Study of rare earth elements in the coals of the Shubarkol deposit

The work studies mineralogical and geochemical features of the Jurassic coals of the Shubarkol deposit. The samples were examined using the method of scanning electron microscopy (SEM-EDX) Hitachi S-3400N, which was carried out at the Uranium Geology Research and Development Center at the Department of Geoecology and Geochemistry of TPU. Coal geochemistry was studied by instrumental neutron activation analysis (INAA) at the nuclear geochemical laboratory of the Department of Geoecology and Geochemistry of National Research Tomsk Polytechnic University (TPU). The choice of this object of study was determined by the tasks of research including the study of the patterns of accumulation of abnormal concentrations of REE, the effect of various factors of the geological environment on the levels of their accumulation in coals, as well as the conditions of its concentration and forms of occurrence in coals to expand the mineral resource base of Kazakhstan for rare earth elements. According to the results of scanning microscopic analysis, aluminosilicates, sulfides and sulfates with inclusions of microparticles of rare and rare earth elements were found in the composition of the Shubarkol deposit coals. According to the INNA results, abnormal concentrations of Sc, Ta, Nb, Hf, Zr, Ba, Sr, Ce and REE were found. Weathering processes led mainly to the loss and redistribution of REE in the coal seams of the Shubarkol deposit, which in turn led to increasing the content of rare earth elements from the bottom up the section. As a result of the action of multiple processes, increased concentrations of rare earth metals, mainly of the yttrium group, were formed. The absence of negative europium anomaly was determined, which confirms the original rocks composition peculiarity. The maximum contents of rare-earth metals are confined to weathered coals; for the medium-heavy group (Nd, PM, Sm, Eu), they are almost a hundredfold higher than the clarke in the upper continental crust. The tenfold excess of the clarke for elements from Gd to Lu was found in clayey sandstones and siltstones; for the rest of the rocks of the deposit the excess over the clarke is significantly lower. It was found that the coals of the deposit belong to the H-type and L-type of REE distribution. During the formation of oxidized H-type coals, clayey matter of terrigenous ash predominated as a carrier of REE, while unoxidized L-type coals were formed with the introduction of REE into the coal accumulation basin mainly in the composition of clay minerals and LREE-phosphates. Here the main source of REE was apparently the weathering crust over acidic rocks.

Separation and Preconcentration of Cr(VI) as Ion Associate Using Solid Phase Extraction

A method of separation and preconcentration of Cr(VI) was developed based on sorption on modified silica gel (C18) of an ion associate of Cr(VI) anion with a quaternary base. The study was performed with the following quaternary onium salts: [1-(ethoxycarbonyl)- pentadecyl]trimethylammonium bromide, 1-hexadecylpyridinium chloride, benzyl(dodecyl)- dimethylammonium bromide, butyl(triphenyl)phosphonium bromide and tetraphenylarsonium chloride. Benzyl(dodecyl)dimethylammonium bromide was found the optimum ion-pairing reagent. Sample containing Cr(III) and Cr(VI) in the presence of 0.005 mol/l of benzyl(dodecyl)dimethylammonium bromide was pumped with a peristaltic pump through the column containing the sorbent. The optimum pH range 4-5 was maintained with 0.05 mol/l phosphate buffer. Elution was accomplished using 95 vol.% ethanol and the recovery of Cr(VI) was (96 ± 6)% in the concentration range 0.005-1 mg/l of Cr(VI); even in a tenfold excess of Cr(III) the recovery of Cr(VI) was 99.8% with the relative standard deviation of repeatability about 2.4% Cr in the eluate was determined by emission flame spectrometry (Cr I 425.435 nm) in an air-acetylene or N2O-acetylene flame with the limits of detection 10 or 2 ng/ml, respectively. Hence, with a typical preconcentration factor of 200, the limits of detection in natural aqueous samples were 50 and 10 pg/ml, respectively. Calibrations were linear at least up to 10 mg/l.

Homoleptische Carbenkomplexe, V [1]. Chelatartige Percarbenkomplexe des Palladiums und Platins / Homoleptic Carbene Complexes, V [1]. Chelating Percarbene Complexes of Palladium and Platinum

Ten palladium and platinum complexes each containing two chelating bis(diaminocarbene) ligands have been synthesized in a one pot-reaction from PdI2, PtI2 or K2PtCl4, a tenfold excess (forty equivalents) of isocyanide and 1,2- or 1,3-diamines. An X-ray investigation of (8) revealed a stereochemistry with the two spiro-linked seven-membered metallacycles strongly bending out of the PtC4 coordination plane in opposite directions. In addition, three palladium bis-chelates with mixed amine/carbene bidentate ligands were obtained from reactions of PdI2 with only four equivalents of isocyanide and the diamine.

Chromatography of Mo(VI) and W(VI) chelates with 2,3-dihydroxynaphthalene

Mo(VI) and W(VI) were separated in the form of their anionic chelates with 2,3-dihydroxynaphthalene (DHN) by reversed phase ion-pair chromatography. The effect of the organic modifier content and concentration of tetrabutylammonium cations (TBA) in the mobile phase and the effect of concentration of DHN in the injected sample on the separation were studied. The best results were attained by using a mobile phase containing DHN (0.5 mmol dm-3), TBA counter-ions (10 mmol dm-3) and phosphate buffer (50 mmol dm-3) in a medium of 30% (v/v) methanol and 30% (v/v) acetonitrile at pH 7 and by injecting Mo(VI) and W(VI) samples containing DHN in a tenfold excess. On a CGC glass column 150 . 3.3 mm i.d. packed with Separon SGX C18 (5μm), the solutes were separated at resolutions of Rij = 1.0 (DHN-Mo) and 1.6 (Mo-W). The detection limits at 240 nm were 0.5 and 0.2 nmol for Mo(VI) and W(VI), respectively.

Candidacidal activity of the neutrophil myeloperoxidase system can be protected from excess hydrogen peroxide by the presence of ammonium ion

Excessive concentrations of hydrogen peroxide inhibit the neutrophil myeloperoxidase system, presumably by inactivating the hypochlorous acid produced by this system. Ammonium ion generated by neutrophils and other cells can react with hypochlorous acid to produce monochloramine, an oxidant with good microbicidal activity, but relative resistance to inactivation by other compounds. In an assay based on the oxidation of 5-thio-2-nitrobenzoic acid, hydrogen peroxide reacted more readily with sodium hypochlorite (used as a source of hypochlorous acid) than with monochloramine. Also, in this assay Candida albicans yeast inactivated the oxidant activity of hypochlorous acid more completely than they did that of monochloramine. The killing of Candida by sodium hypochlorite, as determined in a standard colony count microbicidal assay, was inhibited by equimolar and greater concentrations of hydrogen peroxide; killing of this organism by monochloramine was not affected by a tenfold excess concentration of hydrogen peroxide. In microbicidal assays using 4 mU of myeloperoxidase and optimal or excessive concentrations of hydrogen peroxide or glucose and glucose oxidase to generate hydrogen peroxide, the excessive concentrations inhibited killing of Candida, but not Staphylococcus aureus. The inhibition of Candida killing could be reversed by addition of ammonium ion to convert hypochlorous acid to monochloramine. These results indicate that for certain organisms such as C albicans, conversion of hypochlorous acid to monochloramine by reactions with ammonium ion may extend the range of hydrogen peroxide concentrations under which killing by the myeloperoxidase system can occur by protecting the necessary microbicidal oxidants from inactivation by excess hydrogen peroxide.

Candidacidal activity of the neutrophil myeloperoxidase system can be protected from excess hydrogen peroxide by the presence of ammonium ion

Excessive concentrations of hydrogen peroxide inhibit the neutrophil myeloperoxidase system, presumably by inactivating the hypochlorous acid produced by this system. Ammonium ion generated by neutrophils and other cells can react with hypochlorous acid to produce monochloramine, an oxidant with good microbicidal activity, but relative resistance to inactivation by other compounds. In an assay based on the oxidation of 5-thio-2-nitrobenzoic acid, hydrogen peroxide reacted more readily with sodium hypochlorite (used as a source of hypochlorous acid) than with monochloramine. Also, in this assay Candida albicans yeast inactivated the oxidant activity of hypochlorous acid more completely than they did that of monochloramine. The killing of Candida by sodium hypochlorite, as determined in a standard colony count microbicidal assay, was inhibited by equimolar and greater concentrations of hydrogen peroxide; killing of this organism by monochloramine was not affected by a tenfold excess concentration of hydrogen peroxide. In microbicidal assays using 4 mU of myeloperoxidase and optimal or excessive concentrations of hydrogen peroxide or glucose and glucose oxidase to generate hydrogen peroxide, the excessive concentrations inhibited killing of Candida, but not Staphylococcus aureus. The inhibition of Candida killing could be reversed by addition of ammonium ion to convert hypochlorous acid to monochloramine. These results indicate that for certain organisms such as C albicans, conversion of hypochlorous acid to monochloramine by reactions with ammonium ion may extend the range of hydrogen peroxide concentrations under which killing by the myeloperoxidase system can occur by protecting the necessary microbicidal oxidants from inactivation by excess hydrogen peroxide.

Nonheme iron in sickle erythrocyte membranes: association with phospholipids and potential role in lipid peroxidation

Previous studies documented the abnormal association of heme and heme proteins with the sickle RBC membrane. We have now examined RBC ghosts and inside-out membranes (IOM) for the presence of nonheme iron as detected by its formation of a colored complex with ferrozine. Sickle ghosts have 33.8 +/- 18.2 nmol nonheme iron/mg membrane protein, and sickle IOM have 4.3 +/- 3.0 nmol/mg. In contrast, normal RBC ghosts and IOM have no detectable nonheme iron. The combination of heme and nonheme iron in sickle IOM averages nine times the amount of membrane- associated iron in normal IOM. Kinetics of the ferrozine reaction show that some of this nonheme iron on IOM reacts slowly and is probably in the form of ferritin, but most (72% +/- 18%) reacts rapidly and is in the form of some other biologic chelate. The latter iron compartment is removed by deferoxamine and by treatment of IOM with phospholipase D, which suggests that it represents an abnormal association of iron with polar head groups of aminophospholipids. The biologic feasibility of such a chelate was demonstrated by using an admixture of iron with model liposomes. Even in the presence of tenfold excess adenosine diphosphate, iron partitions readily into phosphatidylserine liposomes; there is no detectable association with phosphatidylcholine liposomes. To examine the bioavailability of membrane iron, we admixed membranes and t-butylhydroperoxide and found that sickle membranes show a tenfold greater peroxidation response than do normal membranes. This is not due simply to a deficiency of vitamin E, and this is profoundly inhibited by deferoxamine. Thus, while thiol oxidation in sickle membranes previously was shown to correlate with heme iron, the present data suggest that lipid peroxidation is related to nonheme iron. In control studies, we did not find this pathologic association of nonferritin, nonheme iron with IOM prepared from sickle trait, high-reticulocyte, postsplenectomy, or iron-overloaded individuals. These data provide additional support for the concept that iron decompartmentalization is a characteristic of sickle RBCs.

Nonheme iron in sickle erythrocyte membranes: association with phospholipids and potential role in lipid peroxidation

Previous studies documented the abnormal association of heme and heme proteins with the sickle RBC membrane. We have now examined RBC ghosts and inside-out membranes (IOM) for the presence of nonheme iron as detected by its formation of a colored complex with ferrozine. Sickle ghosts have 33.8 +/- 18.2 nmol nonheme iron/mg membrane protein, and sickle IOM have 4.3 +/- 3.0 nmol/mg. In contrast, normal RBC ghosts and IOM have no detectable nonheme iron. The combination of heme and nonheme iron in sickle IOM averages nine times the amount of membrane- associated iron in normal IOM. Kinetics of the ferrozine reaction show that some of this nonheme iron on IOM reacts slowly and is probably in the form of ferritin, but most (72% +/- 18%) reacts rapidly and is in the form of some other biologic chelate. The latter iron compartment is removed by deferoxamine and by treatment of IOM with phospholipase D, which suggests that it represents an abnormal association of iron with polar head groups of aminophospholipids. The biologic feasibility of such a chelate was demonstrated by using an admixture of iron with model liposomes. Even in the presence of tenfold excess adenosine diphosphate, iron partitions readily into phosphatidylserine liposomes; there is no detectable association with phosphatidylcholine liposomes. To examine the bioavailability of membrane iron, we admixed membranes and t-butylhydroperoxide and found that sickle membranes show a tenfold greater peroxidation response than do normal membranes. This is not due simply to a deficiency of vitamin E, and this is profoundly inhibited by deferoxamine. Thus, while thiol oxidation in sickle membranes previously was shown to correlate with heme iron, the present data suggest that lipid peroxidation is related to nonheme iron. In control studies, we did not find this pathologic association of nonferritin, nonheme iron with IOM prepared from sickle trait, high-reticulocyte, postsplenectomy, or iron-overloaded individuals. These data provide additional support for the concept that iron decompartmentalization is a characteristic of sickle RBCs.

Inhibitory action of chemically deglycosylated human chorionic gonadotrophin on hormone-induced steroid production by dispersed cells from human corpus luteum

ABSTRACT The biological activity of deglycosylated human chorionic gonadotrophin (hCG) prepared by treatment of the native hormone with anhydrous hydrogen fluoride was evaluated using suspensions of dispersed cells from biopsies of human corpus luteum obtained during the luteal phase of normal menstrual cycles. A reproducible pattern of response to hCG in terms of progesterone production by luteal cells was established for a range of luteal ages. Deglycosylation of hCG led to a diminished level of maximum response to the hormone. Co-incubation of luteal cells with a level of hCG just sufficient to elicit a maximum response and increasing concentrations of deglycosylated hCG led to a progressive inhibition of the hormonal response; at a concentration of 103 ng deglycosylated hCG/ml (a tenfold excess of deglycosylated hCG over the native hormone), hCG-induced progesterone production was reduced by about 50%. Deglycosylated hCG therefore acts as a partial antagonist for the action of hCG on human luteal cells. J. Endocr. (1984) 101, 327–332

Photometric determination of aluminium and zinc with salicylaldehyde semicarbazone

The effect of some tensides on the absorption, excitation, and fluorescence spectra of Al and Zn complexes of salicylaldehyde semicarbazone in aqueous-alcoholic solutions and on their extractability into ethyl acetate has been studied. The shape of the absorption spectra is unaffected by the presence of the tensides while the time of the complex formation is shorter. The complexes are extractable into ethyl acetate in the presence of the anionactive tenside tested, sodium lauryl sulphate. The optimum conditions for the spectrophotometric and fluorometric determination of Al and Zn have been established. The limit of determination is 2 ng ml-1 (pH 3.8-4.8) for Al and 50 ng ml-1 (pH 8.4-8.6) for Zn. Using thiosulphate or fluoride as masking agents, Zn can be determined in a concentration of 2 μg ml-1 in the presence of the same quantity of Al or Cu, or in the presence of a tenfold excess of Fe, with a relative standard deviation of 1.5%.