Erratum: Analytical Sciences, 2016, Vol. 32, No. 2, p. 167, Simultaneous Quantification of Iodine and Other Elements in Infant Formula by ICP-MS Following an Acid Digestion with Nitric Acid and Hydrogen Peroxide.

On page 168, the left column, line 26 to 29, the sentence,Working standard solutions (1, 5, 7.5, and 10 ng mL(-1)) were prepared from the iodine stock solution by dilution with 7.0% (v v(-1)) nitric acid, 5.0% (v v(-1)) acetic acid and 1.2% (v v(-1)) hydrogen peroxide.should readWorking standard solutions (1, 5, 7.5, and 10 ng mL(-1)) were prepared from the iodine stock solution by dilution with 7.0% (v v(-1)) nitric acid and 5.0% (v v(-1)) acetic acid.

Simultaneous Quantification of Iodine and Other Elements in Infant Formula by ICP-MS Following an Acid Digestion with Nitric Acid and Hydrogen Peroxide.

A method for quantifying iodine in infant formula is described. Nitric acid and hydrogen peroxide converted iodine into iodate in microwave-assisted digestion and prevented iodine volatilization and memory effects. Acetic acid as a carbon source was added to both the sample and standard solutions as a countermeasure against carbon charge transfer to iodine and the addition of acetic acid helped to enhance the sensitivity. The instrument limit of quantification was 0.1 ng mL(-1) and the relative standard deviation was less than 3%. The spike recoveries were between 94.8 and 106%. Good agreement with the values obtained using the tetramethylammonium hydroxide method was obtained for infant formula sold in several countries. This method permitted the simultaneous determination of iodine and 12 other important elements (Na, Mg, P, K, Ca, Cr, Mn, Fe, Cu, Zn, Se and Mo) in infant formula.

Fabrication of 3-nm-thick Si3N4 membranes for solid-state nanopores using the poly-Si sacrificial layer process.

To improve the spatial resolution of solid-state nanopores, thinning the membrane is a very important issue. The most commonly used membrane material for solid-state nanopores is silicon nitride (Si3N4). However, until now, stable wafer-scale fabrication of Si3N4 membranes with a thickness of less than 5 nm has not been reported, although a further reduction in thickness is desired to improve spatial resolution. In the present study, to fabricate thinner Si3N4 membranes with a thickness of less than 5 nm in a wafer, a new fabrication process that employs a polycrystalline-Si (poly-Si) sacrificial layer was developed. This process enables the stable fabrication of Si3N4 membranes with thicknesses of 3 nm. Nanopores were fabricated in the membrane using a transmission electron microscope (TEM) beam. Based on the relationship between the ionic current through the nanopores and their diameter, the effective thickness of the nanopores was estimated to range from 0.6 to 2.2 nm. Moreover, DNA translocation through the nanopores was observed.

[Rapid and simultaneous determination method for analysis of minerals in infant formula using ICP-MS].

A rapid and simultaneous method by using inductively coupled plasma mass spectrometry (ICP-MS) was developed for determination of 19 elements in infant formula. Fast and efficient sample digestion was achieved by a microwave-assisted nitric acid procedure. An acetic acid was added to both these treated solutions and standard solutions as a countermeasure for carbon charge transfer in As, Se elements. The observed calibration curves showed good linearity (r(2)>0.9993) and the quantification limit was low. The recoveries of elements were 95.0-108% and the relative standard deviations (RSD) of this method were 0.3-4.2%. The analyzed values were in good agreement with the certified values in a NIST standard reference material. This study showed that the ICP-MS method is useful for major to trace multi-elemental determination in infant formula.

Apoptotic injury in cultured human hepatocytes induced by HMG-CoA reductase inhibitors.

Hepatotoxicity is the major complaint during therapy with lipid-lowering agents such as statins, although the cellular mechanisms underlying the statin-induced liver injury are not fully understood. Using cultured human hepatocytes, we investigated the effects of lipophilic as well as hydrophilic statins on the cell viability. Lipophilic statins, including simvastatin, lovastatin, cerivastatin, fluvastatin and atorvastatin, reduced the viability of hepatocytes as assessed by the mitochondrial enzyme activity to reduce WST-8, however, a hydrophilic pravastatin did not cause cell injury. The simvastatin-induced loss of cell viability was attenuated by mevalonate or geranylgeranyl pyrophosphate. Simvastatin-induced DNA fragmentation and increased the number of cells stained with annexin V and terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling, both of which were reversed by caspase inhibitors such as zDEVD-fmk, zLEHD-fmk and zIETD-fmk. Consistent with these data, the activities of caspase-3, caspase-9 and caspase-8 were elevated by simvastatin. Simvastatin reduced the protein content and mRNA expression for bcl-2 without affecting bax mRNA expression. On the other hand, both lipophilic and hydrophilic statins significantly reduced the content of endogenous cholesterol. These findings suggest that lipophilic statins cause an apoptotic injury in human hepatocytes by stimulating caspase-3 subsequent to the activation of caspase-9 and caspase-8, in which the inhibition of 3-hydroxy-3-methylglutaryl coenzyme A reductase may be involved.

Cell-specific toxicity of fibrates in human embryonal rhabdomyosarcoma cells.

The effects of a variety of fibrates on the cell viability were examined in human embryonal rhabdomyosarcoma cells (HRMSC). Five fibrates, including fenofibrate, clofibrate, gemfibrozil, bezafibrate and ciprofibrate, all concentration-dependently reduced the cell viability determined by the mitochondrial enzyme activity. The cell injury occurred time-dependently and was marked at 24-48 h. The toxic action of fibrates was specific to HRMSC, since bezafibrate did not induce any marked changes in the viability of human microvascular endothelial cells or arterial smooth muscle cells. Synergistic cell injury was observed after a combined treatment with bezafibrate and simvastatin, although simvastatin alone reduced the cell viability. The cell injury was characterized by a typical nuclear damage, as evidenced by Hoechst 33342 staining and deoxynucleotidyl transferase dUTP nick-end label-positive staining. Similar cell-specific injury was induced by 8(S)-hydroxyeicosatetraenoic acid, a potent peroxisome proliferator-activated receptor alpha (PPARalpha) agonist. Consistent with these data, a marked expression for PPARalpha mRNA was observed in HRMSC but not in the endothelial or smooth muscle cells. Therefore, it is suggested that fibrates cause a cell-specific injury in HRMSC via activation of PPARalpha. Moreover, our present cell injury model using HRMSC may be useful for elucidating the mechanisms of clinical rhabdomyolysis induced by lipid-lowering agents.