Spin-polarized electronic structure of the core-shell ZnO/ZnO:Mn nanowires probed by x-ray absorption and emission spectroscopy

The combination of x-ray spectroscopy methods complemented with theoretical analysis unravels the coexistence of paramagnetic and antiferromagnetic phases in the Zn_0.9Mn_0.1O shell deposited onto array of wurtzite ZnO nanowires. The shell is crystalline with orientation toward the ZnO growth axis, as demonstrated by X-ray linear dichroism. EXAFS analysis confirmed that more than 90% of Mn atoms substituted Zn in the shell while fraction of secondary phases was below 10%. The value of manganese spin magnetic moment was estimated from the Mn K{\beta} X-ray emission spectroscopy to be 4.3{\mu}B which is close to the theoretical value for substitutional Mn_Zn. However the analysis of L_2,3 x-ray magnetic circular dichroism data showed paramagnetic behaviour with saturated spin magnetic moment value of 1.95{\mu}B as determined directly from the spin sum rule. After quantitative analysis employing atomic multiplet simulations such difference was explained by a coexistence of paramagnetic phase and local antiferromagnetic coupling of Mn magnetic moments. Finally, spin-polarized electron density of states was probed by the spin-resolved Mn K-edge XANES spectroscopy and consequently analyzed by band structure calculations.Comment: Supplementary information available at http://www.rsc.org/suppdata/ja/c3/c3ja50153a/c3ja50153a.pdf J. Anal. At. Spectrom., 201

Effect of interactions on vortices in a nonequilibrium polariton condensate

We demonstrate the creation of vortices in a macroscopically occupied polariton state formed in a semiconductor microcavity. A weak external laser beam carrying orbital angular momentum (OAM) is used to imprint a vortex on the condensate arising from the polariton optical parametric oscillator (OPO). The vortex core radius is found to decrease with increasing pump power, and is determined by polariton-polariton interactions. As a result of OAM conservation in the parametric scattering process, the excitation consists of a vortex in the signal and a corresponding antivortex in the idler of the OPO. The experimental results are in good agreement with a theoretical model of a vortex in the polariton OPO

Synthesis and characterization of MnCrO4, a new mixed-valence antiferromagnet

A new orthorhombic phase, MnCrO4, isostructural with MCrO 4 (M = Mg, Co, Ni, Cu, Cd) was prepared by evaporation of an aqueous solution, (NH4)2Cr2O7 + 2 Mn(NO 3)2, followed by calcination at 400 C. It is characterized by redox titration, Rietveld analysis of the X-ray diffraction pattern, Cr K edge and Mn K edge XANES, ESR, magnetic susceptibility, specific heat and resistivity measurements. In contrast to the high-pressure MnCrO4 phase where both cations are octahedral, the new phase contains Cr in a tetrahedral environment suggesting the charge balance Mn2+Cr 6+O4. However, the positions of both X-ray absorption K edges, the bond lengths and the ESR data suggest the occurrence of some mixed-valence character in which the mean oxidation state of Mn is higher than 2 and that of Cr is lower than 6. Both the magnetic susceptibility and the specific heat data indicate an onset of a three-dimensional antiferromagnetic order at TN ≈ 42 K, which was confirmed also by calculating the spin exchange interactions on the basis of first principles density functional calculations. Dynamic magnetic studies (ESR) corroborate this scenario and indicate appreciable short-range correlations at temperatures far above T N. MnCrO4 is a semiconductor with activation energy of 0.27 eV; it loses oxygen on heating above 400 C to form first Cr 2O3 plus Mn3O4 and then Mn 1.5Cr1.5O4 spinel. © 2013 American Chemical Society

Токсичність МАРК у карциномах щитоподібної залози. Механізми пригнічення сигнального каскаду (огляд літератури та власних даних)

The aim of the work: to study the activity and expression of the main effector protein kinase cascade in tumors of thyroid gland. There is a strong evidence that the Ras/Raf/MEK/ERK (МАРК) signaling cascade promotes cell proliferation and malignancy by stimulating cell growth and division, as well as inhibiting apoptosis. The mitogenic MAPK cascade associates growth factor signals at cell surface receptors with the transcription factors AP-1, NF-κB, Ets, leading to the induction of c-Fos, cyclin D1 and c-Myc. These factors regulate the expression of genes that control survival, angiogenesis, growth, proliferation, and cell motility. However, the hyperactivity of this cascade in tumor tissues can lead to sensescence, growth retardation, apoptosis or increased autophagy. This phenomenon was called "oncogenic toxicity".Цель работы: исследование в опухолях щитовидной железы активности и экспрессии главной эффекторной протеинкиназы каскада – ERK1/2. Получены убедительные доказательства того, что сигнальный каскад Ras/Raf/MEK/ERK (МАРК) способствует пролиферации и злокачественной трансформации клеток путем стимуляции клеточного роста и деления, а также подавления апоптоза. Митогенный МАРК-каскад связывает сигналы факторов роста на рецепторах клеточной поверхности с транскрипционными факторами АР-1, NF-κB, Ets, что приводит к индукции с-Fos, циклина D1 и с-Мус. Эти факторы регулируют экспрессию генов, контролирующих выживание, ангиогенез, рост, пролиферацию и подвижность клеток. Однако гиперактивность этого каскада в опухолевых тканях может привести к сенесценции, задержке роста, апоптозу или усилению аутофагии. Этот феномен назвали “токсичностью онкогенов”.Мета роботи: дослідження в пухлинах щитоподібної залози (ЩЗ) активності та експресії головної ефекторної протеїнкінази каскаду – ERK1/2. Отримано переконливі докази того, що сигнальний каскад Ras/Raf/MEK/ERK (МАРК) сприяє проліферації і злоякісній трансформації клітин шляхом стимуляції клітинного росту і ділення, а також пригнічення апоптозу. Мітогенний МАРК-каскад пов’язує сигнали факторів росту на рецепторах клітинної поверхні з транскрипційними факторами АР-1, NF-κB, Ets, що приводить до індукції с-Fos, цикліну D1 і с-Мус. Ці фактори регулюють експресію генів, що контролюють виживання, ангіогенез, ріст, проліферацію і мобільність клітин. Однак гіперактивність цього каскаду в пухлинних тканинах може привести до сенесценції, затримки росту, апоптозу або посилення автофагії. Цей феномен назвали “токсичністю онкогенів”