The effects of aging temperature and time on the hardness and impact toughness of a copper-bearing high-strength low-carbon steel were investigated. The hardness of the aged samples reached maxima after 1 h and 5 h of aging at 500 and 450℃, respectively; this increase in hardness was followed by a decrease in hardness until a temperature of 700℃, at which secondary hardening was observed. The impact toughness of the aged steel was found to be higher for 5 h of aging. Transmission electron microscopy confirmed the presence of carbide and copper precipitates; also, the secondary hardening could be the result of the transformation of austenite (formed in the aging treatment) to martensite. Differential scanning calorimetry of the steel was performed to better understand the precipitation behavior. The results revealed that the precipitation of the steel exhibited two significant stages of copper precipitate nucleation and coarsening of the precipitates, with corresponding activation energies of 49 and 238 kJ·mol-1, respectively. 相似文献
According to Vening Meinesz-Moritz (VMM) global inverse isostatic problem, either the Moho density contrast (crust-mantle density contrast) or the Moho geometry can be estimated by solv-ing a non-linea... 相似文献
ATM is the most significant molecule involved in monitoring the genomic integrity of the cell. Any damage done to DNA relentlessly
challenges the cellular machinery involved in recognition, processing and repair of these insults. ATM kinase is activated
early to detect and signal lesions in DNA, arrest the cell cycle, establish DNA repair signaling and faithfully restore the
damaged chromatin. ATM activation plays an important role as a barrier to tumorigenesis, metabolic syndrome and neurodegeneration.
Therefore, studies of ATM-dependent DNA damage signaling pathways hold promise for treatment of a variety of debilitating
diseases through the development of new therapeutics capable of modulating cellular responses to stress. In this review, we
have tried to untangle the complex web of ATM signaling pathways with the purpose of pinpointing multiple roles of ATM underlying
the complex phenotypes observed in AT patients. 相似文献
This paper is a technical study of the systematic observations and computations made by Mu?yī al-Dīn al-Maghribī (d. 1283) at the Maragha observatory (north-western Iran, c. 1259–1320) in order to newly determine the parameters of the Ptolemaic lunar model, as explained in his Talkhī? al-majis?ī, “Compendium of the Almagest.” He used three lunar eclipses on March 7, 1262, April 7, 1270, and January 24, 1274, in order to measure the lunar epicycle radius and mean motions; an observation on April 20, 1264, to determine the lunar eccentricity; an observation on August 29, 1264, to test the model; and another on March 15, 1262, for measuring the lunar parallax. In the second period of activity at the Maragha observatory, Shams al-Dīn Mu?ammad al-Wābkanawī (c. 1254–1320) adopted all of al-Maghribī’s parameter values in his Zīj, but decreased his value for the mean longitude of the moon at epoch by 0;13,11$^{\circ }$. By comparing the times of the new moons and lunar eclipses in the period of 1270–1320 as computed from the astronomical tables of the Maragha tradition with the true modern ones, it is argued that this correction was very probably the result of actual observations. 相似文献
The remodeling of the mitochondrial network is a critical process in maintaining cellular homeostasis and is intimately related to mitochondrial function. The interplay between the formation of new mitochondria (biogenesis) and the removal of damaged mitochondria (mitophagy) provide a means for the repopulation of the mitochondrial network. Additionally, mitochondrial fission and fusion serve as a bridge between biogenesis and mitophagy. In recent years, the importance of these processes has been characterised in multiple tissue- and cell-types, and under various conditions. In skeletal muscle, the robust remodeling of the mitochondrial network is observed, particularly after injury where large portions of the tissue/cell structures are damaged. The significance of mitochondrial remodeling in regulating skeletal muscle regeneration has been widely studied, with alterations in mitochondrial remodeling processes leading to incomplete regeneration and impaired skeletal muscle function. Needless to say, important questions related to mitochondrial remodeling and skeletal muscle regeneration still remain unanswered and require further investigation. Therefore, this review will discuss the known molecular mechanisms of mitochondrial network remodeling, as well as integrate these mechanisms and discuss their relevance in myogenesis and regenerating skeletal muscle.