A thermodynamic optimization for the Al – Mn system is performed by considering reliable literature data and newly measured phase equilibria on the Al-rich side. Using X-ray diffraction, differential thermal analysis, and scanning electron microscopy with energy dispersive X-ray spectroscopy methods, the melting behavior of λ-Al4Mn was correctly elucidated, and two invariant reactions associated with λ-Al4Mn (L + μ-Al4Mn λ-Al4Mn at 721 ± 2 °C and L + λ-Al4Mn Al6Mn at 704 ± 2 °C) are observed. The model Al12Mn4(Al, Mn)10 previously used for Al8Mn5 was modified to be Al12Mn5(Al, Mn)9 based on crystal structure data. In addition, the high-temperature form of Al11Mn4 is included in the assessment. Employing fewer adjustable parameters than previous assessments, the present description of the Al – Mn system yields a better overall agreement with the experimental phase diagram and thermodynamic data. The obtained thermodynamic description for the Al – Mn system is then combined with those in the Al – Mg and Mg – Mn systems to form a basis for a ternary assessment. The thermodynamic parameters for ternary liquid and ternary compound Mn2Mg3Al18 (τ) are evaluated on the basis of critically assessed experimental data. The enthalpy of formation for τ resulting from CALPHAD (CALculation of PHAse Diagrams) approach agrees reasonably with that via first-principles methodology. Comparisons between the calculated and measured phase equilibria in the Al – Mg – Mn system show that the accurate experimental information is satisfactorily accounted for by the present description. A reaction scheme for the whole ternary system is presented for practical applications.

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Glutaminolysis is important for metabolism and biosynthesis of cancer cells, and GLS is essential in the process. Selenite is widely regarded as a chemopreventive agent against cancer risk. Emerging evidence suggests that it also has chemotherapeutic potential in various cancer types, but the mechanism remains elusive. We demonstrate for the first time that supranutritional dose of selenite suppresses glutaminolysis by promoting GLS1 protein degradation and apoptosis. Mechanistically, selenite promotes association of APC/C-CDH1 with GLS1 and leads to GLS1 degradation by ubiquitination, this process is related to induction of PTEN expression. In addition, GLS1 expression is increased in human colorectal cancer tissues compared with normal mucosae. Our data provide a novel mechanistic explanation for the anti-cancer effect of selenite from a perspective of cell metabolism. Moreover, our results indicate that glutaminolysis especially GLS1 could be an attractive therapeutic target in colorectal cancer.