A strict upper limit of the Fe content (about 80 at. %) for the formation of a single amorphous phase with good magnetic softness hinders the improvement in J(s) of the Fe-based amorphous alloys. The alloys with the high Fe content exceeding the limit commonly have the
as-quenched structure consisting of coarse alpha-Fe grains in an amorphous matrix, which inevitably results in inferior magnetic softness. The simultaneous addition of proper amounts of P and Cu is found to be significantly effective in decreasing the grain size of alpha-Fe phase, formed in an amorphous matrix in the as-quenched Fe(82)Si(9)B(9) amorphous alloys with high Fe content exceeding the limit. Fe-rich Fe(81.7)Si(9)B(7)P(2)Cu(0.3) heteroamorphous alloy with an as-quenched structure consisting of extremely small alpha-Fe-like clusters of about 3 nm or smaller in diameter, randomly dispersed within PF-04929113 clinical trial the amorphous matrix, exhibits the lower coercivity of 7 A m(-1) and the higher J(s) of 1.56 T than the typical Fe-based monolithic amorphous alloy at an as-quenched state. (C) 2009 American Institute of
Physics. [DOI: 10.1063/1.3060579]“
“Objective The goal of this paper is to discuss cancer-related fatigue (CRF) and address issues related to the investigation into potential biological and genetic causal mechanisms. The objectives are to: (1) describe CRF as a component of quality Cl-amidine of life (QOL); (2) address measurement issues that have slowed progress toward an understanding of mechanisms underlying this symptom; (3) review biological pathways and genetic approaches that have promise for the exploration of causal mechanisms of CRF; and (4) offer directions for future research.
Methods Review, synthesis, and interpretation of
the literature.
Results Until recently, CRF and QOL have been understood primarily as subjective patient-reported experiences. With increased understanding of human genetics, theories and research are being expanded to incorporate biological and genetic understandings of these subjective experiences. Proposed biological and genetic mechanisms of CRF that have been examined include cytokine dysregulation, hypothalamic-pituitary-adrenal (HPA) axis dysfunction, five hydroxy tryptophan (5-HT) neurotransmitter dysregulation, circadian selleck inhibitor rhythm disruption, alterations in adenosine triphosphate (ATP) and muscle metabolism, and vagal afferent activation. Approaches to the study of genetic mechanisms have also been addressed including candidate genes, genome-wide scanning, and gene expression. Based on the review and synthesis of the literature, directions for future research are proposed.
Conclusions Understanding the biological and genetic basis of CRF has the potential to contribute to a more complete understanding of the genetic determinants of QOL.