Thermodynamics-Guided High-Throughput Discovery of Eutectic High-Entropy Alloys for Rapid Solidification.

Excellent castability, significantly refined microstructure, and good mechanical properties make eutectic high-entropy alloys (EHEAs) a natural fit for rapid solidification processes, e.g., additive manufacturing. Previous investigations have focused on developing EHEAs through trial and error and mixing known binary eutectic materials. However, eutectic compositions obtained from near-equilibrium conditions do not guarantee a fully eutectic microstructure under rapid solidifications. In this work, a thermodynamically guided high-throughput framework is proposed to design EHEAs for rapid solidification. Empirical formulas derived from past experimental observations and thermodynamic computations are applied and considered phase growth kinetics under rapid solidification (skewed phase diagram). The designed alloy candidate, Co25.6Fe17.9Ni22.4Cr19.1Ta8.9Al6.1 (wt.%), contains nanostructured eutectic lamellar and shows a high Vickers hardness of 675 Hv. In addition to this specific composition, the alloy design toolbox enables the development of new EHEAs for rapid solidification without the limitation of previous knowledge.

Thermodynamics-guided alloy and process design for additive manufacturing.

In conventional processing, metals go through multiple manufacturing steps including casting, plastic deformation, and heat treatment to achieve the desired property. In additive manufacturing (AM) the same target must be reached in one fabrication process, involving solidification and cyclic remelting. The thermodynamic and kinetic differences between the solid and liquid phases lead to constitutional undercooling, local variations in the solidification interval, and unexpected precipitation of secondary phases. These features may cause many undesired defects, one of which is the so-called hot cracking. The response of the thermodynamic and kinetic nature of these phenomena to high cooling rates provides access to the knowledge-based and tailored design of alloys for AM. Here, we illustrate such an approach by solving the hot cracking problem, using the commercially important IN738LC superalloy as a model material. The same approach could also be applied to adapt other hot-cracking susceptible alloy systems for AM.

[Method for determining concentration of dichlorvos in serum by gas chromatography].

OBJECTIVE: To develop a method for determining the concentration of dichlorvos in serum by gas chromatography and to provide a basis for clinical diagnosis and monitoring of dichlorvos poisoning. METHODS: The serum (0.5 ml)collected from patients with dichlorvos poisoning was mixed with ethyl acetate (2.0 ml) and underwent shaking/extraction; the obtained liquid was subjected to standing (5 min) and centrifuging (4000 rpm); the obtained supernatant was collected and blow-dried with nitrogen and was then dissolved in ethanol (50 µl); 1.0 µl of the obtained liquid was collected and loaded into a glass-packed column; gas chromatography was performed using a nitrogen-phosphorus detector. RESULTS: A linear relationship was found when the concentration of dichlorvos in serum was 5.0 ∼ 50.0 µg/ml, with a regression equation of y = 804.13x-691.8 (r = 0.9992). The minimum detectable concentration was 2.0 µg/ml, the recovery rate was 86.8% ∼ 94.5%, the relative standard deviation (RSD) was 4.6% ∼ 5.5%, with an intra-day RSD of 4.52% ∼ 5.21% and an inter-day RSD of 3.56% ∼ 5.52%. CONCLUSION: This determination method is easy to operate, efficient, and accurate, and can be used for quickly diagnosing dichlorvos poisoning and quantitatively evaluating treatment outcome.

[The impact of L-carnitine administration on the serum level of myocardium injury markers in patients with acute carbon monoxide poisoning].

OBJECTIVE: To examine the serum level of myocardial injury markers in patients with carbon monoxide (CO) poisoning, the correlation between these markers and the severity of the disease, and the therapeutic effects of L-carnitine administration. METHODS: 69 patients, chosen from 309 cases of acute carbon monoxide poisoning (ACOP) for abnormally high level of serum myocardial injury markers (myoglobin, Mb; MB isoenzyme of creatine kinase, CK-MB; cardiac troponin-I, cTnI) at the time of admission, were randomly divided into control group (n = 34) and observation group (n = 35). The patients in control group were given Xingnaojing (20 ml/d i.v. drip), and the observation group Xingnaojing (20 ml/d)+L-carnitine (2 g/d i.v. drip), in addition to the conventional oxygen supply and symptom-focused therapy. The plasma concentration of carboxyhemoglobin (HbCO, as index for CO poisoning severity), Mb, CK-MB, and cTnI in these patients were further examined 24 hours, 72 hours and 1 week after the treatment, for difference between the two groups, and the correlation between the serum level of HbCO and the myocardial injury markers. RESULTS: At the time of admission, the incidence of abnormal findings in myocardial injury markers were 2.5% (5/204), 46.8% (36/77) and 100.0% (28/28) in patients with mild (HbCO: 10% ~ 19%), moderate (20% ~ 39%) and severe (≥40%) CO poisoning, respectively. The incidence of abnormal findings in injury markers was significantly correlated to the HbCO concentration (x(2)=170.3549, P < 0.0001). Before the treatment, no significant difference was found in any of the indexes [HbCO: (31.1 ± 17.6)%, (32.3 ± 16.9)%, Mb (µg/L): 154.2 ± 51.8, 165.4 ± 48.6, CK-MB (µg/L): 8.7 ± 3.3, 9.6 ± 3.8), and cTnI (µg/L): 2.7 ± 1.2, 2.8 ± 1.5, all P > 0.05] between the control and observation group. However, it was found in: Mb (24 hours: 74.0 ± 36.5 vs. 97.1 ± 35.8, 72 hours: 40.1 ± 6.8 vs. 69.0 ± 11.2), cTnI (24 hours: 1.9 ± 0.5 vs. 2.3 ± 0.7, 72 hours: 1.2 ± 0.3 vs. 1.8 ± 0.4) both 24 hours and 72 hours after the treatment, and CK-MB, 24 hours after treatment (10.6 ± 4.1 vs. 13.0 ± 3.9) with the values in observation group significantly lower (P < 0.05 or P < 0.01); 1 week after the treatment, the concentration of all the injury markers returned to the normal levels with no significant difference between the two groups. Meanwhile, no significant difference was found between the two groups in HbCO concentration throughout the due-course of the therapy. CONCLUSIONS: The incidence of abnormal findings in serum myocardial injury markers was positively correlated with HbCO concentration after CO poisoning. L-carnitine may protect the myocardium and striated muscles against injury in patients with CO poisoning.

[Cholinesterase activity is not parallel to symptoms in patients suffering from organophosphorous pesticide poisoning through skin or by gastrointestinal tract].

OBJECTIVE: To sum up the experience of treating patients suffering from organophosphorous pesticide poisoning either through skin or through gastrointestinal tract. METHODS: The cholinesterase activity was less than 0.50 in all patients. They were divided into two groups: poisoning through skin (skin group) and by gastrointestinal route (gastrointestinal group). The number of poisoning through skin or gastrointestinal tract was 34 (19 cases of middle degree and 15 cases of severe degree) and 50 (22 cases of middle degree and 28 cases of severe degree), respectively. The blood cholinesterase activities were determined during the disease course, the clinical symptoms and signs were recorded, and the quantity of atropine used for treatment in respective group was also recorded. RESULTS: There were no difference in the cholinesterase activities at the same degree between two groups before treatment (P>0.05). But the symptoms of the patients in gastrointestinal group were more serious than in skin group. The cholinesterase activities of the patients in the skin group were higher significantly than that in the gastrointestinal group at 24, 48 and 72 hours after treatment (P<0.05 or P<0.01). The total amount of atropine to achieve atropinization was less in the skin group than that of the gastrointestinal group. The time for restoration of cholinesterase activity was shorter in skin group than the gastrointestinal group (both P<0.01). CONCLUSION: With the same level of enzymatic activity of cholinesterase, the symptoms of the patients poisoned via gastrointestinal tract are more serious than poisoning through skin, and the quantity of atropine is used very much more. Reactivation of the cholinesterase is earlier in patients poisoned by skin route.