Effect of spheroidized microstructure on the impact toughness and electrochemical performance of a high-carbon steel

The influence of cementite spheroidization on the impact toughness and electrochemical properties of a high-carbon steel has been thoroughly investigated in this study. Heavy warm rolling, followed by 2 h of annealing, has resulted in near-complete spheroidization, leading to a microstructure consisting of nano-cementite globules dispersed in the ultrafine-grained ferritic matrix. The Charpy impact test exhibited superior impact toughness with increased spheroidization. It is validated by the presence of abundant dimples in the fractographs of spheroidized specimens, in contrast to the as-received one that experienced a brittle failure due to its lamellar pearlitic structure. Potentiodynamic polarization and electrochemical impedance spectroscopy (EIS) carried out in a 3.5% NaCl solution revealed that the corrosion resistance of the alloy gets improved with the increase in the degree of spheroidization. This is attributed to the lower susceptibility of the spheroidized specimen to microgalvanic corrosion owing to the minimum area of contact between nano-spheroidized cementite and ferrite, as elucidated with the help of EIS results aided by equivalent electrical circuit model.     

Surface effects in nanocrystalline silicon

Exposure to ammonia (NH₃) increases the dark current (DC) in nanocrystalline silicon. Light soaking (LS) for short periods also enhances the dark current, which remains at a high value for a long time. Pumping alone is unable to restore the initial annealed state, but annealing brings it back. The final state obtained by LS and NH₃ exposure depends on the order in which they are performed. Evaporated selenium (Se) deposited on nanocrystalline silicon decreases the DC. These effects cannot be explained entirely by the presence of a-Si : H alone, in our sample. DC and photoluminescence (PL) measurements indicate the presence of two types of center in our sample, which behave differently when exposed to NH₃.     

Intercarrier bandwidth exchange: an engineering framework

A mismatch between demand and supply for bandwidth is common in transport carrier networks. This mismatch is generally a result of the disparity between a carrier's capacity buildout and its anticipated customer demand. A carrier with temporary bandwidth deficit or lack of presence in a geographical region and a carrier with surplus capacity in the right locations can be brought together by the emerging bandwidth exchange technology. Bandwidth exchange offers a win-win solution, in which the carrier with a deficit avoids losing revenue by buying capacity from the carrier with surplus, and the latter makes additional revenue by retail sale of its excess capacity. While the concept of real-time purchase and exchange of bandwidth has attracted a lot of attention, many technical challenges stand in the way of making it a reality. The purpose of this article is to provide an engineering framework for enabling real-time bandwidth exchange with committed quality of service and service level agreement among transport carriers. Special emphasis is given to identifying the architectural requirements and the enabling infrastructure necessary for building a viable bandwidth exchange that can be used for creating revenue out of surplus stranded capacity. Indepth analysis of cross-carrier service level agreement specification, capacity publication, route design, and service provisioning are also provided in the article.     

Prolonged tamoxifen exposure selects a breast cancer cell clone that is stable in vitro and in vivo

The effects of long-term tamoxifen exposure on cell growth and cell cycle kinetics were compared between oestrogen receptor (ER)-positive (MCF-7) and ER-negative (MDA-MB-231) cell lines. In the MCF-7 cell line, prolonged tamoxifen exposure (0.5 mumol/l for > 100 days) blocked cells in G0-G1 of the cell cycle, and slowed the doubling time of cells from 30 to 59 h. These effects corresponded to an increase in the cellular accumulation of tamoxifen over time [mean area under concentration curve (AUC) = 77.92 mumoles/10(6)/cells/day]. In contrast, in the MDA-MB-231 cell line, long-term tamoxifen exposure had no obvious effect on the doubling time, and reduced cellular tamoxifen accumulation (mean AUC = 50.50 mumoles/10(6)/cells/day) compared to the MCF-7 cells. Flow cytometric analysis of MDA-MB-231 cells demonstrated that a new tetraploid clone emerged following 56 days of tamoxifen exposure. Inoculation of the MDA-MB-231 tetraploid clone and MDA-MB-231 wildtype cells into the opposite flanks of athymic nude mice resulted in the rapid growth of tetraploid tumours. The tetraploid tumours maintained their ploidy following tamoxifen treatment for nine consecutive serial transplantations. Histological examination of the fifth transplant generation xenografts revealed that the tetraploid tumour had a 25-30 times greater mass, area of haemorrhage and necrosis, a slightly higher mitotic index and was more anaplastic than the control neoplasm. The control wildtype MDA-MB-231 tumours maintained a stable ploidy following tamoxifen treatment until the eighth and ninth transplantation, when a tetraploid population appeared, suggesting that tamoxifen treatment may select for this clone in vivo. These studies suggest that prolonged tamoxifen exposure may select for new, stable, fast growing cell clones in vitro as well as in vivo.     

Binding free energy calculations of galectin-3-ligand interactions

Galectins show remarkable binding specificity towards ß-galactosides.A recently developed method for calculating binding free energiesbetween a protein and its substrates has been used to evaluatethe binding specificity of galectin-3. Five disaccharides anda tetrasaccharide were used as the substrates. The calculatedbinding free energies agree quite well with the experimentaldata and the ranking of binding affinities is well reproduced.For all the six protein–ligand complexes it was observedthat electrostatic interactions oppose binding whereas the non-polarcontributions drive complex formation. The observed bindingspecificity of galectin-3 for galactosides rather than glucosidesis discussed in light of our results.