Mining flotation reagents: Quantitative and robust analysis of metal-xanthate complexes in water.

Xanthates, common mining flotation reagents, strongly bind thiophilic metals such as copper (Cu), lead (Pb), cadmium (Cd), and zinc (Zn) and consequentially change their bioavailability and mobility upon their discharge into the environment. However, accurate quantification of the metal-xanthate complexes has remained elusive. This study develops a novel and robust method that realizes the accurate quantification of the metal-xanthate complexes resulted from single and multiple reactions of three typical xanthates (ethyl, isopropyl, and butyl xanthates) and four thiophilic metals (Cu, Pb, Cd, and Zn) in water samples. This method uses sulfur (S2-) dissociation, followed by tandem solid phase extraction of C18 + PWAX and subsequent LC-MS/MS analysis. It has a wide linearity range (1-1000 µg/L, R2 ≥ 0.995), low method detection limits (0.002-0.036 µg/L), and good recoveries (70.6-107.0 %) at 0.01-10 mg/L of xanthates. Applications of this method showed ubiquitous occurrence of the metal-xanthate complexes as the primary species in flotation wastewaters, which the concentrations were 4.6-28.9-fold higher than those previously determined. It is the first quantitative method established for the analysis of metal-xanthate complexes in water samples, which is of great importance to comprehensively understand the fate and risks of xanthates in the environment.

miR-7a/b attenuates post-myocardial infarction remodeling and protects H9c2 cardiomyoblast against hypoxia-induced apoptosis involving Sp1 and PARP-1.

miRs (microRNAs, miRNAs) intricately regulate physiological and pathological processes. Although miR-7a/b protects against cardiomyocyte injury in ischemia/reperfusion injury, the function of miR-7a/b in myocardial infarction (MI)-induced cardiac remodeling remains unclear. Here, we sought to investigate the function of miR-7a/b in post-MI remodeling in a mouse model and to determine the underlying mechanisms involved. miR-7a/b overexpression improved cardiac function, attenuated cardiac remodeling and reduced fibrosis and apoptosis, whereas miR-7a/b silencing caused the opposite effects. Furthermore, miR-7a/b overexpression suppressed specific protein 1 (Sp1) and poly (ADP-ribose) polymerase (PARP-1) expression both in vivo and in vitro, and a luciferase reporter activity assay showed that miR-7a/b could directly bind to Sp1. Mithramycin, an inhibitor of the DNA binding activity of Sp1, effectively repressed PARP-1 and caspase-3, whereas knocking down miR-7a/b partially counteracted these beneficial effects. Additionally, an immunoprecipitation assay indicated that hypoxia triggered activation of the binding activity of Sp1 to the promoters of PARP-1 and caspase-3, which is abrogated by miR-7a/b. In summary, these findings identified miR-7a/b as protectors of cardiac remodeling and hypoxia-induced injury in H9c2 cardiomyoblasts involving Sp1 and PARP-1.

[Research on relationship of survivin gene expression with malignant proliferation and apoptosis of brain glioma].

OBJECTIVE: To investigate the expression level of inhibitor of apoptosis protein survivin gene in human brain glioma and its role in malignant proliferation and antiapoptosis of brain glioma. METHODS: Eighty-three cases of brain glioma specimen was chosen, protein expression of survivin and proliferating cell nuclear antigen (PCNA) was investigated by immunohistochemistry streptavidin-biotin complex (SABC) method, the immunoreactivity score (IRS) of survivin and the proliferative index (PI) were counted. Apoptotic cells were screened by TdT-mediated dUTP-biotin nick-end labeling (TUNEL) method, and the apoptotic index (AI) of brain glioma was calculated. RESULTS: The survivin IRS, PI and AI of brain glioma were 3.8 +/- 3.9, (28.4 +/- 19.5)% and (1.0 +/- 0.8)% respectively, and all of them were elevated with the increase of pathological grade of brain glioma (P < 0.01 for all). PI in survivin positive group was significantly higher than that in survivin negative group (P < 0.01), and PI was positively correlated with survivin IRS (r = 0.740, P < 0.01). There was no significant difference between AI in survivin positive group and that in survivin negative group (P > 0.05), however, AI was negatively correlated with survivin IRS (r = -0.307, P < 0.01). CONCLUSIONS: Survivin is overexpressed in brain glioma, and which may play important roles in malignant proliferation and antiapoptosis of brain glioma.

[Changes and effects of group II metabotropic glutamate receptors in the cerebral cortex of rats after diffuse brain injuries coupled with hypopiesia secondary brain insults].

OBJECTIVE: To study the changes and effects of group II metabotropic glutamate receptors (mGluR) after diffuse brain injuries (DBI) coupled with hypopiesia secondary brain insults (SBI). METHODS: Male SD rats were randomized into four groups: normal control, sham-operated, DBI alone and DBI coupled with SBI group. The SBI model was made on the basis of Marmarou's model. The mRNAs of the mGluRs were detected at 1, 3, 6, 12, 24, 48 and 72 hours after injuries by in-situ hybridization, and the positive neurons were counted. RESULTS: Statistical analysis showed no significance between normal control group and sham-operated group, DBI group in mGluR 2, 3 mRNA (all P>0.05). The number of mGluR 2, 3 positive neurons decreased at 12 hours after injury and the peak occurred at 48 hours after injury in the injured cerebral cortex in DBI alone group (both P<0.05). However, in DBI with SBI group, there was a significant decrease of the number of mGluR2, 3 positive neurons at 6 hours after injury and the peak happened at 24 hours after injury (both P<0.05). CONCLUSION: mGluR2, 3, factors with the function of protecting brain, might play an important role in the path physiology of DBI and SBI.

Experiment and observation on invasion of brain glioma in vivo.

Research on invasion and metastasis of glioma in vivo was performed by implanting C6 glioma cells transfected with enhanced green fluorescent protein (EGFP) gene into the brain of SD rats. Firstly, C6 glioma cells were transfected with a plasmid vector (pEGFP-N3) containing the EGFP gene. Stable EGFP-expressing clones were isolated and examination for these cells by flow cytometry and electron microscope was done. Secondly, EGFP-expressing cells were stereotactically injected into the brain parenchyma of SD rats to establish xenotransplanted tumor. Four weeks later rats were killed and continuous brain sections were examined using fluorescence microscopy after adjacent sections were examined by immunohistochemistry or routine hematoxylin and eosin staining for the visualization and detection of tumor cell invasion. Xenotransplanted tumor was primarily cultured to determine the storage of EGFP gene in vivo. The results showed that EGFP-transfected C6 glioma cells maintained stable high-level EGFP expression in the central nervous system during their growth in vivo. EGFP fluorescence clearly demarcated the primary tumor margin and readily allowed for the visualization of distant micrometastasis and invasion on the single-cell level. Small locally invasive foci, including those immediately adjacent to the leading invasive edge of the tumor, were virtually undetectable by routine hematoxylin and eosin staining and immunohistochemistry. These results suggested that EGFP-transfected C6 cells can be visualized by fluorescence microscopy after intracranial implantation. This model is an excellent experimental animal model in research on invasion and metastasis of brain glioma in vivo.