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Reverse anionic flotation of carbonate-containing iron ores is quite a challenging process. Studies on this ores conducted in many laboratories or beneficiation plants have obtained poor concentrate grades and separation between quartz and iron minerals, even when valuable minerals are adequately liberated. The presence of carbonate minerals, such as siderite, causes a detrimental effect on quartz flotation recovery (froth product) and separation selectivity between quartz and iron minerals. In this work, the effect of carbonate minerals on quartz flotation from iron mineral was investigated using sodium oleate as collector, starch and calcium as regulators. Microflotation, adsorption, PHREEQC calculation, and Fourier transform infrared spectroscopy (FTIR) measurements were conducted in the investigation. Carbonate minerals (i.e., siderite and dolomite) adversely affected the floatability of quartz and separation between quartz and hematite. Starch dosage experiment results clearly showed that the reduction of quartz recovery in the presence of carbonate minerals was mainly related to starch. In addition, mineral dissolution and sodium carbonate dosage experiments evidently exhibited that CO 3 2 − dissolved species of carbonate minerals passively affected quartz flotation recovery. By contrast, both starch and CO 3 2 − dissolved species of carbonate minerals adversely affected the flotation recovery. FTIR showed that the strong drop-off in quartz recovery in the presence of carbonate minerals was due to the adsorption of CaCO 3 precipitations on quartz surfaces and further their interaction with starch molecules. The appearance of CaCO 3 precipitations was caused by reaction of Ca 2 + from the hydrolysis of CaCl 2 and CO 3 2 − dissolved species of carbonate minerals. To decrease the passive effect, a potential strategy to improve the flotation performance of iron ores that contain carbonate minerals at strong alkaline pH is suggested to remove carbonate minerals before separation between hematite and quartz.

Background Reperfusion therapy is widely utilized for acute myocardial infarction (AMI), so ischemia/reperfusion (I/R) of the heart is frequently encountered in clinical practice. The curative effects of reperfusion therapy for AMI are favourable in most cases, but reperfusion can also cause harmful effect to cardiomyocytes. Hydroxysafflor yellow A (HSYA) is an effective therapeutic agent to alleviate I/R injury, but the mechanisms underlying this therapeutic effect are unknown. Methods and results The H9c2 cardiomyocyte cell line was incubated with or without HSYA during hypoxia, then it was reoxygenated. In the presence of HSYA, reoxygenation resulted in the upregulated expression and activity of heme oxygenase-1 (HO-1), phosphorylation of Akt, translocation of nuclear factor Nrf2, and most importantly, a reduction in A/R-induced apoptosis. An HO-1 inhibitor completely suppressed HO-1 enzymatic activity upregulated by HSYA and notably diminished the anti-apoptotic effect of HSYA. An inhibitor of PI3K, completely blocked Akt phosphorylation induced by HSYA and partly negated HSYA-induced upregulation of HO-1, translocation of nuclear factor Nrf2 and suppression of apoptosis in the H9c2 cardiomyocytes. Conclusions Our study suggests that HSYA can provide protection to H9c2 cardiomyocytes against A/R-induced apoptosis. This protective effect largely depends on the upregulation of HO-1 expression through the PI3K/Akt/Nrf2 signaling pathway.