a 20-year period (1993–2012). Except for three model simulations, all others were driven offline by (or nudged to) reanalysed meteorology. The overarching goal of TransCom-VSLS was to provide a reconciled model estimate of the stratospheric source gas injection (SGI) of bromine from these gases, to constrain the current measurement-derived range, and to investigate inter-model differences due to emissions and transport processes. Models ran with standardised idealised chemistry, to isolate differences due to transport, and we investigated the sensitivity of results to a range of VSLS emission inventories. Models were tested in their ability to reproduce the observed seasonal and spatial distribution of VSLS at the surface, using measurements from NOAA's long-term global monitoring network, and in the tropical troposphere, using recent aircraft measurements – including high-altitude observations from the NASA Global Hawk platform. The models generally capture the observed seasonal cycle of surface CHBr3 and CH2Br2 well, with a strong model–measurement correlation (r  ≥  0.7) at most sites. In a given model, the absolute model–measurement agreement at the surface is highly sensitive to the choice of emissions. Large inter-model differences are apparent when using the same emission inventory, highlighting the challenges faced in evaluating such inventories at the global scale. Across the ensemble, most consistency is found within the tropics where most of the models (8 out of 11) achieve best agreement to surface CHBr3 observations using the lowest of the three CHBr3 emission inventories tested (similarly, 8 out of 11 models for CH2Br2). In general, the models reproduce observations of CHBr3 and CH2Br2 obtained in the tropical tropopause layer (TTL) at various locations throughout the Pacific well. Zonal variability in VSLS loading in the TTL is generally consistent among models, with CHBr3 (and to a lesser extent CH2Br2) most elevated over the tropical western Pacific during boreal winter. The models also indicate the Asian monsoon during boreal summer to be an important pathway for VSLS reaching the stratosphere, though the strength of this signal varies considerably among models. We derive an ensemble climatological mean estimate of the stratospheric bromine SGI from CHBr3 and CH2Br2 of 2.0 (1.2–2.5) ppt,  ∼  57 % larger than the best estimate from the most recent World Meteorological Organization (WMO) Ozone Assessment Report. We find no evidence for a long-term, transport-driven trend in the stratospheric SGI of bromine over the simulation period. The transport-driven interannual variability in the annual mean bromine SGI is of the order of ±5 %, with SGI exhibiting a strong positive correlation with the El Niño–Southern Oscillation (ENSO) in the eastern Pacific. Overall, our results do not show systematic differences between models specific to the choice of reanalysis meteorology, rather clear differences are seen related to differences in the implementation of transport processes in the models. </jats:p

Cloning and heterologous expression of bovine pyroglutamyl peptidase type-1 in Escherichia coli : purification , biochemical and kinetic characterisation

We describe the cloning, expression and purification of the bovine XM866409 form of pyroglutamyl-aminopeptidase I. The amino acid sequence, deduced from the nucleotide sequence, revealed that it consists of 209 amino acid residues and showed to have 98% homology with the human AJ278828 form of the enzyme. Three amino acid residues at positions 81, 205 and 208 were found to vary among the two sequences. The bovine enzyme was expressed in XL10-gold Esherichia coli cells. Immobilizied Ni-ion affinity chromatography was used to purify the expressed protein resulting in a yield of 3.3mg of PAP1 per litre culture. The purified enzyme had a specific activity of 1700 units/ml. SDS-PAGE produced a single band for bovine PAP1 with a molecular weight of ~23-24 kDa which is in good agreement with previously reported data on PAP1. Kinetic constants Km and Kcat were 59μΜ and 3.5s-1, respectively. It possessed an optimum pH between 9-9.5, a temperature of 37°C and showed an absolute requirement for a thiol-reducing agent (10mM DTT). EDTA didn’t prove to have an effect on enzyme activity. Competitive inhibition was seen with pyroglutamyl peptides pGlu-His-Pro-NH2 (TRH; Ki= 44.1 uM), pGlu-Ala- OH (Ki=141 uM) and pGlu-Val-OH (Ki=652.17)

Experimental Assessment of the Role of Acetaldehyde in Alcoholic Cardiomyopathy

Alcoholism is one of the major causes of non-ischemic heart damage. The myopathic state of the heart due to alcohol consumption, namely alcoholic cardiomyopathy, is manifested by cardiac hypertrophy, compromised ventricular contractility and cardiac output. Several mechanisms have been postulated for alcoholic cardiomyopathy including oxidative damage, accumulation of triglycerides, altered fatty acid extraction, decreased myofilament Ca(2+ )sensitivity, and impaired protein synthesis. Despite intensive efforts to unveil the mechanism and ultimate toxin responsible for alcohol-induced cardiac toxicity, neither has been clarified thus far. Primary candidates for the specific toxins are ethanol, its first and major metabolic product - acetaldehyde (ACA) and fatty acid ethyl esters. Evidence from our lab suggests that ACA directly impairs cardiac function and promotes lipid peroxidation resulting in oxidative damage. The ACA-induced cardiac contractile depression may be reconciled with inhibitors of Cytochrome P-450 oxidase, xanthine oxidase and lipid peroxidation Unfortunately, the common methods to investigate the toxicity of ACA have been hampered by the fact that direct intake of ACA is toxic and unsuitable for chronic study, which is unable to provide direct evidence of direct cardiac toxicity for ACA. In order to overcome this obstacle associated with the chemical properties of ACA, our laboratory has used the chronic ethanol feeding model in transgenic mice with cardiac over-expression of alcohol dehydrogenase (ADH) and an in vitro ventricular myocyte culture model. The combination of both in vivo and in vitro approaches allows us to evaluate the role of ACA in ethanol-induced cardiac toxicity and certain cellular signaling pathways leading to alcoholic cardiomyopathy