Bloedite (Na 2 SO 4 •MgSO 4 •4H 2 O) is an important natural chemical resource. So far, it has not been developed and utilized effectively because of its separation difficulties. To develop a new technology to produce Na 2 SO 4 and Mg−N compound fertilizers by a CO(NH 2 ) 2 salting-out method to separate bloedite, the mutual solubilities of the ternary system Na 2 SO 4 −CO(NH 2 ) 2 −H 2 O and the quaternary system Na 2 SO 4 −MgSO 4 −CO(NH 2 ) 2 −H 2 O at 25 °C were measured, and the phase digrams of these two systems were investigated. According to the phase diagram analysis, it indicates that, by using the CO(NH 2 ) 2 salting-out method, Na 2 SO 4 and MgSO 4 in bloedite can achieve better separation and anhydrous sodium sulfate can be directly obtained. The yield of Na 2 SO 4 was 90.98 % in the case of the mother solution without cycling and utilizing. Adding a certain amount of CO(NH 2 ) 2 into the mother solution after Na 2 SO 4 separation, MgSO 4 •CO(NH 2 ) 2 •2H 2 O can be obtained. After separating MgSO 4 •CO(NH 2 ) 2 •2H 2 O from the solution, the remain mother solution was recycled to dissolve bloedite. The new technology can get stable recycle production.

There is a great deal of H 2 O 2 loss and low production benefit in the traditional technology of urea peroxide production. To develop a new method of producing urea peroxide, the mutual solubilities in the quaternary system Na 2 CO 3 −CO(NH 2 ) 2 −H 2 O 2 −H 2 O were measured, and the corresponding diagrams were plotted at 0 °C and 25 °C. Based on the analysis about the phase diagram, this work put forward a new technology of the combination production of urea peroxide and sodium percarbonate. Urea peroxide was first produced at 0 °C; then sodium percarbonate was produced according to the reaction of Na 2 CO 3 with the residual solution after urea peroxide production at 25 °C. After sodium percarbonate production, the residual solution was evaporated and concentrated and then used to produce urea peroxide, and thereby the stable recycle production of CO(NH 2 ) 2 •H 2 O 2 and Na 2 CO 3 •1.5H 2 O 2 could be realized.

Background: Oocyte vitrification has been widely used in the treatment of infertility and fertility preservation. However, vitrification-induced mitochondrial damage adversely affects oocyte development. Several studies have reported that mitochondrial calcium uptake protein 1 (MICU1) regulates the uptake of mitochondrial calcium by the mitochondrial calcium uniporter (MCU) and subsequently controls aerobic metabolism and oxidative stress in mitochondria, but research considering oocytes remains unreported. We evaluated whether the addition of MICU1 modulators enhances mitochondrial activity, pyruvate metabolism, and developmental competence after warming of MII oocytes. Methods: Retrieved MII oocytes of mice were classified as vitrified or control groups. After thawing, oocytes of vitrified group were cultured with or without DS16570511 (MICU1 inhibitor) and MCU-i4 (MICU1 activator) for 2 h. Results: Mitochondrial Ca2+ concentration, pyruvate dephosphorylation level, and MICU1 expression of MII oocytes were significantly increased after vitrification. These phenomena were further exacerbated by the addition of MCU-i4 and reversed by the addition of DS16570511 after warming. However, the mitochondrial membrane potential (MMP) and adenosine triphosphate (ATP) in vitrified-warmed MII oocytes drop significantly after vitrification, which was improved after MCU-i4 treatment and decreased significantly after DS16570511 treatment. The vitrification process was able to elicit a development competence reduction. After parthenogenetic activation, incubation of the thawed oocytes with MCU-i4 did not alter the cleavage and blastocyst rates. Moreover, incubation of the thawed oocytes with DS16570511 reduced the cleavage and blastocyst rates. Conclusions: MICU1-mediated increasing mitochondrial calcium uptake after vitrification of the MII oocytes promoted the pyruvate oxidation, and this process may maintain oocyte development competence by compensating for the consumption of ATP under stress state.

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