A chemical method for removing calcium sulfate saturated solutions(0.016 mol/L CaSO_(4))using barium chloride(BaCl_(2)∙2H_(2)O)and sodium phosphate(Na_(3)PO_(4))was experimentally studied.The main interest is to remov...A chemical method for removing calcium sulfate saturated solutions(0.016 mol/L CaSO_(4))using barium chloride(BaCl_(2)∙2H_(2)O)and sodium phosphate(Na_(3)PO_(4))was experimentally studied.The main interest is to remove these ions from the solution through the precipitation of two solid species:sulfate(SO_(4)^(2−))as barite(BaSO4),and calcium(Ca^(2+))as hydroxyapatite(Ca_(5)(PO_(4))_(3)OH).Additionally,a solid/liquid separation method(i.e.,flotation)was explored,using oleic acid and dodecylamine as collectors.The results show that,the chemical treatment of saturated solutions at 60℃,pH 11.5 and using 3.9 g/L BaCl_(2)·2H_(2)O and 1.6 g/L Na_(3)PO_(4),promotes the precipitation of barium sulfate and calcium-deficient hydroxyapatite(Ca_(10−x)(HPO_(4))_(x)(PO_(4))_(6−x)(OH)_(2−x)),with residual concentrations of calcium and sulfate below 0.10 and 5 mg/L,respectively.The residual calcium concentration increases to 28 mg/L when using the same amount of reactants,at temperature and pH values below those quoted.The highest flotation recovery of hydroxyapatite with oleic acid at pH 9.5 was about 80%,while that of barite floated with dodecylamine at pH 6.5 was about 90%.展开更多
目的探讨磺基-N-琥珀酰亚胺油酸酯(sulfo-N-succinimidyloleate,SSO)调控二氧化硅(silicon dioxide,SiO_(2))诱导的巨噬细胞脂质代谢紊乱的机制。方法于2023年3月,以常规体外培养大鼠肺泡巨噬细胞NR8383,随机分为对照组(C组)、SSO染毒组...目的探讨磺基-N-琥珀酰亚胺油酸酯(sulfo-N-succinimidyloleate,SSO)调控二氧化硅(silicon dioxide,SiO_(2))诱导的巨噬细胞脂质代谢紊乱的机制。方法于2023年3月,以常规体外培养大鼠肺泡巨噬细胞NR8383,随机分为对照组(C组)、SSO染毒组、SiO_(2)染毒组和SiO_(2)+SSO染毒组,使用SSO和SiO_(2)分别单独或联合染毒NR8383细胞36 h构建细胞模型。免疫荧光和BODIPY 493/503染色分别检测白细胞分化抗原36(cluster of differentiation,CD36)和细胞内脂质的水平,Western blot检测细胞内CD36、肝脏X受体(liver X receptors,LXR)、磷酸化哺乳动物雷帕霉素靶蛋白(P-mammalian target of rapamycin,P-mTOR)、胆碱磷酸转移酶1(cholinephosphotransferase 1,CHPT1)的蛋白表达水平,脂质代谢组学筛选差异脂质代谢物及富集的途径。多组比较采用单因素方差分析,组内两两比较用LSD检验。结果SiO_(2)染毒导致巨噬细胞CD36、P-mTOR表达增加(P=0.012、0.020),LXR表达降低(P=0.005),细胞内脂质水平升高,给予SSO干预后,与SiO_(2)染毒组比较,SiO_(2)+SSO染毒组巨噬细胞CD36表达降低(P=0.023),LXR表达升高(P=0.000)。代谢组学筛选出C组和SiO_(2)染毒组中有87个差异代谢物,SiO_(2)染毒组和SiO_(2)+SSO染毒组中有19个差异代谢物,两个组中差异代谢物存在5个交集,分别为PS(22∶1/14∶0)、DG(O-16∶0/18∶0/0∶0)、PGP(i-13∶0/i-20∶0)、PC(18∶3/16∶0)、鞘氨酸(SPA)。两个比较组差异代谢物均主要富集在甘油磷脂代谢和鞘脂代谢通路。对甘油磷脂代谢通路中的差异基因CHPT1进行验证,SiO_(2)染毒后导致巨噬细胞CHPT1表达降低(P=0.041)。结论SSO可能通过调控PS(22∶1/14∶0)、DG(O-16∶0/18∶0/0∶0)、PGP(i-13∶0/i-20∶0)、PC(18∶3/16∶0)、SPA以及甘油磷脂代谢和鞘脂代谢通路改善SiO_(2)诱导的巨噬细胞脂质代谢紊乱。展开更多
基金the personnel of Cinvestav-IPN Unidad Saltillo as well as the scholarships awarded by CONACYT(México).
文摘A chemical method for removing calcium sulfate saturated solutions(0.016 mol/L CaSO_(4))using barium chloride(BaCl_(2)∙2H_(2)O)and sodium phosphate(Na_(3)PO_(4))was experimentally studied.The main interest is to remove these ions from the solution through the precipitation of two solid species:sulfate(SO_(4)^(2−))as barite(BaSO4),and calcium(Ca^(2+))as hydroxyapatite(Ca_(5)(PO_(4))_(3)OH).Additionally,a solid/liquid separation method(i.e.,flotation)was explored,using oleic acid and dodecylamine as collectors.The results show that,the chemical treatment of saturated solutions at 60℃,pH 11.5 and using 3.9 g/L BaCl_(2)·2H_(2)O and 1.6 g/L Na_(3)PO_(4),promotes the precipitation of barium sulfate and calcium-deficient hydroxyapatite(Ca_(10−x)(HPO_(4))_(x)(PO_(4))_(6−x)(OH)_(2−x)),with residual concentrations of calcium and sulfate below 0.10 and 5 mg/L,respectively.The residual calcium concentration increases to 28 mg/L when using the same amount of reactants,at temperature and pH values below those quoted.The highest flotation recovery of hydroxyapatite with oleic acid at pH 9.5 was about 80%,while that of barite floated with dodecylamine at pH 6.5 was about 90%.
文摘目的探讨磺基-N-琥珀酰亚胺油酸酯(sulfo-N-succinimidyloleate,SSO)调控二氧化硅(silicon dioxide,SiO_(2))诱导的巨噬细胞脂质代谢紊乱的机制。方法于2023年3月,以常规体外培养大鼠肺泡巨噬细胞NR8383,随机分为对照组(C组)、SSO染毒组、SiO_(2)染毒组和SiO_(2)+SSO染毒组,使用SSO和SiO_(2)分别单独或联合染毒NR8383细胞36 h构建细胞模型。免疫荧光和BODIPY 493/503染色分别检测白细胞分化抗原36(cluster of differentiation,CD36)和细胞内脂质的水平,Western blot检测细胞内CD36、肝脏X受体(liver X receptors,LXR)、磷酸化哺乳动物雷帕霉素靶蛋白(P-mammalian target of rapamycin,P-mTOR)、胆碱磷酸转移酶1(cholinephosphotransferase 1,CHPT1)的蛋白表达水平,脂质代谢组学筛选差异脂质代谢物及富集的途径。多组比较采用单因素方差分析,组内两两比较用LSD检验。结果SiO_(2)染毒导致巨噬细胞CD36、P-mTOR表达增加(P=0.012、0.020),LXR表达降低(P=0.005),细胞内脂质水平升高,给予SSO干预后,与SiO_(2)染毒组比较,SiO_(2)+SSO染毒组巨噬细胞CD36表达降低(P=0.023),LXR表达升高(P=0.000)。代谢组学筛选出C组和SiO_(2)染毒组中有87个差异代谢物,SiO_(2)染毒组和SiO_(2)+SSO染毒组中有19个差异代谢物,两个组中差异代谢物存在5个交集,分别为PS(22∶1/14∶0)、DG(O-16∶0/18∶0/0∶0)、PGP(i-13∶0/i-20∶0)、PC(18∶3/16∶0)、鞘氨酸(SPA)。两个比较组差异代谢物均主要富集在甘油磷脂代谢和鞘脂代谢通路。对甘油磷脂代谢通路中的差异基因CHPT1进行验证,SiO_(2)染毒后导致巨噬细胞CHPT1表达降低(P=0.041)。结论SSO可能通过调控PS(22∶1/14∶0)、DG(O-16∶0/18∶0/0∶0)、PGP(i-13∶0/i-20∶0)、PC(18∶3/16∶0)、SPA以及甘油磷脂代谢和鞘脂代谢通路改善SiO_(2)诱导的巨噬细胞脂质代谢紊乱。
