Effect In Mn1 Research Articles

Magnetostriction and Magnetocaloric Effect in Mn1 – xFexAs Alloys

Magnetostriction and Magnetocaloric Effect in Mn1 – xFexAs Alloys

Effect of manganese stoichiometry at B-site on magneto-transport and magnetic properties of La0.67Sr0.33MnO3manganites

To study the effect of manganese non-stoichiometry at B-site, a series of manganites with compositional formula La0.67Sr0.33Mn1±xO3 (where x = 0, 0.05 and 0.1) was synthesized by oxalate precursor method. X-ray diffraction data confirm the rhombohedral structure of La0.67Sr0.33Mn1±xO3 along with minor phases of Mn3O4. The average grain size is found to be 266 nm for x = 0 whereas its magnitude decreases with excess or deficiency in manganese concentration. An increase in the manganese non-stoichiometry leads to the coexistence of ferromagnetic and antiferromagnetic interactions. The effect of Mn1±x on the magnetotransport properties could be understood on the basis of collective behaviour of magnetic spins, double exchange mechanism and ratio of Mn4+/Mn3+ ions. A crossover from negative to positive magnetoresistance behavior above metal-insulator transition temperature was observed for LSP-0.95 sample, whereas a positive magnetoresistance over the entire temperature region was noticed for LSP-1.10 sample.

Critical behavior and magnetocaloric effect across the magnetic transition in Mn1+xFe4\u2212xSi3

The nature of the magnetic transition, critical scaling of magnetization, and magnetocaloric effect in Mn1+xFe4−xSi3 (x = 0 to 1) are studied in detail. Our measurements show no thermal hysteresis across the magnetic transition for the parent compound which is in contrast with the previous report and corroborate the second order nature of the transition. The magnetic transition could be tuned continuously from 328 K to 212 K with Mn substitution at the Fe site. The Mn substitution leads to a linear increase in the unit cell volume and a slight reduction in the effective moment. A detailed critical analysis of the magnetization data for x = 0.0 and 0.2 is performed in the critical regime using the modified Arrott plots, Kouvel-Fisher plot, universal curve scaling, and scaling analysis of magnetocaloric effect. The magnetization isotherms follow modified Arrott plots with critical exponent (βsimeq 0.308, γsimeq 1.448, and δsimeq 5.64) for the parent compound (x = 0.0) and (βsimeq 0.304, γsimeq 1.445, and δsimeq 5.64) for x = 0.2. The Kouvel-Fisher and universal scaling plots of the magnetization isotherms further confirm the reliability of our critical analysis and values of the exponents. These values of the critical exponents are found to be same for both the parent and doped samples which do not fall under any of the standard universality classes. The exchange interaction decays as J(r) ~ r−3.41 following the renormalization group theory and the observed critical exponents correspond to lattice dimensionality d = 2, spin dimensionality n = 1, and the range of interaction σ = 1.41. This value of σ(<2) indicates long-range interaction between magnetic spins. A reasonable magnetocaloric effect ΔSmsimeq −6.67 J/Kg-K and −5.84 J/Kg-K for x = 0.0 and 0.2 compounds, respectively, with a huge relative cooling power (RCP ~ 700 J/Kg) for 9 T magnetic field change is observed. The universal scaling of magnetocaloric effect further mimics the second order character of the magnetic transition. The obtained critical exponents from the critical analysis of magnetocaloric effect agree with the values deduced from the magnetic isotherm analysis.

Tuning transition temperature of magnetocaloric Mn1.8Fe0.2(P0.59Si0.41)x alloys for cryogenic magnetic refrigeration

Giant magnetocaloric effect in Mn1.8Fe0.2(P0.59Si0.41)x ( x = 1.00, 1.01, 1.02, 1.03, 1.04) alloys is assessed for cryogenic temperature applications. We found that the Curie temperature can be tuned from. 300 K to 99 K by increase of Mn/Fe and P/Si ratios. We systematically optimized metal/non-metal ratio and homogenization condition to maximize the volume fraction of the Fe2P-type phase. A giant isothermal magnetic entropy changes of 10.6 and 14.0 J/kgK under a magnetic field of 2.0 and 5.0 T is obtained at 117.0 K for Mn1.8Fe0.2(P0.59Si0.41)1.03 alloy. This work demonstrates low-cost Mn-Fe-P-Si alloys with giant MCE are competitive candidates compare to the rare-earth-containing magnetocaloric compounds for cryogenic applications.

Reversible magnetocaloric effect and critical behaviors in Mn1.9−xCoxSn compounds

The structure, magnetic properties and magnetocaloric effect in the Mn1.9−xCoxSn (x = 0, 0.2, 0.4) compounds have been investigated. The reversible magnetic-entropy changes of Mn1.9Sn and Mn1.7Co0.2Sn are 2.13 (209 K) and 1.08 (113 K) J kg−1 K−1, respectively, for magnetic field change between 0–5 T. The critical exponents in Mn1.9Sn and Mn1.7Co0.2Sn compounds have been determined. In the critical region, the data points of magnetization, field and temperature near fall into two universal curves. By analysis on the critical exponents, we thought that the short-range ferri-magnetic order occurs in x = 0 compound at T < and in x = 0.2 one at T > The analysis on long-range attractive interactions reveals the dominant long-range interactions in the vicinity of in both compounds, besides a little short-range ferro- or ferri-magnetic order.

Transformation behavior and magnetocaloric effect in Mn1−xCrxCoGe (x = 0.04 and 0.11) melt-spun ribbons tailored by heat treatment

Recently, MnNiGe and MnCoGe intermetallic compounds have received a considerable attention due to the coupled tunable martensitic and magnetic transitions as well as giant magnetocaloric effect (MCE) they exhibit. In this work, by doping with Cr and varying of the annealing regime, a merged magnetostructural transition between a ferromagnetic orthorhombic and a paramagnetic hexagonal structure was received near room temperature in Mn1−xCrxCoGe melt-spun ribbons with x=0.04 and 0.11. Structural and magnetic characterizations have been performed by X-ray diffraction, differential scanning calorimetry and magnetization measurements. It is found that, in ribbons with x=0.04 (0.11) annealed at 1148K, the peak value of the magnetic entropy change and the refrigerant capacity through the orthorhombic to hexagonal transition strongly increase with the annealing time from 7.3 (9.4) Jkg−1K−1 to 10.6 (13.7) Jkg−1K−1 and from 182 (235) Jkg−1 to 214 (267) Jkg−1, respectively, at 5T for the time increase from 4h to 8h. Compared to bulk alloys of similar composition, the fabricated melt-spun ribbons show much broader working temperature range and a higher cooling efficiency.

Tunable magnetostructural coupling and large magnetocaloric effect in Mn1−xNi1−xFe2xSi1−xGax

A common method of realizing a magnetostructural coupling for MnNiSi is chemically alloying it with a ternary compound possessing a stable Ni2In-type structure. In this way, the substituting elements and levels are determined by the stoichiometry of counterpart compounds. In this work, chemical co-substitutions of Fe and Ga at three different atomic sites of MnNiSi were performed. The selections of substitution elements and levels were based on the site occupation rule and an analysis of the site-dependent substitutional effects on structural stability, Curie temperatures, and magnetic moment of MnNiSi. A broad Curie temperatures window of 285K spanning room temperature was established in Mn1−xNi1−xFe2xSi1−xGax. Strong magnetostructural transformations with large magnetization difference were realized in this window. A relatively large magnetic entropy change of −38.1J/kgK was observed for a field change of 5T near room temperature in the alloy with x=0.15.

Kinetic arrest of the ferrimagnetic state in indium-doped Mn1.82Co0.18Sb

Substituting Mn with small amounts of Co in Mn2Sb leads to kinetic arrest and magnetic frustration effects. By adding small amounts of In in place of Sb, the tetragonality and thereby the kinetic arrest properties can be modified and controlled. We investigate the kinetic arrest effect in Mn1.82Co0.18Sb1−xInx with x = 0 and 0.5 at the first-order antiferromagnetic-ferrimagnetic magnetostructural transition. Kinetic arrest is observed in both systems, whereby the arrest is partial under 5 T field for Mn1.82Co0.18Sb and full for Mn1.82Co0.18Sb0.95In0.05. The FI state remains arrested as long as the cooling-field is maintained.

The effect of Mn1.5Co1.5O4 coatings on the development of near surface microstructure for Haynes 230 oxidized at 800 °C in air

The effect of reactively sintered Mn1.5Co1.5O4 (MCO) coatings on the development of surface microstructure for Haynes 230 (H230) oxidized in air at 800°C has been studied using a combination of thermo-gravimetric analysis and electron microscopy techniques. The bare alloy exhibits a parabolic rate constant of 8.8×10−9mg2cm−4s−1, and forms a two-layer oxide scale with a continuous chromia layer and a thinner discontinuous MnCr2O4 overlayer. For the MCO-coated H230, the reduction step of the reactive sintering process converts the MCO coating to a mixture of Co and MnO with a thin Cr-rich oxide layer at the interface with the alloy substrate. Following the re-oxidation step, there is a 200nm chromia layer and a 400nm cubic spinel reaction layer (RL) between the alloy and the MCO. These layers thicken to 800nm and 1.2μm, respectively after 1000h oxidation. These observations are compared to our previous studies of MCO-coated Crofer 22 APU, and the implications for long-term SOFC performance are discussed.

Abstract 1694: Over expression of MN1 induces therapy resistance in a murine model of AML

Abstract Acute myeloid leukemia (AML) is an accumulation of immature myeloid precursors that leads to marrow failure and death. This disease affects approximately 12,000 people per year in the United States, causing 9,000 deaths. Despite decades of active research the overall 5 year survival remains a dismal 30-40%. The backbone of initial therapy for the last 30 years is combination chemotherapy containing cytarabine (Ara-C) and an anthracycline. Resistance is a major problem and most patients diagnosed with AML will ultimately die from resistant disease. The MN1 gene encodes a transcription co-factor that has been found over-expressed in multiple AML patient samples. There are several reports that over-expression of MN1 confers a worse prognosis in AML. High MN1 expressers are less likely to achieve a remission and have lower 3 year survival rates. Additionally, over expression of MN1 in murine bone marrow leads to AML in transplanted recipients and predicts for resistance to ATRA in elderly AML patients. However, the effect of MN1 over expression on response to standard chemotherapy is currently unknown. To answer this question we used a murine model of AML driven by MLL-ENL. Blasts were infected with retroviral vectors that contained MN1 and a GFP reporter. Partially infected blast populations were then exposed to various concentrations of either Ara-C or doxorubicin and the ratio of GFP positive and negative cells was compared to untreated controls. When blasts were exposed to 150 nM Ara-C the GFP+ percentage went from 21.10 (+/- 0.5302) in the control samples to 35.68 (+/-1.230) in the treated samples. This result was even more profound when cells were treated with 15 ng/ml doxorubicin where the percentage went from 21.10 (+/- 0.5302) to 80.27 (+/-1.615). Bother results were highly statistically significant by two tailed student's t test with p values of 0.004 and &amp;lt; 0.0001 respectively. Consistent with these data purified blast populations over expressing MN1 showed resistance to both doxorubicin and Ara-C. This effect was the result of reduced induction of apoptosis as MN1 over expressing blasts showed decreased levels of annexin V staining after exposure to vary amounts of Ara-C or doxorubicin. In order to determine if MN1 conferred resistance to Ara-C and doxorubicin in vivo we injected sublethally irradiated recipients with a partially infected population of blasts. Eight days after injection of blasts animals were treated with 100 mg/kg Ara-C plus 3 mg/kg doxorubicin daily for 5 days or observed. Animals treated with Ara-C plus doxorubicin had 90.58% (+/-0.6638) GFP+ blasts compared to 55.38% (+/-5.245) in control animals. This result was highly statistically significant with a p value of &amp;lt; 0.0001 by two tailed student's t test. These data suggest that over expression of MN1 in this model confers resistance to Ara-C and doxorubicin in vitro and in vivo and provides a biological explanation for the clinical observation that it confers a worse prognosis. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 1694. doi:10.1158/1538-7445.AM2011-1694

Over Expression of MN1 Confers Resistance to Chemotherapy In Vitro and In Vivo

AbstractAbstract 969Acute myeloid leukemia (AML) is an accumulation of immature myeloid precursors that leads to progressive marrow failure and death. This disease affects approximately 12,000 people per year in the United States, causing 9,000 deaths. Despite decades of active research the overall 5 year survival remains a dismal 30–40%. The backbone of initial therapy for the last 30 years is combination chemotherapy containing cytarabine (Ara-C) and an anthracycline. Resistance to these therapies is a major problem and most patients diagnosed with AML will ultimately die from resistant disease.AML is characterized by heterogeneous genetic alterations that can be used to delineate prognosis. Using standard karyotyping techniques patients can be divided into good, intermediate and poor prognostic categories. There is a clear link between these chromosomal aberrations and response to chemotherapy as complete remission rates are significantly different between groups. Patients with no detectable cytogenetic abnormality fall into an intermediate prognostic group with a very heterogeneous outcome. Recent work has begun to uncover submicroscopic genetic alterations that effect prognosis for these patients. These alterations can be mutations, over or under expression of a particular gene.The MN1 gene encodes a transcription co-factor first identified by its involvement in a balanced translocation in a patient with a meningioma. Since its initial description it has been found over-expressed in multiple AML patient samples. There are several reports that over-expression of MN1 confers a worse prognosis in AML. High MN1 expressers were less likely to achieve a remission and had a lower 3 year survival rate. Additionally, over expression of MN1 in murine bone marrow leads to AML in transplanted recipients and predicts for resistance to ATRA in elderly AML patients. However, the effect of MN1 over expression on response to standard chemotherapy is currently unknown.To answer this question we used a murine model of AML driven by MLL-ENL. AML blasts were infected with retroviral vectors that contained MN1 and a GFP reporter. Partially infected blast populations were then exposed to various concentrations of either Ara-C or doxorubicin and the ratio of GFP positive and negative cells was compared to untreated controls. When blasts were exposed to 150 nM Ara-C the GFP+ percentage went from 21.10 (+/− 0.5302) in the control samples to 35.68 (+/−1.230) in the treated samples. This result was even more profound when cells were treated with 15 ng/ml doxorubicin where the percentage went from 21.10 (+/− 0.5302) to 80.27 (+/−1.615). Both results were highly statistically significant by two tailed student's t test with p values of 0.004 and <0.0001 respectively. Consistent results were obtained in multiple different infections and with separately derived MLL-ENL lines. These data demonstrate that blasts expressing MN1 had an advantage when exposed to either Ara-C or doxorubicin although the effect was far more pronounced with doxorubicin exposure. MN1 expressing blasts were also resistant to the combination of Ara-C and doxorubicin.In order to determine if MN1 conferred resistance to Ara-C and doxorubicin in vivo we injected sublethally irradiated, Ly5.1+ C57Bl6 recipients with a partially infected population of blasts. Ly5.1+ animals do not express the Ly5.2 allele; thus, staining cells for Ly5.2 allows differentiation of leukemic cells from endogenous marrow. Eight days after injection of blasts animals were treated with 100 mg/kg Ara-C plus 3 mg/kg doxorubicin daily for 5 days or observed. On day 6 animals were sacrificed and bone marrow from bilateral femurs was harvested, stained for Ly5.2 and analyzed by flow cytometery. Animals treated with Ara-C plus doxorubicin had 90.58% (+/−0.6638) Ly5.2+, GFP+ blasts compared to 55.38% (+/−5.245) in control animals. This result was highly statistically significant with a p value of <0.0001 by two tailed student's t test. This observation was reproducible in a separately derived MLL-ENL driven cell line.These data suggest that over expression of MN1 in this murine AML model confers resistance to both Ara-C and doxorubicin in vitro and in vivo and provides a biological explanation for the clinical observation that it confers a worse prognosis. The mechanisms involved in this resistance are currently under study. Disclosures:No relevant conflicts of interest to declare.

Co doping enhanced giant magnetocaloric effect in Mn1−xCoxAs films epitaxied on GaAs (001)

A giant magnetocaloric effect was found in series of Mn1−xCoxAs films epitaxied on GaAs (001). The maximum magnetic entropy change caused by a magnetic field of 4 T is as large as 25 J/kg K around room temperature, which is about twice the value of pure MnAs film. The observed small thermal hysteresis is more suitable for practical application. Growing of layered Mn1−xCoxAs films with Co concentration changing gradually may draw layered active magnetic regenerator refrigerators closer to practical application. Our experimental result may provide the possibility for the combination of magnetocaloric effect and microelectronic circuitry.

The “colossal” magnetocaloric effect in Mn1−xFexAs: What are we really measuring?

Recently, a so-called “colossal” magnetocaloric effect (MCE) was reported in Mn1−xFexAs [A. de Campos et al., Nat. Mater. 5, 802 (2006)]. However, the value of ΔS that was determined appears markedly overestimated since it results from the inadequate use of the Maxwell relation. Here, we report on recent measurements of ΔS in Mn1−xFexAs from which a correct MCE value is deduced by using the Clausius–Clapeyron equation. This result is asserted by careful use of the Maxwell relation.

Giant magnetocaloric effect in Mn1−x(Ti0.5V0.5)xAs: Experiments and calculations

In this paper, we present the giant magnetocaloric effect exhibited by the Mn1−x(Ti0.5V0.5)xAs compound with x=0.1. The ordering temperature decreases from 318K in the case of MnAs (x=0) to 266K in the case of Mn0.9Ti0.05V0.05As (x=0.1). A large magnetic entropy change −ΔSm attributed to a first order magnetic transition has been observed. For Mn0.9Ti0.05V0.05As, the maximum of −ΔSm occurs near TC=266K and is about 30J∕kgK for an applied field change of 2T, a value very close to that (∼31J∕kgK) measured in MnAs. For materials with a first order transition at TC, the observed magnetocaloric effect enhancement can be explained by magnetoelastic effects which are due to structural changes. A model based on the phenomenological approach of Bean and Rodbell [Phys. Rev. 126, 104 (1962)] has been developed in order to describe such a behavior. In this paper we apply this model to describe the giant magnetocaloric effect exhibited by Mn1−x(Ti0.5V0.5)xAs (x=0, 0.1) materials.

Ambient pressure colossal magnetocaloric effect in Mn1−xCuxAs compounds

Magnetic refrigeration is a good alternative to gas compression technology due to higher efficiency and environmental concerns. Magnetocaloric materials must exhibit large adiabatic temperature variations and a large entropic effect. MnAs shows the colossal magnetocaloric effect under high pressures or with Fe doping. In this work the authors introduce a class of materials—Mn1−xCuxAs—revealing a peak colossal effect of −175J∕(Kkg) for a 5T field variation at 318K and ambient pressure.

The MN1 oncoprotein synergizes with coactivators RAC3 and p300 in RAR-RXR-mediated transcription

The t(12;22) creates an MN1-TEL fusion gene leading to acute myeloid leukemia. The fusion partner TEL (ETV6) is a member of the ETS family of transcription factors. The nature of the other fusion partner, MN1, has not been investigated in detail until now. We recently described that MN1 activates the transcription activity of the moloney sarcoma virus long terminal repeat, indicating that this protein itself may act as a transcription factor. We show here that MN1 comprises multiple transcription activating domains. A search for a bound DNA sequence revealed that MN1 has affinity for retinoic acid responsive elements. A DR5 retinoic acid responsive element was observed in the LTR. The combination of MN1 and ligand-activated retinoic acid receptor leads to a synergistic induction of expression directed by the LTR. Cotransfection of MN1 with RAC3 or p300, known coactivators of retinoic acid receptors, leads to a further synergistic induction of transcription. In addition, the effect of MN1 can be inhibited by the wild-type adenovirus ElA protein that inhibits p300 function, but not by an E1A mutant lacking the p300-binding site. GAL4-MN1-mediated transcription can be enhanced directly by RAC3 and p300. Taken together, our results indicate that MN1 is a transcription coactivator rather than a sequence-specific transcription factor, and that it may stimulate RAR/RXR-mediated transcription through interaction with p160 and p300.