Search for unconventional superconductors among the YTE 2Si2 compounds (TE = Cr, Co, Ni, Rh, Pd, Pt).

Motivated by the recent discovery of exotic superconductivity in YFe2Ge2 we undertook reinvestigation of formation and physical properties of yttrium-based 1:2:2 silicides. Here we report on syntheses and crystal structures of the YTE 2Si2 compounds with TE = Cr, Co, Ni, Rh, Pd and Pt, and their low-temperature physical properties measurements, supplemented by results of fully relativistic full-potential local-orbital minimum basis band structure calculations. We confirm that most of the members of that family crystallize in a tetragonal ThCr2Si2-type structure (space group I4/mmm) and have three-dimensional Fermi surface, while only one of them (YPt2Si2) forms with a closely-related primitive CaBe2Ge2-type unit cell (space group P4/nmm) and possess quasi-two-dimensional Fermi surface sheets. Physical measurements indicated that BCS-like superconductivity is observed only in YPt2Si2 (T c = 1.54 K) and YPd2Si2 (T c = 0.43 K), while no superconducting phase transition was found in other systems at least down to 0.35 K. Thermal analysis showed no polymorphism in both superconducting phases. No clear relation between the superconductivity and the crystal structure (and dimensionality of the Fermi surface) was observed.

The influence of magnetic sublattice dilution on magnetic order in CeNiGe3 and UNiSi2.

Polycrystalline samples of the Y-diluted antiferromagnet CeNiGe(3) (T(N) = 5.5 K) and Th-diluted ferromagnet UNiSi(2) (T(C) = 95 K) were studied by means of x-ray powder diffraction, magnetization and specific heat measurements performed in a wide temperature range. The lattice parameters of the Ce(1-x)Y(x)NiGe(3) alloys decrease linearly with increasing Y content, while the unit cell volume of U(1-x)Th(x)NiSi(2) increases linearly with increasing Th content. The ordering temperatures of the systems decrease monotonically with increasing x down to about 1.2 K in Ce(0.4)Y(0.6)NiGe(3) and 26 K in U(0.3)Th(0.7)NiSi(2), forming a dome of long-range magnetic order on their magnetic phase diagrams. The suppression of the magnetic order is associated with distinct broadening of the anomalies at T(N,C) due to crystallographic disorder being a consequence of the alloying. Below the magnetic percolation threshold x(c) of about 0.68 and 0.75 in the Ce- and U-based alloys, respectively, the long-range magnetic order smoothly evolves into a short-range one, forming a tail on the magnetic phase diagrams. The observed behaviour of Ce(1-x)Y(x)NiGe(3) and U(1-x)Th(x)NiSi(2) is characteristic of diluted magnetic alloys.

Temperature-dependent Raman and IR studies of multiferroic MnWO4 doped with Ni2+ ions.

Temperature-dependent Raman and IR studies of MnWO(4) crystal doped with Ni(2+) ions were performed in the 4.2-300 K range. These studies were complemented by magnetization and specific heat measurements in the 2-100K range, which revealed that MnWO(4) crystal doped with Ni(2+) ions exhibits two phase transitions at 13.9 and 12.5K. Temperature evolution of Raman wavenumbers and linewidths revealed anomalous behaviour at low temperatures. These anomalies have been attributed to spin-phonon coupling, which appear due to onset of antiferromagnetic spin ordering. The observed anomalies extend above T(N)=13.9 K. This behaviour is consistent with the fact that MnWO(4) is a moderately magnetically frustrated material.

Evolution from a localized to an intermediate valence regime in Ce2Cu(2-x)Ni(x)In.

Polycrystalline samples of the solid solution Ce2Cu(2-x)Ni(x)In were studied by means of x-ray powder diffraction, magnetic susceptibility and electrical resistivity measurements performed in a wide temperature range. Partial substitution of copper atoms by nickel atoms results in a quasi-linear decrease of the lattice parameters and the unit cell volume of the system. The lattice compression leads to an increase in the exchange integral and yields a reversal in the order of the magnetic 4f(1) and nonmagnetic 4f(0) states, being in line with the Doniach phase diagram. In the localized regime, where an interplay of the Kondo scattering and the crystalline electric field effect occurs, the rise in the hybridization strength is accompanied by a relative reduction in the scattering conduction electrons on excited crystal field levels.

Magnetic properties and electronic structures of intermediate valence systems CeRhSi2 and Ce2Rh3Si5.

The crystal structures and the physical (magnetic, electrical transport and thermodynamic) properties of the ternary compounds CeRhSi(2) and Ce(2)Rh(3)Si(5) (orthorhombic CeNiSi(2)- and U(2)Co(3)Si(5)-type structures, respectively) were studied over wide ranges of temperature and magnetic field strength. The results revealed that both materials are valence fluctuating systems, in line with previous literature reports. Direct evidence for valence fluctuations was obtained by means of Ce L(III)-edge x-ray absorption spectroscopy and Ce 3d core-level x-ray photoelectron spectroscopy. The experimental data were confronted with the results of ab initio calculations of the electronic band structures in both compounds.

Emergence of a superconducting state from an antiferromagnetic phase in single crystals of the heavy fermion compound Ce2PdIn8.

Single crystals of Ce2PdIn8 were studied by means of magnetic susceptibility, electrical resistivity, and specific heat measurements. The compound was found to be a heavy fermion clean-limit superconductor with Tc=0.68 K. Most remarkably, the superconductivity in this system emerges out of the antiferromagnetic state that sets in at TN=10 K, and both cooperative phenomena coexist in a bulk at ambient pressure conditions.

Violation of critical universality at the antiferromagnetic phase transition of YbRh2Si2.

We report on precise low-temperature specific-heat measurements, C(T), of YbRh2Si2 in the vicinity of the antiferromagnetic phase transition on a single crystal of superior quality (residual resistivity ratio of approximately 150). We observe a very sharp peak at T_{N}=72 mK with absolute values as high as C/T=8 J/mol K2. A detailed analysis of the critical exponent alpha around T_{N} reveals alpha=0.38 which differs significantly from those of the conventional universality classes in the Ginzburg-Landau theory, where alpha< or =0.11. Thermal-expansion measurements corroborate this large positive critical exponent. These results provide insight into the nature of the critical magnetic fluctuations at a temperature-driven phase transition close to a quantum critical point.

Kondo-cluster-glass state near a ferromagnetic quantum phase transition.

We report on a comprehensive study of CePd(1-x)Rh(x) (0.6 0, providing evidence for the absence of a quantum critical point. Instead, a peculiar "Kondo-cluster-glass" state is found for x >or= 0.65, and the non-Fermi-liquid effects in the specific heat, ac susceptibility, and magnetization are compatible with the quantum Griffiths phase scenario.

Molecular dosimetry in rat urine of aflatoxin-N7-guanine and other aflatoxin metabolites by multiple monoclonal antibody affinity chromatography and immunoaffinity/high performance liquid chromatography.

The development of molecular dosimetry methods will simplify the identification of people at high risk for cancer. A combined monoclonal antibody immunoaffinity chromatography/high performance liquid chromatography method has been devised to isolate and quantify aflatoxin-DNA adducts and other metabolites in rat urine samples. We report the production of 11 different monoclonal antibodies recognizing aflatoxin B1, aflatoxin Q1, aflatoxin G1, aflatoxicol, and aflatoxin M1 and the application of these antibodies to a multiple monoclonal antibody affinity chromatography technique. Using the multiple monoclonal antibody affinity column with rat urines obtained from dosed animals, between 90 and 95% of total aflatoxin metabolites can be bound to the column and isolated. Analytical immunoaffinity chromatography/high performance liquid chromatography analysis of these isolated aflatoxins reveals that more than 55% of the aflatoxins in rat urine are aflatoxin-dihydrodiol, aflatoxin-N7-guanine, aflatoxin Q1, aflatoxin M1, aflatoxin P1, and aflatoxin B1, accounting for 1.5, 9.6, 1.8, 34.5, 8.0, and 1.0% of the total aflatoxins, respectively. Further, a perchloric acid digestion of the aflatoxin-N7-guanine peak was used to confirm its identity by its conversion to guanine. The measurement of aflatoxin-N7-guanine excretion in rat urine was examined to assess its utility as a marker of DNA adduct formation in the liver, and a dose-dependent excretion in urine was found with a correlation coefficient of 0.99. A comparison of the dose-dependent residual levels of aflatoxin binding to liver DNA with the amount of aflatoxin-N7-guanine excreted in urine showed a correlation coefficient of 0.98. Besides the nucleic acid adduct excretion data, aflatoxin M1 and aflatoxin P1 were evaluated as molecular dosimeters in the urine. Aflatoxin M1 was found to be an excellent marker, whereas no linear relationship between dose and aflatoxin P1 excretion in urine was found.

Molecular dosimetry of urinary aflatoxin-DNA adducts in people living in Guangxi Autonomous Region, People's Republic of China.

Hepatocellular carcinoma is one of the five leading human cancers causing at least 250,000 deaths each year. One of the major risk factors for this disease is exposure to dietary aflatoxins, and the development of appropriate molecular dosimetry biomarkers would facilitate the identification of individuals at risk. This study was undertaken to explore the relationship between dietary intake of aflatoxins and the excretion of the major aflatoxin-DNA adduct and other metabolites into the urine of chronically exposed people. The following protocol was developed for this investigation in Guangxi Autonomous Region, People's Republic of China, where the diets of 30 males and 12 females (ages, 25-64 years) were monitored for 1 week and aflatoxin intake levels determined each day. Starting on the fourth day, total urine volumes were obtained in consecutive 12-h fractions for 3 or 4 days. High performance liquid chromatography and competitive radioimmunoassay analyses were done on each of the urine samples, and the relationships between excretion of total aflatoxin metabolites, aflatoxin-N7-guanine, aflatoxin M1, aflatoxin P1, and aflatoxin B1, and aflatoxin B1 intake values were determined. The average intake of aflatoxin B1 by men was 48.4 micrograms/day, giving a total mean exposure during the study period of 276.8 micrograms. The average daily intake by women was 77.4 micrograms/day, resulting in a total average exposure during the 7-day period of 542.6 micrograms aflatoxin B1. Initial efforts to characterize aflatoxin metabolites in urine samples were with an analysis by competitive radioimmunoassay. The analysis by linear regression of the association between aflatoxin B1 intake/day and total aflatoxin metabolite excretion/day showed a correlation coefficient of only 0.26. These findings stimulated the immunoaffinity/analytical high performance liquid chromatography analysis for individual metabolites. When the data were analyzed by linear regression analysis, the aflatoxin N7-guanine excretion and aflatoxin B1 intake from the previous day showed a correlation coefficient of 0.65 and P less than 0.000001. Similar analysis for aflatoxin M1 resulted in a correlation coefficient of 0.55 and P less than 0.00001, whereas there was no positive statistical association between exposure in the diet and aflatoxin P1 excretion, despite aflatoxin P1 being quantitatively a major metabolite. Analysis of the total aflatoxin-N7-guanine excretion in the urine during the complete collection period plotted against the total aflatoxin B1 exposure in the diet for each of the individuals, smoothing the day to day variations, revealed a correlation coefficient of 0.80 and P less than 0.0000001.(ABSTRACT TRUNCATED AT 400 WORDS)

Distribution of aflatoxins in tissues of growing pigs fed an aflatoxin-contaminated diet amended with a high affinity aluminosilicate sorbent.

The effect of hydrated sodium calcium aluminosilicate (HSCAS) added to the diet of swine fed an aflatoxin-contaminated diet on tissue aflatoxin levels was investigated. Pigs were fed control (less than 10 ng/g B1 + B2), contaminated (500-600 ng/g B1 + B2), and contaminated +0.5% HSCAS diets. Tissues analyzed for the presence of aflatoxin B1, B2, and M1 residues included liver, muscle, kidney, and adipose. Addition of HSCAS to the contaminated diet significantly reduced the amount of M1 in liver, kidney, and muscle tissue. Aflatoxin B1 was not reduced in liver or kidney, but was decreased in muscle.

Aflatoxin-DNA adduct formation in chronically dosed rats fed a choline-deficient diet.

Nutritional modulation of male Fischer rats by a choline-deficient/methionine-low diet dramatically increases hepatocarcinogenesis and reduces time to first tumors induced by aflatoxin B1 (AFB1). The effect of this diet on hepatic aflatoxin-DNA adduct burden in male Fischer rats dosed with a carcinogenic regimen of AFB1 was examined in this study. After 3 weeks of ingestion of a choline-deficient/methionine-low diet or control semi-purified diet, rats were administered a carcinogenic regimen of 25 micrograms [3H]AFB1 for 5 days a week over 2 weeks. Six choline-deficient and four control diet rats were killed 2 h after each dose, and liver DNA isolated. In addition, hepatic DNA was isolated from animals 1, 2, 3, and 11 days after the last [3H]AFB1 administration. At all time points HPLC analysis of aflatoxin-DNA adducts was performed to confirm radiometric determinations of DNA binding levels. No significant quantitative differences in AFB1-DNA adduct formation between the dietary groups were observed following the first exposure to [3H]AFB1; however, total aflatoxin-DNA adduct levels in the choline-deficient animals were significantly increased during the multiple dose schedule. When total aflatoxin-DNA adduct levels were integrated over the 10 day dose period, a 41% increase in adduct burden was determined for the choline-deficient animals. While this increase in DNA damage is consistent with the hypothesis that DNA damage is related to tumor outcome, the biochemical basis for this effect still needs to be elucidated.

Modulation of aflatoxin metabolism, aflatoxin-N7-guanine formation, and hepatic tumorigenesis in rats fed ethoxyquin: role of induction of glutathione S-transferases.

The effects of dietary administration of ethoxyquin (EQ) on aflatoxin B1 (AFB1) metabolism, DNA adduct formation and removal, and hepatic tumorigenesis were examined in male Fischer rats. Rats were fed a semipurified diet containing 0.4% EQ for 1 wk, gavaged with 250 micrograms of AFB1 per kg 5 times a wk during the next 2 wk, and, finally, restored to the control diet 1 wk after cessation of dosing. At 4 mo, focal areas of hepatocellular alteration were identified and quantitated by staining sections of liver for gamma-glutamyl transpeptidase. Treatment with EQ reduced by greater than 95% both area and volume of liver occupied by gamma-glutamyl transpeptidase-positive foci. Utilizing the same multiple dosing protocol, patterns of covalent modifications of DNA by AFB1 were determined. EQ produced a dramatic reduction in the binding of AFB1 to hepatic DNA: 18-fold initially and 3-fold at the end of the dosing period. Although binding was detectable at 3 and 4 mo postdosing, no effect of EQ was observed, suggesting that these persistent adducts are not of primary relevance to AFB1 carcinogenesis. Analysis of nucleic acid bases by high-performance liquid chromatography revealed no qualitative differences in adduct species between treatment groups. The inhibitory effect of EQ on AFB1 binding to DNA and tumorigenesis appears related to induction of detoxication enzymes. Rats fed 0.4% EQ for 7 days showed a 5-fold increase in hepatic cytosolic glutathione S-transferase (GST)-specific activities. Multiple molecular forms of GST were induced, and concomitant elevations in messenger RNA levels coding for the synthesis of GST subunits were observed. Correspondingly, biliary elimination of AFB1-glutathione conjugate was increased 4.5-fold in animals on the EQ diet during the first 2 h following p.o. administration of 250 micrograms of AFB1 per kg. Thus, induction by EQ of enzymes important to AFB1 detoxication, such as GST, can lead to enhanced carcinogen elimination, as well as reductions of AFB1-DNA adduct formation and subsequent expression of preneoplastic lesions, and, ultimately, neoplasia.