Persistent luminescence behavior of materials doped with Eu2+ and Tb3+

In this work, the persistent luminescence mechanisms of Tb3+ (in CdSiO3) and Eu2+ (in BaAl2O4) based on solid experimental data are compared. The photoluminescence spectroscopy shows the different nature of the inter- and intraconfigurational transitions for Eu2+ and Tb3+, respectively. The electron is the charge carrier in both mechanisms, implying the presence of electron acceptor defects. The preliminary structural analysis shows a free space in CdSiO3 able to accommodate interstitial oxide ions needed by charge compensation during the initial preparation. The subsequent annealing removes this oxide leaving behind an electron trap. Despite the low band gap energy for CdSiO3, determined with synchrotron radiation UV-VUV excitation spectroscopy of Tb3+, the persistent luminescence from Tb3+ is observed only with UV irradiation. The need of high excitation energy is due to the position of F-7(6) level deep below the bottom of the conduction band, as determined with the 4f(8)-> 4f(7)5d(1) and the ligand-to-metal charge-transfer transitions. Finally, the persistent luminescence mechanisms are constructed and, despite the differences, the mechanisms for Tb3+ and Eu2+ proved to be rather similar. This similarity confirms the solidity of the interpretation of experimental data for the Eu2+ doped persistent luminescence materials and encourages the use of similar models for other persistent luminescence materials. (C) 2012 Optical Society of America

Magnetic properties of selected 3d- and 4f-systems on alpha-Al 2 O 3 substrates

In this work the growth and the magnetic properties of the transition metals molybdenum, niobium, and iron and of the highly-magnetostrictive C15 Laves phases of the RFe2 compounds (R: Rare earth metals: here Tb, Dy, and Tb{0.3}Dy{0.7} deposited on alpha-Al2O3 (sapphire) substrates are analyzed. Next to (11-20) (a-plane) oriented sapphire substrates mainly (10-10) (m-plane) oriented substrates were used. These show a pronounced facetting after high temperature annealing in air. Atomic force microscopy (AFM) measurements reveal a dependence of the height, width, and angle of the facets with the annealing temperature. The observed deviations of the facet angles with respect to the theoretical values of the sapphire (10-1-2) and (10-11) surfaces are explained by cross section high resolution transmission electron microscopy (HR-TEM) measurements. These show the plain formation of the (10-11) surface while the second, energy reduced (10-1-2) facet has a curved shape given by atomic steps of (10-1-2) layers and is formed completely solely at the facet ridges and valleys. Thin films of Mo and Nb, respectively, deposited by means of molecular beam epitaxy (MBE) reveal a non-twinned, (211)-oriented epitaxial growth as well on non-faceted as on faceted sapphire m-plane, as was shown by X-Ray and TEM evaluations. In the case of faceted sapphire the two bcc crystals overgrow the facets homogeneously. Here, the bcc (111) surface is nearly parallel to the sapphire (10-11) facet and the Mo/Nb (100) surface is nearly parallel to the sapphire (10-1-2) surface. (211)-oriented Nb templates on sapphire m-plane can be used for the non-twinned, (211)-oriented growth of RFe2 films by means of MBE. Again, the quality of the RFe2 films grown on faceted sapphire is almost equal to films on the non-faceted substrate. For comparison thin RFe2 films of the established (110) and (111) orientation were prepared. Magnetic and magnetoelastic measurements performed in a self designed setup reveal a high quality of the samples. No difference between samples with undulated and flat morphology can be observed. In addition to the preparation of covering, undulating thin films on faceted sapphire m-plane nanoscopic structures of Nb and Fe were prepared by shallow incidence MBE. The formation of the nanostructures can be explained by a shadowing of the atomic beam due to the facets in addition to de-wetting effects of the metals on the heated sapphire surface. Accordingly, the nanostructures form at the facet ridges and overgrow them. The morphology of the structures can be varied by deposition conditions as was shown for Fe. The shape of the structures vary from pearl-necklet strung spherical nanodots with a diameter of a few 10 nm to oval nanodots of a few 100 nm length to continuous nanowires. Magnetization measurements reveal uniaxial magnetic anisotropy with the easy axis of magnetization parallel to the facet ridges. The shape of the hysteresis is depending on the morphology of the structures. The magnetization reversal processes of the spherical and oval nanodots were simulated by micromagnetic modelling and can be explained by the formation of magnetic vortices.

Expression and Regulation of Human Cytochrome P450 4F Isoforms in Tissue Samples and Under TNF-Alpha Challenges

CYP4F (Cytochrome P4504F) enzymes metabolize endogenous molecules including leukotrienes, prostaglandins and arachidonic acid. The involvement of these endogenous compounds in inflammation has led to the hypothesis that changes in the inflamed tissue environment may affect the expression of CYP4Fs during the pro-inflammatory state, which in turn may modulate inflammatory conditions during the anti-inflammatory state. We demonstrated that inflamed tissues have different levels of CYP4F isoform expression profiles in a number of human samples when compared to the average population. The CYP4F isoform expression levels change with the degree of inflammation present in tissue. Further investigation in cell culture studies revealed that inflammatory cytokines, in particular TNF-α, play a role in regulating the expression of the CYP4F family. One of the isoforms, CYP4F11, had different characteristics than that of the other five CYP4F family members. CYP4F11 metabolizes xenobiotics while the other isoforms metabolize endogenous compounds with higher affinity. CYP4F11 also was expressed at high quantities in the brain, and was up-regulated by TNF-α, while the other isoforms were not expressed at high quantities in the brain and were down-regulated by TNF-α. We identified the AP-1 protein of the JNK pathway as the signaling protein that causes significant increase in CYP4F11 expression. Since TNF-α stimulation causes a simultaneous activation of both JNK pathway and NF-κB signaling, we investigated further the role that NF-κB plays on expression of the CYP4F11 gene. We concluded that although there is a significant increase in CYP4F11 expression in the presence of TNF-α, the activation of NF-κB signaling inhibits CYP4F11 expression in a time dependent manner. The expression of CYP4F11 is only significantly increased after 24 hours of treatment with TNF-α; at shorter time points NF-κB signaling overpowers the JNK pathway activation. We believe that these findings may in the future lead to improved drug design for modulating inflammation.

Characterization of cytochrome P450 4F subfamily: Functional role and response in inflammation

CYP4F subfamily comprises a group of enzymes that metabolize LTB4 to biologically less active metabolites. These inactive hydroxy products are incapable of chemotaxis and recruitment of inflammatory cells. This has led to a hypothesis that CYP4Fs may modulate inflammatory conditions serving as a signal of resolution. ^ We investigated the regulation of rat CYP4F gene expression under various inflammatory prompts including a bacterial lipopolysaccharide (LPS) treated model system, controlled traumatic brain injury (TBI) model as well as using direct cytokine challenges. CYP4Fs showed an isoform specific response to LPS. The pro-inflammatory cytokines IL-1β, IL-6 and TNF-α produced an overall inductive CYP4F response whereas IL-10, an anti-inflammatory cytokine, suppressed CYP4F gene expression in primary hepatocytes. The molecular mechanism behind IL-6 mediated CYP4F induction was partially STAT3 dependent. ^ An alternate avenue of triggering the inflammatory cascade is TBI, which is known to cause several secondary effects leading to multiorgan dysfunction syndrome. The results from this study elicited that trauma to the brain can produce acute inflammatory changes in organs distant from the injury site. Local production of LTB4 after CNS injury caused mobilization of inflammatory cells such as neutrophils to the lung. In the resolution phase, CYP4F expression increased with time along with the associated activity causing a decline in LTB4 concentration. This marked a significant reduction in neutrophil recruitment to the lung which led to subsequent recovery and repair. In addition, we showed that CYP4Fs are localized primarily in pulmonary endothelium. We speculate that the temporally regulated LTB4 clearance in the endothelium may be a novel target for treatment of pulmonary inflammation following injury. ^ In humans, several CYP4F isoforms have been identified and shown to metabolize LTB4 and other endogenous eicosanoids. However, the specific activity of the recently cloned human CYP4F11 is unknown. In the final part of this thesis, CYP4F11 protein was expressed in yeast in parallel to CYP4F3A. To our surprise, CYP4F11 displayed a different substrate profile than CYP4F3A. CYP4F3A metabolized eicosanoids while CYP4F11 was a better catalyst for therapeutic drugs. Thus, besides their endogenous function in clearing inflammation, CYP4Fs also may play a part in drug metabolism. ^

Characterization of cytochrome P450 4F subfamily: Response in traumatic brain injury and gene regulation

CYP4F enzymes metabolize endogenous molecules including arachidonic acid, leukotrienes and prostaglandins. The involvement of these eisosanoids in inflammation has led to the hypothesis that CYP4Fs may modulate inflammatory conditions after traumatic brain injury (TBI). In rat, TBI elicited changes in mRNA expression of CYP4Fs as a function of time in the cerebrum region. These changes in CYP4F mRNA levels inversely correlated with the cerebral leukotriene B4 (LTB4) level following injury at the same time points. TBI also resulted in changes in CYP4F protein expression and localization around the injury site, where CYP4F1 and CYP4F6 immunoreactivity increased in surrounding astrocytes and CYP4F4 immunoreactivity shifted from endothelia of cerebral vessels to astrocytes. The study with rat primary astrocytes indicated that pro-inflammatory cytokines TNFα and IL-1β could affect the transcription of CYP4Fs to a certain degree, whereas the changing pattern in the primary astrocytes appeared to be different from that in the in vivo TBI model.^ In addition, the regulation of CYP4F genes has been an unsolved issue although factors including cytokines and fatty acids appear to affect CYP4Fs expression in multiple models. In this project, HaCaT cells were used as an in vitro cellular model to define signaling pathways involved in the regulation of human CYP4F genes. Retinoic acids inhibited CYP4F11 expression, whereas cytokines TNFα and IL-1β induced transcription of CYP4F11 in HaCaT cells. The induction of CYP4F11 by both cytokines could be blocked by a JNK specific inhibitor, indicating the involvement of the JNK pathway in the up-regulation of CYP4F11. Retinoic acids are known to function in gene regulation through nuclear receptors RARs and RXRs. The RXR agonist LG268 greatly induced transcription of CYP4F11, whereas RAR agonist TTNPB obviously inhibited CYP4F11 transcription, indicating that the down-regulation of CYP4F11 by retinoic acid was mediated by RARs, and that inhibition of CYP4F11 by retinoic acid may also be related to the competition for RXR receptors. Thus, the CYP4F11 gene is regulated by signaling pathways including the RXR pathway and the JNK pathway. In contrast, the regulation mechanism of other CYP4Fs by retinoic acids appears to be different from that of CYP4F11.^

Function of the p86 subunit of eukaryotic initiation factor (iso)4F as a microtubule-associated protein in plant cells.

The isozyme form of eukaryotic initiation factor 4F [eIF-(iso)4F] from wheat germ is composed of a p28 subunit that binds the 7-methylguanine cap of mRNA and a p86 subunit having unknown function. The p86 subunit was found to have limited sequence similarity to a kinesin-like protein encoded by the katA gene of Arabidopsis thaliana. Native wheat germ eIF-(iso)4F and bacterially expressed p86 subunit and p86-p28 complex bound to taxol-stabilized maize microtubules (MTs) in vitro. Binding saturation occurred at 1 mol of p86 per 5-6 mol of polymerized tubulin dimer, demonstrating a substoichiometric interaction of p86 with MTs. No evidence was found for a direct interaction of the p28 subunit with MTs. Unlike kinesin, cosedimentation of eIF-(iso)4F with MTs was neither reduced by MgATP nor enhanced by adenosine 5'-[gamma-imido]triphosphate. Both p86 subunit and p86-p28 complex induced the bundling of MTs in vitro. The p86 subunit was immunolocalized to the cytosol in root maize cells and existed in three forms: fine particles, coarse particles, and linear patches. Many coarse particles and linear patches were colocalized or closely associated with cortical MT bundles in interphase cells. The results indicate that the p86 subunit of eIF-(iso)4F is a MT-associated protein that may simultaneously link the translational machinery to the cytoskeleton and regulate MT disposition in plant cells.

(Appendix 1) Coral analysis and isostatic rebound effects from different Holes of IODP Expedition 310

Past sea-level records provide invaluable information about the response of ice sheets to climate forcing. Some such records suggest that the last deglaciation was punctuated by a dramatic period of sea-level rise, of about 20 metres, in less than 500 years. Controversy about the amplitude and timing of this meltwater pulse (MWP-1A) has, however, led to uncertainty about the source of the melt water and its temporal and causal relationships with the abrupt climate changes of the deglaciation. Here we show that MWP-1A started no earlier than 14,650 years ago and ended before 14,310 years ago, making it coeval with the Bølling warming. Our results, based on corals drilled offshore from Tahiti during Integrated Ocean Drilling Project Expedition 310, reveal that the increase in sea level at Tahiti was between 12 and 22 metres, with a most probable value between 14 and 18 metres, establishing a significant meltwater contribution from the Southern Hemisphere. This implies that the rate of eustatic sea-level rise exceeded 40 millimetres per year during MWP-1A.

Microscopic Theory of Anchoring Transitions at the Surfaces of Pure Liquid-Crystals and their Mixtures .1. The Fowler Approximation

We have generalized earlier work on anchoring of nematic liquid crystals by Sullivan, and Sluckin and Poniewierski, in order to study transitions which may occur in binary mixtures of nematic liquid crystals as a function of composition. Microscopic expressions have been obtained for the anchoring energy of (i) a liquid crystal in contact with a solid aligning surface; (ii) a liquid crystal in contact with an immiscible isotropic medium; (iii) a liquid crystal mixture in contact with a solid aligning surface. For (iii), possible phase diagrams of anchoring angle versus dopant concentration have been calculated using a simple liquid crystal model. These exhibit some interesting features including re-entrant conical anchoring, for what are believed to be realistic values of the molecular parameters. A way of relaxing the most drastic approximation implicit in the above approach is also briefly discussed.

p38/MKP-1-regulated AKT coordinates macrophage transitions and resolution of inflammation during tissue repair

Repair of damaged tissue requires the coordinated action of inflammatory and tissue-specific cells to restore homeostasis, but the underlying regulatory mechanisms are poorly understood. In this paper, we report new roles for MKP-1 (mitogen-activated protein kinase [MAPK] phosphatase-1) in controlling macrophage phenotypic transitions necessary for appropriate muscle stem cell¿dependent tissue repair. By restricting p38 MAPK activation, MKP-1 allows the early pro- to antiinflammatory macrophage transition and the later progression into a macrophage exhaustion-like state characterized by cytokine silencing, thereby permitting resolution of inflammation as tissue fully recovers. p38 hyperactivation in macrophages lacking MKP-1 induced the expression of microRNA-21 (miR-21), which in turn reduced PTEN (phosphatase and tensin homologue) levels, thereby extending AKT activation. In the absence of MKP-1, p38-induced AKT activity anticipated the acquisition of the antiinflammatory gene program and final cytokine silencing in macrophages, resulting in impaired tissue healing. Such defects were reversed by temporally controlled p38 inhibition. Conversely, miR-21¿AKT interference altered homeostasis during tissue repair. This novel regulatory mechanism involving the appropriate balance of p38, MKP-1, miR-21, and AKT activities may have implications in chronic inflammatory degenerative diseases.

Synthesis and magnetic properties of heteronuclear 3d-4f compound

A novel heteronuclear 3d-4f compound having formula NdCu3L3·13H2O (where H3L = Schiff base derived from 5-bromosalicylaldehyde and glycylglycine and L³ = C11H8 N2O4Br) was obtained. It was characterized by elemental and thermal analyses and magnetic measurements. The Cu(II)-Nd(III) compound is stable up to 323 K. During dehydration process the water molecules are lost in two stages. The magnetic susceptibility data for this complex change with temperature according to the Curie-Weiss law with theta = -35 K. The magnetic moment values decrease from 5.00µB at 303 K to 4.38µB at 76 K.