Degradation of Contaminants of Emerging Concern by Electrochemical Oxidation: Coupling of Ultraviolet and Ultrasound Radiations.

In this work, we study the electrochemical oxidation of methyl red, a dye present in textile industrial effluents, which is selected as the model for the degradation of Contaminants of Emerging Concern. The influence of the initial pollutant concentration (1-5 mg dm-3), applied current density (2-15 mA cm-2), and the coupling of ultraviolet or ultrasound radiation have been studied using a titanium plate as anode. The results show that electrochemical oxidation is able to efficiently remove methyl red, and the process efficiency decreases with the initial pollutant concentration. At high applied current densities, efficiency drastically decreases due to a less effective mass transfer of the pollutant on the anodic surface. On one hand, the coupling of ultrasound entails an antagonistic effect on the process efficiency, which is probably due to a massive formation of oxidant radicals followed by a fast recombination process. On the other hand, the coupling of ultraviolet radiation increases the process efficiency. Concomitantly to the oxidation processes, titanium electrode produces rising TiO2-anatase nanoparticles, boosting the mineralization process. This new finding sets up a significant improvement over conventional photocatalysis treatments using TiO2-anatase as a catalyst due to synergistic effects coming from the coupling of the electrochemical oxidation and photocatalysis process with Ti anode.

Large Magnetoelectric Coupling Near Room Temperature in Synthetic Melanostibite Mn2 FeSbO6.

Multiferroic materials exhibit two or more ferroic orders and have potential applications as multifunctional materials in the electronics industry. A coupling of ferroelectricity and ferromagnetism is hereby particularly promising. We show that the synthetic melanostibite mineral Mn2 FeSbO6 (R3‾ space group) with ilmenite-type structure exhibits cation off-centering that results in alternating modulated displacements, thus allowing antiferroelectricity to occur. Massive magnetoelectric coupling (MEC) and magnetocapacitance effect of up to 4000 % was detected at a record high temperature of 260 K. The multiferroic behavior is based on the imbalance of cationic displacements caused by a magnetostrictive mechanism, which sets up an unprecedented example to pave the way for the development of highly effective MEC devices operational at or near room temperature.

Double Double Cation Order in the High-Pressure Perovskites MnRMnSbO6.

Cation ordering in ABO3 perovskites adds to their chemical variety and can lead to properties such as ferrimagnetism and magnetoresistance in Sr2 FeMoO6 . Through high-pressure and high-temperature synthesis, a new type of "double double perovskite" structure has been discovered in the family MnRMnSbO6 (R=La, Pr, Nd, Sm). This tetragonal structure has a 1:1 order of cations on both A and B sites, with A-site Mn(2+) and R(3+) cations ordered in columns and Mn(2+) and Sb(5+) having rock salt order on the B sites. The MnRMnSbO6 double double perovskites are ferrimagnetic at low temperatures with additional spin-reorientation transitions. The ordering direction of ferrimagnetic Mn spins in MnNdMnSbO6 changes from parallel to [001] below TC =76 K to perpendicular below the reorientation transition at 42 K at which Nd moments also order. Smaller rare earths lead to conventional monoclinic double perovskites (MnR)MnSbO6 for Eu and Gd.

Synthesis, structures and magnetic properties of the dimorphic Mn2CrSbO6 oxide.

The perovskite polymorph of Mn(2)CrSbO(6) compound has been synthesized at 8 GPa and 1473 K. It crystallizes in the monoclinic P21/n space group with cell parameters a = 5.2180 (2) Å, b = 5.3710(2) Å, c = 7.5874(1) Å and ß = 90.36(1)°. Magnetic susceptibility and magnetization measurements show the simultaneous antiferromagnetic ordering of Mn(2+) and Cr(3+) sublattices below TN = 55 K with a small canting. Low temperature powder neutron diffraction reveals a commensurate magnetic structure with spins confined to the ac-plane and a propagation vector κ = [1/2 0 1/2]. The thermal treatment of this compound induces an irreversible phase transition to the ilmenite polymorph, which has been isolated at 973 K and crystallizes in R3[combining macron] space group with cell parameters a = 5.2084 (4) Å and c = 14.4000 (11) Å. Magnetic susceptibility, magnetization and powder neutron diffraction data confirm the antiferromagnetic helical ordering of spins in an incommensurate magnetic structure with κ = [00 0.46] below 60 K, and the temperature dependence of the propagation vector up to κ = [00 0.54] at about 10 K.

Spin-glass behavior and incommensurate modulation in high-pressure perovskite BiCr0.5Ni0.5O3.

The BiCr(0.5)Ni(0.5)O(3) perovskite has been obtained at high pressure. Neutron and synchrotron diffraction data show a Pnma orthorhombic structure with a = 5.5947(1) Å, b = 7.7613(1) Å, and c = 5.3882(1) Å at 300 K and random B-site Cr/Ni distribution. Electron diffraction reveals an incommensurate modulation parallel to the b axis. The combination of either Cr-O-Ni (J > 0) or Cr-O-Cr/Ni-O-Ni (J < 0) nearest-neighbor spin interactions results in a random-bond spin-glass configuration. Magnetization, neutron diffraction, and muon-spin-relaxation measurements demonstrate that variations in the local bonding and charge states contribute to the magnetic frustration.

High-pressure synthesis, structural and complex magnetic properties of the ordered double perovskite Pb2NiReO6.

The ordered double perovskite Pb2NiReO6 has been prepared at 6 GPa and temperatures ranging from 1273 to 1373 K. Its crystal structure determined by X-ray powder diffraction and selected area electron diffraction shows monoclinic symmetry with centrosymmetric space group I2/m (a = 5.6021(1) Å, b = 5.6235(1) Å, c = 7.9286(1) Å and ß = 90.284°(1)). High angle annular dark field microscopy studies reveal the existence of compositional microdomains. The compound displays a re-entrant spin-glass transition from a ferrimagnetic ordering below T(N) ~ 37 K between the Re(+5) and Ni(+3) (high spin configuration) magnetic sublattices to a spin-glass configuration. Magnetic field dependent magnetization measurements revealed wasp-waisted hysteresis loops at 5 K. These shaped features originate from the antiferromagnetic/ferromagnetic (AFM/FM) competing interactions.

Spinel to CaFe2O4 transformation: mechanism and properties of beta-CdCr2O4.

The CdCr(2)O(4) spinel transforms to a 10.6% denser new polymorph of the CaFe(2)O(4)-type structure at 10 GPa and 1100 degrees C. This new polymorph has a honeycomb-like structure because of double rutile-type chains formed by [Cr-O(6)] edge-shared octehedra. This crystal structure is prone to be magnetically frustrated and presents low-dimensional antiferromagnetism at 25 K < T < 150 K, accompanied by more complex interactions as the temperature decreases. These transitions are evidenced by magnetic susceptibility and heat capacity measurements. We also discuss a possible structural mechanism for the transformation.

Antiferromagnetism and spin reorientation in "PbCrO3".

The perovskite "PbCrO(3)" was synthesized at high pressure and high temperature. Its magnetic properties have been investigated by means of magnetization, specific heat, and resistivity measurements. Earlier workers had concluded it to have a G-type antiferromagnetic structure. However, our measurements suggest a rather more complex situation: first, a weak ferromagnetic transition of the Cr(IV) spins occurs at 245 K; this is followed by a temperature-driven spin reorientation starting at 185 K and ending at 62 K. Since zero-magnetic-field spin reorientation in the "PbCrO(3)" perovskite should not be expected, an intrinsic "magnetoelectric effect", associated with the lone-pair Pb electrons, seems to be responsible for the observed smooth rotation of the Cr-spins.

Letter to the Editor: E-cadherin, laminin and collagen IV expression in the evolution from dysplasia to oral squamous cell carcinoma

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Expresión de E-cadherina, laminina y colágeno IV en la evolución de displasia a carcinoma epidermoide oral / E-cadherin, laminin and collagen IV expression in the evolution from dysplasia to oral squamous cell carcinoma

Objetivos: Estudiar la pérdida o reducción de la adhesión celular mediada por E-cadherina en leucoplasias, carcinomas epidermoides y metástasis ganglionares. Estudiar la pérdida de continuidad de la expresión de laminina y colágeno IV en la membrana basal epitelial en el desarrollo biológico de las leucoplasias y carcinomas orales.Material y metodo: Hemos estudiado 124 muestras de pacientes portadores de leucoplasias y carcinomas orales con diversos diagnósticos que abarcan desde epitelio normal (13 muestras), displasias leves (2), displasias moderadas (12), carcinomas in situ (13) carcinomas microinvasores (11) Carcinoma epidermoide oral (64 muestras) y metástasis ganglionar(9). Se construyeron 7 bloques de tissue microarrays con aguja de 2mm y se realizó un estudio mediante técnica inmunohistoquímica para E-cadherina (clona 36, T.D. ABD Company), Laminina (078P, Biogenex) y Colágeno IV (PHM12, Biogenex).Resultados: En Displasias Leves y Moderadas presentan pérdida de expresión de E-cadherina, Laminina, y ColágenoIV (20%). En Carcinomas in situ y Microinvasores, presentaron pérdida de expresión de E-cadherina (73%), y en Laminina y Colágeno IV (57%). En los carcinomas epidermoides, encontramos pérdida de expresión de E-cadherina (90%) y discontinuidad en la M. basal (70%). Todas las metástasis ganglionares presentaron pérdida de E-cadherina y discontinuidad en Laminina y Colágeno IV.Conclusiones: La pérdida de expresión de E-cadherina se incrementa al aumentar el grado de displasia de las lesiones. La perdida de continuidad en la expresión de laminina y Colágeno IV sigue una evolución paralela desde displasias a metástasis ganglionares. La disminución en la expresión de los tres marcadores ha sido significativa en la evolución de las lesiones orales

Objectives: Study the loss or reduction of the cellular adhesion mediated for E-cadherin in oral leukoplakias, oral squamouscell carcinomas and metastatic nodules. Study the loss of continuity of the laminin and collagen IV expression in the epithelial basal membrane from the biological development of the oral leukoplakias and oral carcinomas.Material and method: we have studied 124 samples of patient payees leukoplakias and oral carcinomas with diverse diagnosis that embrace from normal epithelium (13 samples), mild dysplasias (2), moderate dysplasias (12), “in situ” carcinomas (13), microinvasive carcinomas (11) oral squamous cell carcinomas (64 samples) and metastatic nodules (9). 7 blocks of tissue microarrays were built with needle of 2mm and was carried out a study by means of immunohistochemicaltechnique for E-cadherin (clone 36, Biogenex), Laminin (078P, Biogenex) and Collagen IV (PHM12, Biogenex).Results: In Mild and Moderate Dysplasias the results present loss of E-cadherin, Laminin, and Collagen IV (20%) expression. “in situ” and microinvasive carcinomas, the results presented loss of E-cadherin expression (73%), and loss in Laminin and Collagen IV expression (57%). In the squamous cell carcinomas , we find E-cadherin underexpression (90%) and discontinuity in the Basal Membrane. (70%). All the metastatic nodules presented loss of E-cadherin expressionand discontinuity in Laminin and Collagen IV expression.Conclusions: The loss of E-cadherin expression is increased when increasing the dysplasia grade of lesions. The loss of continuity in the laminin and Collagen IV expression follow a parallel evolution from dysplasias to metastatic nodules. The underexpression of the three markers has been significant in the evolution of the oral lesions

E-cadherin, laminin and collagen IV expression in the evolution from dysplasia to oral squamous cell carcinoma.

OBJECTIVES: Study the loss or reduction of the cellular adhesion mediated for E-cadherin in oral leukoplakias, oral squamous cell carcinomas and metastatic nodules. Study the loss of continuity of the laminin and collagen IV expression in the epithelial basal membrane from the biological development of the oral leukoplakias and oral carcinomas. MATERIAL AND METHOD: we have studied 124 samples of patient pays leukoplakias and oral carcinomas with diverse diagnosis that embrace from normal epithelium (13 samples), mild dysplasias (2), moderate dysplasias (12), in situ carcinomas (13), microinvasive carcinomas (11) oral squamous cell carcinomas (64 samples) and metastatic nodules (9). 7 blocks of tissue microarrays were built with needle of 2mm and was carried out a study by means of immunohistochemical technique for E-cadherin (clone 36, Biogenex), Laminin (078P, Biogenex) and Collagen IV (PHM12, Biogenex). RESULTS: In Mild and Moderate Dysplasias the results present loss of E-cadherin, Laminin, and Collagen IV (20%) expression. in situ and microinvasive carcinomas, the results presented loss of E-cadherin expression (73%), and loss in Laminin and Collagen IV expression (57%). In the squamous cell carcinomas , we find E-cadherin underexpression (90%) and discontinuity in the Basal Membrane. (70%). All the metastatic nodules presented loss of E-cadherin expression and discontinuity in Laminin and Collagen IV expression. CONCLUSIONS: The loss of E-cadherin expression is increased when increasing the dysplasia grade of lesions. The loss of continuity in the laminin and Collagen IV expression follow a parallel evolution from dysplasias to metastatic nodules. The underexpression of the three markers has been significant in the evolution of the oral lesions.

Expresión proteica de p53 y proliferación celular en leucoplasias orales / Proteic expressión of p53 and cellular proliferation in oral leukoplakias

Objetivos: Conocer la expresión proteica de las alteraciones genéticas que se producen en las etapas precoces de la cancerización del campo de cavidad oral en nuestro medio. Estudiar la proliferación celular mediante Ki-67 y la expresión de la proteína p53 para valorar si las alteraciones en la expresión proteica de estos marcadores suceden de forma secuencial a través de las distintas etapas en la cancerización del campo de la cavidad oral. Material y métodos: Se realizó un estudio mediante técnicas de inmunohistoquímica sobre 53 pacientes que presentaron lesiones de leucoplasia oral, atendidos por el Servicio de O.R.L del Hospital Universitario de Salamanca, desde 1.990 hasta 2000. Se incluyen en el estudio 11 muestras de epitelio normal, 15 displasias leves y moderadas, 15 carcinomas in situ, y 12 carcinomas microinvasores. Resultados: Encontramos la proliferación celular aumentada y sobreexpresión de p53 a medida que avanzamos en el grado de severidad histopatológica de las lesiones. Las alteraciones más precoces son el aumento significativo de la proliferación celular en displasias leves y moderadas y el aumento de expresión de p53. Conclusión: La leucoplasia oral es un estado precanceroso quec onstituye una lesión cancerizable debido a las alteraciones genéticas que intervienen en la evolución de la lesión. El estudio inmunohistoquímico y molecular de las lesiones es un medio rutinario que permite conocer la expresión proteica de las alteraciones genéticas, que puede ayudar en el diagnóstico precoz y tratamientode esta patología, teniendo especial relevancia el estudio de Ki-67 en etapas iniciales y p53 en lesiones más avanzadas

OBJECTIVES: We intend to know the protein expression of genetic alterations that take place in the early stages in the field cancerization of oral cavity in our means as well as to study the cellular proliferation by means of Ki-67 and the protein product expression of p53 to value if the alterations in the protein products expression of these markers happen in a sequential pathway through the different stages in the field cancerization of oral cavity. MATERIALS AND METHODS: A study was made by immunohistochemistry on 53 patients that presented lesions of oral leukoplaquia, assisted by the ENT service at University Hospitalof Salamanca, from 1.990 up to 2000. 11 samples of normal epithelium,15 mild to moderate dysplasias, 15 in situ carcinomas and 12 microinvasive carcinomas are included in the study. RESULTS: we find an increased cellular proliferation and p53 over-expression as we advance in the grade of severity histopathologic of these lesions. The most early alterations are a significant increase of cell proliferation in mild and moderate dysplasias and an increased p53 over-expression. CONCLUSIONS: Oral leukoplaquia is a precancerous stage that constitutes a canzerisable lesion due to the genetic alterations that mediate in the evolution of lesion. Routine Immunohistochemical and molecular study of these lesions allow us to know the protein expression of genetic alterations that can help in the early diagnosis and treatment of this pathology, having special relevance the study of Ki-67 in early stages and p53 inadvanced lesions

Proteic expression of p53 and cellular proliferation in oral leukoplakias.

OBJECTIVES: We intend to know the protein expression of genetic alterations that take place in the early stages in the field cancerization of oral cavity in our means as well as to study the cellular proliferation by means of Ki-67 and the protein product expression of p53 to value if the alterations in the protein products expression of these markers happen in a sequential pathway through the different stages in the field cancerization of oral cavity. MATERIALS AND METHODS: A study was made by immunohistochemistry on 53 patients that presented lesions of oral leukoplaquia, assisted by the ENT service at University Hospital of Salamanca, from 1.990 up to 2000. 11 samples of normal epithelium, 15 mild to moderate dysplasias, 15 in situ carcinomas and 12 microinvasive carcinomas are included in the study. RESULTS: we find an increased cellular proliferation and p53 over-expression as we advance in the grade of severity histopathologic of these lesions. The most early alterations are a significant increase of cell proliferation in mild and moderate dysplasias and an increased p53 over-expression. CONCLUSIONS: Oral leukoplaquia is a precancerous stage that constitutes a cancerisable lesion due to the genetic alterations that mediate in the evolution of lesion. Routine Immunohistochemical and molecular study of these lesions allow us to know the protein expression of genetic alterations that can help in the early diagnosis and treatment of this pathology, having special relevance the study of Ki-67 in early stages and p53 in advanced lesions.