The effects of Ca content on intragranular acicular ferrite nucleation in the CGHAZ of Al-Ca-Ti deoxidised shipbuilding steel

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This study reveals the effects of Ca content (0.0002–0.0025 wt%) on the CGHAZ toughness of Al-Ca-Ti steels. Increasing the Ca content transforms inclusions from Ti 2 O 3 -MnS to CaO·6Al 2 O 3 -CaTiO 3 -MnS(-CaS), raising the effective inclusion density from 72.11 to 114.35 mm −2 . First-principles and lattice mismatch calculations reveal the superior lattice matching between CaTiO 3 and MnS, facilitating Mn-depleted zone formation around Ca-containing inclusions. Moreover, CaO·6Al 2 O 3 -CaTiO 3 -MnS(-CaS) exhibits lower lattice mismatch with ferrite (<6%) compared to Ti 2 O 3 -MnS, significantly promoting primary IAF nucleation. Consequently, with increasing Ca content, the primary IAF length grows from 7.7 to 11.3 μm, and the secondary IAF count increases from 2.1 to 3.7 per inclusion, enhancing CGHAZ impact toughness from 18 to 162 J.

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Alterations in cation homeostasis during and after recovery from myocardial ischemia may account for some of the reversible and irreversible components of myocardial cell injury. To investigate possible mechanisms involved, we exposed cultured layers of spontaneously contracting chick embryo ventricular cells to media containing 1 mM cyanide (CN) and 20 mM 2-deoxyglucose (2-DG), and zero glucose for up to 6 h, and then allowed cultured cells to recover in serum-free culture medium for 24 h. Changes in Na, K, and Ca contents, 42K uptake and efflux, ATP content, cell water content, and lactate dehydrogenase (LDH) release were measured, and compared with changes produced by exposure to 10(-3) M ouabain and severe hypoxia. Exposure to CN and 2-DG caused marked increase in cell Na (sevenfold) and Ca (fivefold) contents, and a decrease in K content (one-fifth normal), coincident with ATP depletion to one-tenth normal levels. This produced only slight cell injury, evidenced by increased LDH release. Recovery for 24 h resulted in return to near normal values (expressed in nanomoles per milligram of protein) of Na, Ca, and ATP contents. However, there was failure of cell K content to return to normal, associated with a persistent reduced net uptake of 42K, and an increase in the rate of 42K efflux. These abnormalities in K homeostasis were associated with a decrease in cell volume and water content per milligram of protein. More marked ATP depletion (to 1/100 normal values) was produced by hypoxia plus 2-DG and zero glucose, and was associated with much more severe cell injury manifested by LDH loss. Ouabain exposure resulted in a much greater Ca gain (20-30-fold), relative to increase in Na content, than did either CN and 2-DG or hypoxia; and ouabain effects were not reversible (after a 15-fold or greater increase in Ca content was produced) and were associated with significant LDH release. We conclude that these cells are resistant to cell injury caused by moderately severe Ca overload and ATP depletion produced by exposure to CN and 2-DG. However, metabolic inhibition of ATP production produces persistent abnormalities in K homeostasis, associated with functional abnormalities.

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