Direct observations of nucleation in a nondilute multicomponent alloy

The chemical pathways leading to gamma-prime(L1_2)-nucleation from nondilute Ni-5.2 Al-14.2 Cr at.%, gamma(f.c.c.), at 873 K are followed with radial distribution functions and isoconcentration surface analyses of direct-space atom-probe tomographic images. Although Cr atoms initially are randomly distributed, a distribution of congruent Ni3Al short-range order domains (SRO), =0.6 nm, results from Al diffusion during quenching. Domain site occupancy develops as their number density increases leading to Al-rich phase separation by gamma-prime-nucleation, =0.75 nm, after SRO occurs.Comment: 5 pages, 4 figure

The Earned Income Tax Credit: Antipoverty Effectiveness and Labor Market Effects

The authors begin with a detailed assessment then perform empirical analyses to predict the outcomes of changes to the structure of the program.https://research.upjohn.org/up_press/1099/thumbnail.jp

Effects of solute concentrations on kinetic pathways in Ni-Al-Cr alloys

The kinetic pathways resulting from the formation of coherent L12-ordered y'-precipitates in the g-matrix (f.c.c.) of Ni-7.5 Al-8.5 Cr at.% and Ni-5.2 Al-14.2 Cr at.% alloys, aged at 873 K, are investigated by atom-probe tomography (APT) over a range of aging times from 1/6 to 1024 hours; these alloys have approximately the same volume fraction of the y'-precipitate phase. Quantification of the phase decomposition within the framework of classical nucleation theory reveals that the y-matrix solid-solution solute supersaturations of both alloys provide the chemical driving force, which acts as the primary determinant of the nucleation behavior. In the coarsening regime, the temporal evolution of the y'-precipitate average radii and the y-matrix supersaturations follow the predictions of classical coarsening models, while the temporal evolution of the y'-precipitate number densities of both alloys do not. APT results are compared to equilibrium calculations of the pertinent solvus lines determined by employing both Thermo-Calc and Grand-Canonical Monte Carlo simulation.Comment: Submitted to Acta Materialia, June, 200

Noise and Quality of Life

Noise is defined as an unwanted sound or a combination of sounds that has adverse effects on health. These effects can manifest in the form of physiologic damage or psychological harm through a variety of mechanisms. Chronic noise exposure can cause permanent threshold shifts and loss of hearing in specific frequency ranges. Noise induced hearing loss (NIHL) is thought to be one of the major causes of preventable hearing loss. Approximately 10 million adults and 5.2 million children in the US are already suffering from irreversible noise induced hearing impairment and thirty million more are exposed to dangerous levels of noise each day. The mechanisms of NIHL have yet to be fully identified, but many studies have enhanced our understanding of this process. The role of oxidative stress in NIHL has been extensively studied. There is compelling data to suggest that this damage may be mitigated through the implementation of several strategies including anti-oxidant, anti-ICAM 1 Ab, and anti JNK intervention. The psychological effects of noise are usually not well characterized and often ignored. However, their effect can be equally devastating and may include hypertension, tachycardia, increased cortisol release and increased physiologic stress. Collectively, these effects can have severe adverse consequences on daily living and globally on economic production. This article will review the physiologic and psychologic consequences of noise and its effect on quality of life

Age-related Hearing Loss and its Association with Reactive Oxygen Species and Mitochondrial DNA damage

Age-related hearing loss, known as presbyacusis, is characterized by the progressive deterioration of auditory sensitivity associated with the aging process and is the leading cause of adult auditory deficiency in the USA. Presbyacusis is described as a progressive, bilateral, high-frequency hearing loss that is manifested on audiometric assessment by a moderately sloping pure tone audiogram. Approximately 23% of the population between 65 and 75 years of age, and 40% of the population older than 75 years of age are affected by this condition. It was estimated in 1980 that 11% of the population was 76 years or older and this number is expected to almost double by the year 2030. When one considers that the population over 65 years of age is experiencing the most accelerated development of hearing loss, the potential socioeconomic ramifications are staggering. Curiously, the frequency of presbyacusis varies across different societies. This discrepancy has been attributed to many factors including genetics, diet, socioeconomic factors, and environmental variables. The purpose of this article is to review the various molecular mechanisms underlying presbyacusis and to offer insights into potential methods of mitigating the effects of aging on hearing impairment