Ultrafast spin polarization in a multiferroic manganite BiFe0.5Mn0.5O3 thin film

In this work, we present observations of ultrafast carrier dynamics and spin polarization in a multiferroic manganite BiFe0.5Mn0.5O3 film excited by linearly and circularly polarized femtosecond pulses, respectively. The d-band charge transfer transition is reasonably assigned to Γ3 → Γ5. The transient reflectivity decay on a time scale as fast as only 0.3 ps is consistent with the picture of ultrafast electron-phonon coupling. The ultrafast switching of polarization ellipticity (\u3c 150 fs) originates from a transient coherent spin polarization by optical orientation. The ultrafast spin polarization switching is assigned to the Raman coherence process

Effect of anisotropy on the ground-state magnetic ordering of the spin-one quantum J1XXZJ_{1}^{XXZ}--J2XXZJ_{2}^{XXZ} model on the square lattice

We study the zero-temperature phase diagram of the $J_{1}^{XXZ}$--$J_{2}^{XXZ}$ Heisenberg model for spin-1 particles on an infinite square lattice interacting via nearest-neighbour ($J_1 \equiv 1$) and next-nearest-neighbour ($J_2 > 0$) bonds. Both bonds have the same $XXZ$-type anisotropy in spin space. The effects on the quasiclassical N\'{e}el-ordered and collinear stripe-ordered states of varying the anisotropy parameter $\Delta$ is investigated using the coupled cluster method carried out to high orders. By contrast with the spin-1/2 case studied previously, we predict no intermediate disordered phase between the N\'{e}el and collinear stripe phases, for any value of the frustration $J_2/J_1$, for either the $z$-aligned ($\Delta > 1$) or $xy$-planar-aligned ($0 \leq \Delta < 1$) states. The quantum phase transition is determined to be first-order for all values of $J_2/J_1$ and $\Delta$. The position of the phase boundary $J_{2}^{c}(\Delta)$ is determined accurately. It is observed to deviate most from its classical position $J_2^c = {1/2}$ (for all values of $\Delta > 0$) at the Heisenberg isotropic point ($\Delta = 1$), where $J_{2}^{c}(1) = 0.55 \pm 0.01$. By contrast, at the XY isotropic point ($\Delta = 0$), we find $J_{2}^{c}(0) = 0.50 \pm 0.01$. In the Ising limit ($\Delta \to \infty$) $J_2^c \to 0.5$ as expected.Comment: 20 pages, 5 figure

Copper accumulation and physiological markers of soybean (Glycine max) grown in agricultural soil amended with copper nanoparticles

Environmental Biolog

Microgravity induces inhibition of osteoblastic differentiation and mineralization through abrogating primary cilia

It is well documented that microgravity in space environment leads to bone loss in astronauts. These physiological changes have also been validated by human and animal studies and modeled in cell-based analogs. However, the underlying mechanisms are elusive. In the current study, we identified a novel phenomenon that primary cilia (key sensors and functioning organelles) of rat calvarial osteoblasts (ROBs) gradually shrank and disappeared almost completely after exposure to simulated microgravity generated by a random positioning machine (RPM). Along with the abrogation of primary cilia, the differentiation, maturation and mineralization of ROBs were inhibited. We also found that the disappearance of primary cilia was prevented by treating ROBs with cytochalasin D, but not with LiCl or dynein light chain Tctex-type 1 (Dynlt1) siRNA. The repression of the differentiation, maturation and mineralization of ROBs was effectively offset by cytochalasin D treatment in microgravity conditions. Blocking ciliogenesis using intraflagellar transport protein 88 (IFT88) siRNA knockdown inhibited the ability of cytochalasin D to counteract this reduction of osteogenesis. These results indicate that the abrogation of primary cilia may be responsible for the microgravity's inhibition on osteogenesis. Reconstruction of primary cilia may become a potential strategy against bone loss induced by microgravity.Wengui Shi, Yanfang Xie, Jinpeng He, Jian Zhou, Yuhai Gao, Wenjun Wei, Nan Ding, Huiping Ma, Cory J. Xian, Keming Chen, Jufang Wan

Superconductivity in SmFe1-xMxAsO (M = Co, Rh, Ir)

In this paper we report the comparative study of superconductivity by 3d (Co), 4d (Rh), 5d (Ir) element doping in SmFeAsO. X-ray diffraction patterns indicate that the material has formed the ZrCuSiAs-type structure with a space group P4/nmm. It is found that the antiferromagnetic spin-density-wave (SDW) order in the parent compounds is rapidly suppressed by Co, Rh, and Ir doping, and superconductivity emerges. Both electrical resistance and magnetization measurements show superconductivity up to around 10 K in SmFe1-xMxAsO (M = Co, Rh, Ir). Co, Rh and Ir locate in the same column in the periodic table of elements but have different electronic band structure, so comparative study would add more ingredients to the underlying physics of the iron-based superconductors.Comment: 16 pages, 4 figures, 1 tabl

Growth of BiFeO 3

BiFeO3 microcylinders were synthesized via a hydrothermal condition. SEM observation reveals that with increasing the hydrothermal reaction time from 6 to 15 h, the microcylinders grow from ~0.7 to ~4.1 μm in height, whereas their diameter remains to be 3.7-3.8 μm with a minor change. The microcylinders are mainly made up of sphere-like grains of 100–150 nm in size. A possible growth mechanism of the BiFeO3 microcylinders is proposed. The photocatalytic activity of the as-prepared BiFeO3 samples was evaluated by the degradation of acid orange 7 under simulated sunlight irradiation, revealing that they possess an appreciable photocatalytic activity. Magnetic hysteresis loop measurement shows that the BiFeO3 microcylinders exhibit a typical antiferromagnetic behavior at room temperature

The Epigenetic Modifier PRDM5 Functions as a Tumor Suppressor through Modulating WNT/β-Catenin Signaling and Is Frequently Silenced in Multiple Tumors

BACKGROUND: PRDM (PRDI-BF1 and RIZ domain containing) proteins are zinc finger proteins involved in multiple cellular regulations by acting as epigenetic modifiers. We studied a recently identified PRDM member PRDM5 for its epigenetic abnormality and tumor suppressive functions in multiple tumorigeneses. METHODOLOGY/PRINCIPAL FINDINGS: Semi-quantitative RT-PCR showed that PRDM5 was broadly expressed in human normal tissues, but frequently silenced or downregulated in multiple carcinoma cell lines due to promoter CpG methylation, including 80% (4/5) nasopharyngeal, 44% (8/18) esophageal, 76% (13/17) gastric, 50% (2/4) cervical, and 25% (3/12) hepatocellular carcinoma cell lines, but not in any immortalized normal epithelial cell lines. PRDM5 expression could be restored by 5-aza-2'-deoxycytidine demethylation treatment in silenced cell lines. PRDM5 methylation was frequently detected by methylation-specific PCR (MSP) in multiple primary tumors, including 93% (43/46) nasopharyngeal, 58% (25/43) esophageal, 88% (37/42) gastric and 63% (29/46) hepatocellular tumors. PRDM5 was further found a stress-responsive gene, but its response was impaired when the promoter was methylated. Ectopic PRDM5 expression significantly inhibited tumor cell clonogenicity, accompanied by the inhibition of TCF/β-catenin-dependent transcription and downregulation of CDK4, TWIST1 and MDM2 oncogenes, while knocking down of PRDM5 expression lead to increased cell proliferation. ChIP assay showed that PRDM5 bound to its target gene promoters and suppressed their transcription. An inverse correlation between the expression of PRDM5 and activated β-catenin was also observed in cell lines. CONCLUSIONS/SIGNIFICANCE: PRDM5 functions as a tumor suppressor at least partially through antagonizing aberrant WNT/β-catenin signaling and oncogene expression. Frequent epigenetic silencing of PRDM5 is involved in multiple tumorigeneses, which could serve as a tumor biomarker

The accelerated scaling attractor solution of the interacting agegraphic dark energy in Brans-Dicke theory

We investigate the interacting agegraphic dark energy in Brans-Dicke theory and introduce a new series general forms of dark sector coupling. As examples, we select three cases involving a linear interaction form (Model I) and two nonlinear interaction form (Model II and Model III). Our conclusions show that the accelerated scaling attractor solutions do exist in these models. We also find that these interacting agegraphic dark energy modes are consistent with the observational data. The difference in these models is that nonlinear interaction forms give more approached evolution to the standard $\Lambda$CDM model than the linear one. Our work implies that the nonlinear interaction forms should be payed more attention.Comment: 9 pages, 10 figures, accepted in Eur. Phys. J.

Quantification of SLIT-ROBO transcripts in hepatocellular carcinoma reveals two groups of genes with coordinate expression

<p>Abstract</p> <p>Background</p> <p>SLIT-ROBO families of proteins mediate axon pathfinding and their expression is not solely confined to nervous system. Aberrant expression of <it>SLIT-ROBO </it>genes was repeatedly shown in a wide variety of cancers, yet data about their collective behavior in hepatocellular carcinoma (HCC) is missing. Hence, we quantified <it>SLIT-ROBO </it>transcripts in HCC cell lines, and in normal and tumor tissues from liver.</p> <p>Methods</p> <p>Expression of <it>SLIT-ROBO </it>family members was quantified by real-time qRT-PCR in 14 HCC cell lines, 8 normal and 35 tumor tissues from the liver. ANOVA and Pearson's correlation analyses were performed in R environment, and different clinicopathological subgroups were pairwise compared in Minitab. Gene expression matrices of cell lines and tissues were analyzed by Mantel's association test.</p> <p>Results</p> <p>Genewise hierarchical clustering revealed two subgroups with coordinate expression pattern in both the HCC cell lines and tissues: <it>ROBO1</it>, <it>ROBO2</it>, <it>SLIT1 </it>in one cluster, and <it>ROBO4</it>, <it>SLIT2</it>, <it>SLIT3 </it>in the other, respectively. Moreover, <it>SLIT-ROBO </it>expression predicted <it>AFP</it>-dependent subgrouping of HCC cell lines, but not that of liver tissues. <it>ROBO1 </it>and <it>ROBO2 </it>were significantly up-regulated, whereas <it>SLIT3 </it>was significantly down-regulated in cell lines with high-<it>AFP </it>background. When compared to normal liver tissue, <it>ROBO1 </it>was found to be significantly overexpressed, while <it>ROBO4 </it>was down-regulated in HCC. We also observed that <it>ROBO1 </it>and <it>SLIT2 </it>differentiated histopathological subgroups of liver tissues depending on both tumor staging and differentiation status. However, <it>ROBO4 </it>could discriminate poorly differentiated HCC from other subgroups.</p> <p>Conclusion</p> <p>The present study is the first in comprehensive and quantitative evaluation of <it>SLIT-ROBO </it>family gene expression in HCC, and suggests that the expression of <it>SLIT-ROBO </it>genes is regulated in hepatocarcinogenesis. Our results implicate that <it>SLIT-ROBO </it>transcription profile is bi-modular in nature, and that each module shows intrinsic variability. We also provide quantitative evidence for potential use of <it>ROBO1</it>, <it>ROBO4 </it>and <it>SLIT2 </it>for prediction of tumor stage and differentiation status.</p