Natural aging and reversion behavior of Al-Cu-Li-Ag-Mg alloy Weldalite (tm) 049

This study was initiated to understand the natural aging and reversion behavior of Weldalite (trademark) 049 in tempers without cold work. Of particular interest are: (1) the microstructural basis for the high strength in the T4 condition; (2) an explanation of the reversion phenomenon; and (3) the effect of re-aging at room temperature after a reversion treatment. Mechanical properties were measured and transmission electron microscopy (TEM) analysis performed at various stages of microstructural development during aging, reversion, and subsequent re-aging

Structure and properties during aging of an Al-Cu-Li-Ag-Mg alloy, Weldalite (tm) 049

An Al-Cu-Li-Ag-Mg alloy, Weldalite (trademark) 049, was recently introduced as an ultra-high strength alloy (7000 MPa yield strength in artificially aged tempers) with good weldability. In addition, the alloy exhibits an extraordinary natural aging response (440 MPa yield strength (YS) in the unstretch condition) and a high ductility reversion condition which may be useful as a cold-forming temper. In contrast to other Al-Li alloys, these properties can essentially be obtained with or without a stretch or other coldworking operation prior to aging. Preliminary studies have revealed that the T4 temper (no stretch, natural age) is strengthened by a combination of GP zones and delta prime (Al3Li). The T6 temper (no stretch, aged at 180 C to peak strength) was reported to be strengthened primarily by T(sub 1) phase (Al2CuLi) with a minor presence of a theta prime like (Al2Cu) phase. On the other hand, a similar but lower solute containing alloy was reported to contain omega, (stoichiometry unknown), theta prime, and S prime in the peak strength condition. The purpose of this study is to further elucidate the strengthening phases in Weldalite (trademark) 049 in the unstretched tempers, and to follow the development of the microstructure from the T4 temper through reversion (180 C for 5 to 45 minutes) to the T6 temper

High resolution electron microscopy study of a high Cu variant of Weldalite (tm) 049 and a high strength Al-Cu-Ag-Mg-Zr alloy

Weldalite (trademark) 049 is an Al-Cu-Li-Ag-Mg alloy that is strengthened in artificially aged tempers primarily by very thin plate-like precipitates lying on the set of (111) matrix planes. This precipitate might be expected to be the T(sub 1) phase, Al2CuLi, which has been observed in Al-Cu-Li alloys. However, in several ways this precipitate is similar to the omega phase which also appears as the set of (111) planes plates and is found in Al-Cu-Ag-Mg alloys. The study was undertaken to identify the set of (111) planes precipitate or precipitates in Weldalite (trademark) 049 in the T8 (stretched and artificially aged) temper, and to determine whether T(sub 1), omega, or some other phase is primarily responsible for the high strength (i.e., 700 MPa tensile strength) in this Al-Cu-Li-Ag-Mg alloy

Evaluation of the microstructure of Al-Cu-Li-Ag-Mg Weldalite (tm) alloys, part 4

Weldalite (trademark) 049 is an Al-Cu-Li-Ag-Mg alloy designed to have ultrahigh strength and to serve in aerospace applications. The alloy displays significantly higher strength than competitive alloys in both naturally aged and artificially aged tempers. The strengthening phases in such tempers have been identified to, in part, explain the mechanical properties attained. In general, the alloy is strengthened by delta prime Al3Li and Guinier-Preston (GP) zones in the naturally aged tempers. In artificially aged tempers in slightly underaged conditions, strengthening is provided by several phases including GP zones, theta prime Al2Cu, S prime Al2CuMg, T(sub 1) Al2CuLi, and possibly a new phase. In the peak strength artificially aged tempers, T(sub 1) is the predominant strengthening phase

Contrast-enhanced micro-CT imaging in murine carotid arteries : a new protocol for computing wall shear stress

Background: Wall shear stress (WSS) is involved in the pathophysiology of atherosclerosis. The correlation between WSS and atherosclerosis can be investigated over time using a WSS-manipulated atherosclerotic mouse model. To determine WSS in vivo, detailed 3D geometry of the vessel network is required. However, a protocol to reconstruct 3D murine vasculature using this animal model is lacking. In this project, we evaluated the adequacy of eXIA 160, a small animal contrast agent, for assessing murine vascular network on micro-CT. Also, a protocol was established for vessel geometry segmentation and WSS analysis. Methods: A tapering cast was placed around the right common carotid artery (RCCA) of ApoE(-/-) mice (n = 8). Contrast-enhanced micro-CT was performed using eXIA 160. An innovative local threshold-based segmentation procedure was implemented to reconstruct 3D geometry of the RCCA. The reconstructed RCCA was compared to the vessel geometry using a global threshold-based segmentation method. Computational fluid dynamics was applied to compute the velocity field and WSS distribution along the RCCA. Results: eXIA 160-enhanced micro-CT allowed clear visualization and assessment of the RCCA in all eight animals. No adverse biological effects were observed from the use of eXIA 160. Segmentation using local threshold values generated more accurate RCCA geometry than the global threshold-based approach. Mouse-specific velocity data and the RCCA geometry generated 3D WSS maps with high resolution, enabling quantitative analysis of WSS. In all animals, we observed low WSS upstream of the cast. Downstream of the cast, asymmetric WSS patterns were revealed with variation in size and location between animals. Conclusions: eXIA 160 provided good contrast to reconstruct 3D vessel geometry and determine WSS patterns in the RCCA of the atherosclerotic mouse model. We established a novel local threshold-based segmentation protocol for RCCA reconstruction and WSS computation. The observed differences between animals indicate the necessity to use mouse-specific data for WSS analysis. For our future work, our protocol makes it possible to study in vivo WSS longitudinally over a growing plaque

Conspicuous consumption of the elite: Social and self-congruity in tourism choices

This paper relies on social and economic psychology to explore how the travel choices of Portuguese citizens, with different status levels in their daily lives, perceive and adopt different conspicuous travel patterns because of public exposure. To account for the moderated role of public exposure on conspicuous travel patterns, 36 Portuguese citizens were interviewed. Q-methods were applied to explore the varying senses of conspicuous travel choices among citizens with different levels of public exposure, both individually and relative to each other. Complementary qualitative methods were applied, in order to explore how the interviewees construct tourism conspicuous meanings that match their social or self-representations. The results suggest that social contexts moderate the ways in which individuals perceive and experience conspicuous travel. Further, the results show that public groups with higher exposure tend to prefer subtle signals of conspicuousness, in order to differentiate themselves from the mainstream

Microglial activation and chronic neurodegeneration

Microglia, the resident innate immune cells in the brain, have long been implicated in the pathology of neurode-generative diseases. Accumulating evidence points to activated microglia as a chronic source of multiple neurotoxic factors, including tumor necrosis factor-α, nitric oxide, interleukin-1β, and reactive oxygen species (ROS), driving progressive neuron damage. Microglia can become chronically activated by either a single stimulus (e.g., lipopolysaccharide or neuron damage) or multiple stimuli exposures to result in cumulative neuronal loss with time. Although the mechanisms driving these phenomena are just beginning to be understood, reactive microgliosis (the microglial response to neuron damage) and ROS have been implicated as key mechanisms of chronic and neurotoxic microglial activation, particularly in the case of Parkinson’s disease. We review the mechanisms of neurotoxicity associated with chronic microglial activation and discuss the role of neuronal death and microglial ROS driving the chronic and toxic microglial phenotype

Increased Mitochondrial Calcium Sensitivity and Abnormal Expression of Innate Immunity Genes Precede Dopaminergic Defects in Pink1-Deficient Mice

BACKGROUND: PTEN-induced kinase 1 (PINK1) is linked to recessive Parkinsonism (EOPD). Pink1 deletion results in impaired dopamine (DA) release and decreased mitochondrial respiration in the striatum of mice. To reveal additional mechanisms of Pink1-related dopaminergic dysfunction, we studied Ca²+ vulnerability of purified brain mitochondria, DA levels and metabolism and whether signaling pathways implicated in Parkinson\u27s disease (PD) display altered activity in the nigrostriatal system of Pink1⁻/⁻ mice. METHODS AND FINDINGS: Purified brain mitochondria of Pink1⁻/⁻ mice showed impaired Ca²+ storage capacity, resulting in increased Ca²+ induced mitochondrial permeability transition (mPT) that was rescued by cyclosporine A. A subpopulation of neurons in the substantia nigra of Pink1⁻/⁻ mice accumulated phospho-c-Jun, showing that Jun N-terminal kinase (JNK) activity is increased. Pink1⁻/⁻ mice 6 months and older displayed reduced DA levels associated with increased DA turnover. Moreover, Pink1⁻/⁻ mice had increased levels of IL-1β, IL-12 and IL-10 in the striatum after peripheral challenge with lipopolysaccharide (LPS), and Pink1⁻/⁻ embryonic fibroblasts showed decreased basal and inflammatory cytokine-induced nuclear factor kappa-β (NF-κB) activity. Quantitative transcriptional profiling in the striatum revealed that Pink1⁻/⁻ mice differentially express genes that (i) are upregulated in animals with experimentally induced dopaminergic lesions, (ii) regulate innate immune responses and/or apoptosis and (iii) promote axonal regeneration and sprouting. CONCLUSIONS: Increased mitochondrial Ca²+ sensitivity and JNK activity are early defects in Pink1⁻/⁻ mice that precede reduced DA levels and abnormal DA homeostasis and may contribute to neuronal dysfunction in familial PD. Differential gene expression in the nigrostriatal system of Pink1⁻/⁻ mice supports early dopaminergic dysfunction and shows that Pink1 deletion causes aberrant expression of genes that regulate innate immune responses. While some differentially expressed genes may mitigate neurodegeneration, increased LPS-induced brain cytokine expression and impaired cytokine-induced NF-κB activation may predispose neurons of Pink1⁻/⁻ mice to inflammation and injury-induced cell death