Publications by authors named "Catherine Jenkins"

20 Publications

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North American temperate conifer (Tsuga canadensis) reveals a complex physiological response to climatic and anthropogenic stressors.

New Phytol 2020 12 18;228(6):1781-1795. Epub 2020 Aug 18.

School of Earth and Ocean Sciences, Cardiff University, Main Building, Park Place, Cardiff, CF10 3AT, UK.

Rising atmospheric CO (c) is expected to promote tree growth and lower water loss via changes in leaf gas exchange. However, uncertainties remain if gas-exchange regulation strategies are homeostatic or dynamical in response to increasing c, as well as evolving climate and pollution inputs. Using a suite of tree ring-based δC-derived physiological parameters (ΔC, c, iWUE) and tree growth from a mesic, low elevation stand of canopy-dominant Tsuga canadensis in north-eastern USA, we investigated the influence of rising c, climate and pollution on, and characterised the dynamical regulation strategy of, leaf gas exchange at multidecadal scales. Isotopic and growth time series revealed an evolving physiological response in which the species shifted its leaf gas-exchange strategy dynamically (constant c; constant c/c; constant c - c) in response to rising c, moisture availability and site conditions over 111 yr. Tree iWUE plateaued after 1975, driven by greater moisture availability and a changing soil biogeochemistry that may have impaired a stomatal response. Results suggested that trees may exhibit more complex physiological responses to the changing environmental conditions over multidecadal periods, and complicating the parameterisation of Earth system models and the estimation of future carbon sink capacity and water balance in midlatitude forests and elsewhere.
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http://dx.doi.org/10.1111/nph.16811DOI Listing
December 2020

Cross-Priming Dendritic Cells Exacerbate Immunopathology After Ischemic Tissue Damage in the Heart.

Circulation 2021 Feb 10;143(8):821-836. Epub 2020 Dec 10.

National Heart and Lung Institute, Imperial College London, UK (A.S., H.S.K., A.P., C.J., M.A., R.A.C., M.B., M.D.S., S.E.H., F.S.N., N.R., S.S.).

Background: Ischemic heart disease is a leading cause of heart failure and despite advanced therapeutic options, morbidity and mortality rates remain high. Although acute inflammation in response to myocardial cell death has been extensively studied, subsequent adaptive immune activity and anti-heart autoimmunity may also contribute to the development of heart failure. After ischemic injury to the myocardium, dendritic cells (DC) respond to cardiomyocyte necrosis, present cardiac antigen to T cells, and potentially initiate a persistent autoimmune response against the heart. Cross-priming DC have the ability to activate both CD4 helper and CD8 cytotoxic T cells in response to necrotic cells and may thus be crucial players in exacerbating autoimmunity targeting the heart. This study investigates a role for cross-priming DC in post-myocardial infarction immunopathology through presentation of self-antigen from necrotic cardiac cells to cytotoxic CD8 T cells.

Methods: We induced type 2 myocardial infarction-like ischemic injury in the heart by treatment with a single high dose of the β-adrenergic agonist isoproterenol. We characterized the DC population in the heart and mediastinal lymph nodes and analyzed long-term cardiac immunopathology and functional decline in wild type and -depleted mice lacking DC cross-priming function.

Results: A diverse DC population, including cross-priming DC, is present in the heart and activated after ischemic injury. mice deficient in DC cross-priming are protected from persistent immune-mediated myocardial damage and decline of cardiac function, likely because of dampened activation of cytotoxic CD8 T cells.

Conclusion: Activation of cytotoxic CD8 T cells by cross-priming DC contributes to exacerbation of postischemic inflammatory damage of the myocardium and corresponding decline in cardiac function. Importantly, this provides novel therapeutic targets to prevent postischemic immunopathology and heart failure.
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http://dx.doi.org/10.1161/CIRCULATIONAHA.120.044581DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7899721PMC
February 2021

Development of a pro-arrhythmic ex vivo intact human and porcine model: cardiac electrophysiological changes associated with cellular uncoupling.

Pflugers Arch 2020 10 1;472(10):1435-1446. Epub 2020 Sep 1.

Faculty of Medicine, National Heart and Lung Institute, Imperial College London, Hammersmith Campus, Du Cane Road, London, W12 0NN, UK.

We describe a human and large animal Langendorff experimental apparatus for live electrophysiological studies and measure the electrophysiological changes due to gap junction uncoupling in human and porcine hearts. The resultant ex vivo intact human and porcine model can bridge the translational gap between smaller simple laboratory models and clinical research. In particular, electrophysiological models would benefit from the greater myocardial mass of a large heart due to its effects on far-field signal, electrode contact issues and motion artefacts, consequently more closely mimicking the clinical setting. Porcine (n = 9) and human (n = 4) donor hearts were perfused on a custom-designed Langendorff apparatus. Epicardial electrograms were collected at 16 sites across the left atrium and left ventricle. A total of 1 mM of carbenoxolone was administered at 5 ml/min to induce cellular uncoupling, and then recordings were repeated at the same sites. Changes in electrogram characteristics were analysed. We demonstrate the viability of a controlled ex vivo model of intact porcine and human hearts for electrophysiology with pharmacological modulation. Carbenoxolone reduces cellular coupling and changes contact electrogram features. The time from stimulus artefact to (-dV/dt) increased between baseline and carbenoxolone (47.9 ± 4.1-67.2 ± 2.7 ms) indicating conduction slowing. The features with the largest percentage change between baseline and carbenoxolone were fractionation + 185.3%, endpoint amplitude - 106.9%, S-endpoint gradient + 54.9%, S point - 39.4%, RS ratio + 38.6% and (-dV/dt) - 20.9%. The physiological relevance of this methodological tool is that it provides a model to further investigate pharmacologically induced pro-arrhythmic substrates.
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http://dx.doi.org/10.1007/s00424-020-02446-6DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7476990PMC
October 2020

An enhancer cluster controls gene activity and topology of the SCN5A-SCN10A locus in vivo.

Nat Commun 2019 10 30;10(1):4943. Epub 2019 Oct 30.

Department of Medical Biology, Amsterdam Cardiovascular Sciences, Academic Medical Center, Amsterdam, The Netherlands.

Mutations and variations in and around SCN5A, encoding the major cardiac sodium channel, influence impulse conduction and are associated with a broad spectrum of arrhythmia disorders. Here, we identify an evolutionary conserved regulatory cluster with super enhancer characteristics downstream of SCN5A, which drives localized cardiac expression and contains conduction velocity-associated variants. We use genome editing to create a series of deletions in the mouse genome and show that the enhancer cluster controls the conformation of a >0.5 Mb genomic region harboring multiple interacting gene promoters and enhancers. We find that this cluster and its individual components are selectively required for cardiac Scn5a expression, normal cardiac conduction and normal embryonic development. Our studies reveal physiological roles of an enhancer cluster in the SCN5A-SCN10A locus, show that it controls the chromatin architecture of the locus and Scn5a expression, and suggest that genetic variants affecting its activity may influence cardiac function.
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http://dx.doi.org/10.1038/s41467-019-12856-5DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6821807PMC
October 2019

Epigenetic Restoration of Fetal-like IGF1 Signaling Inhibits Leukemia Stem Cell Activity.

Cell Stem Cell 2018 11 27;23(5):714-726.e7. Epub 2018 Sep 27.

Terry Fox Laboratory, BC Cancer Agency, Vancouver, BC V5Z 1L3, Canada. Electronic address:

Acute leukemias are aggressive malignancies of developmentally arrested hematopoietic progenitors. We sought here to explore the possibility that changes in hematopoietic stem/progenitor cells during development might alter the biology of leukemias arising from this tissue compartment. Using a mouse model of acute T cell leukemia, we found that leukemias generated from fetal liver (FL) and adult bone marrow (BM) differed dramatically in their leukemia stem cell activity with FL leukemias showing markedly reduced serial transplantability as compared to BM leukemias. We present evidence that this difference is due to NOTCH1-driven autocrine IGF1 signaling, which is active in FL cells but restrained in BM cells by EZH2-dependent H3K27 trimethylation. Further, we confirmed this mechanism is operative in human disease and show that enforced IGF1 signaling effectively limits leukemia stem cell activity. These findings demonstrate that resurrecting dormant fetal programs in adult cells may represent an alternate therapeutic approach in human cancer.
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http://dx.doi.org/10.1016/j.stem.2018.08.018DOI Listing
November 2018

RUNX1 promotes cell growth in human T-cell acute lymphoblastic leukemia by transcriptional regulation of key target genes.

Exp Hematol 2018 08 5;64:84-96. Epub 2018 May 5.

Terry Fox Laboratory/Department of Pathology, BC Cancer Agency, Vancouver, BC, Canada. Electronic address:

RUNX1 is frequently mutated in T-cell acute lymphoblastic leukemia (T-ALL). The spectrum of RUNX1 mutations has led to the notion that it acts as a tumor suppressor in this context; however, other studies have placed RUNX1, along with transcription factors TAL1 and NOTCH1, as core drivers of an oncogenic transcriptional program. To reconcile these divergent roles, we knocked down RUNX1 in human T-ALL cell lines and deleted Runx1 or Cbfb in primary mouse T-cell leukemias. RUNX1 depletion consistently resulted in reduced cell proliferation and increased apoptosis. RUNX1 upregulated variable sets of target genes in each cell line, but consistently included a core set of oncogenic effectors including insulin-like growth factor 1 receptor (IGF1R) and NRAS. Our results support the conclusion that RUNX1 has a net positive effect on cell growth in the context of established T-ALL.
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http://dx.doi.org/10.1016/j.exphem.2018.04.008DOI Listing
August 2018

IGF1R Derived PI3K/AKT Signaling Maintains Growth in a Subset of Human T-Cell Acute Lymphoblastic Leukemias.

PLoS One 2016 17;11(8):e0161158. Epub 2016 Aug 17.

Terry Fox Laboratory, BC Cancer Agency, Vancouver, BC, V5Z 1L3, Canada.

Insulin-like growth factor 1 receptor (IGF1R) is a prevalent signaling pathway in human cancer that supports cell growth/survival and thus contributes to aggressive biological behavior. Much work has gone into development of IGF1R inhibitors; however, candidate agents including small molecule tyrosine kinase inhibitors and blocking antibodies have yet to fulfill their promise clinically. Understanding cellular features that define sensitivity versus resistance are important for effective patient selection and anticipation of outgrowth of a resistant clone. We previously identified an important role for IGF signaling in T-cell acute lymphoblastic leukemia (T-ALL) relying primarily upon genetically defined mouse models. We present here an assessment of IGF1R dependence in human T-ALL using a broad panel of 27 established cell lines that capture a spectrum of the genetic variation that might be encountered in clinical practice. We observed that a subset of cell lines are sensitive to IGF1R inhibition and are characterized by high levels of surface IGF1R expression and PTEN positivity. Interestingly, lentiviral expression or knock-down of PTEN in PTEN-negative/positive cell lines, respectively, had limited effects on their response to IGF1R inhibition, suggesting that PTEN contributes to, but does not define IGF dependence. Additionally, we characterize downstream PI3K/AKT signaling as dominant over RAS/RAF/MEK/ERK in mediating growth and/or survival in this context. Finally, we demonstrate that IGF and interleukin-7 (IL-7) fulfill non-overlapping roles in supporting T-ALL growth. These findings are significant in that they reveal cellular features and downstream mechanisms that may determine the response of an individual patient's tumor to IGF1R inhibitor therapy.
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http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0161158PLOS
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4988785PMC
August 2017

Giant reversible anisotropy changes at room temperature in a (La,Sr)MnO3/Pb(Mg,Nb,Ti)O3 magneto-electric heterostructure.

Sci Rep 2016 06 8;6:27501. Epub 2016 Jun 8.

Department of Materials Science and Engineering, Univ. of California, Davis, Davis, CA 95616, USA.

In a model artificial multiferroic system consisting of a (011)-oriented ferroelectric Pb(Mg,Nb,Ti)O3 substrate intimately coupled to an epitaxial ferromagnetic (La,Sr)MnO3 film, electric field pulse sequences of less than 6 kV/cm induce large, reversible, and bistable remanent strains. The magnetic anisotropy symmetry reversibly switches from a highly anisotropic two-fold state to a more isotropic one, with concomitant changes in resistivity. Anisotropy changes at the scale of a single ferromagnetic domain were measured using X-ray microscopy, with electric-field dependent magnetic domain reversal showing that the energy barrier for magnetization reversal is drastically lowered. Free energy calculations confirm this barrier lowering by up to 70% due to the anisotropic strain changes generated by the substrate. Thus, we demonstrate that an electric field pulse can be used to 'set' and 'reset' the magnetic anisotropy orientation and resistive state in the film, as well as to lower the magnetization reversal barrier, showing a promising route towards electric-field manipulation of multifunctional nanostructures at room temperature.
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http://dx.doi.org/10.1038/srep27501DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4897745PMC
June 2016

CD44 promotes chemoresistance in T-ALL by increased drug efflux.

Exp Hematol 2016 Mar 18;44(3):166-71.e17. Epub 2015 Dec 18.

Terry Fox Laboratory, BC Cancer Agency, Vancouver, British Columbia, Canada. Electronic address:

T-Cell acute lymphoblastic leukemia is considered a largely curable disease in children; however, adult patients and children with refractory or relapsed disease have consistently poor outcomes. On the basis of our prior work highlighting CD44 as a marker of leukemia-initiating cells in animal models and because cancer stem cells are postulated to possess intrinsic resistance to conventional chemotherapy, we examined whether CD44 itself might play a role in mediating chemoresistance. We report here that in both genetically defined mouse models and human cell lines, CD44 expression is associated with chemoresistance, and that this effect is mediated in part through enhanced drug efflux. Interestingly, we also observed increased CD44 expression in residual blasts following standard induction chemotherapy, as compared with blasts from matched, pretherapy samples in a subset of pediatric patients undergoing minimal residual disease monitoring as part of a clinical trial. These findings support a functional role for CD44 in promoting chemotherapy resistance and suggest that targeting it directly or its relevant effector pathways may improve clinical responses in T-cell acute lymphoblastic leukemia.
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http://dx.doi.org/10.1016/j.exphem.2015.12.001DOI Listing
March 2016

Leukemia stem cells in T-ALL require active Hif1α and Wnt signaling.

Blood 2015 Jun 1;125(25):3917-27. Epub 2015 May 1.

Terry Fox Laboratory, British Columbia Cancer Agency, Vancouver, BC, Canada.

The Wnt signaling pathway has been shown to play important roles in normal hematopoietic stem cell biology and in the development of both acute and chronic myelogenous leukemia. Its role in maintaining established leukemia stem cells, which are more directly relevant to patients with disease, however, is less clear. To address what role Wnt signaling may play in T-cell acute lymphoblastic leukemia (T-ALL), we used a stably integrated fluorescent Wnt reporter construct to interrogate endogenous Wnt signaling activity in vivo. In this study, we report that active Wnt signaling is restricted to minor subpopulations within bulk tumors, that these Wnt-active subsets are highly enriched for leukemia-initiating cells (LICs), and that genetic inactivation of β-catenin severely reduces LIC frequency. We show further that β-catenin transcription is upregulated by hypoxia through hypoxia-inducible factor 1α (Hif1α) stabilization, and that deletion of Hif1α also severely reduces LIC frequency. Of note, the deletion of β-catenin or Hif1α did not impair the growth or viability of bulk tumor cells, suggesting that elements of the Wnt and Hif pathways specifically support leukemia stem cells. We also confirm the relevance of these findings to human disease using cell lines and patient-derived xenografts, suggesting that targeting these pathways could benefit patients with T-ALL.
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http://dx.doi.org/10.1182/blood-2014-10-609370DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4548498PMC
June 2015

Carbon p electron ferromagnetism in silicon carbide.

Sci Rep 2015 Mar 11;5:8999. Epub 2015 Mar 11.

Helmholtz-Zentrum Dresden-Rossendorf, Institute of Ion Beam Physics and Materials Research, Bautzner Landstr. 400, 01328 Dresden, Germany.

Ferromagnetism can occur in wide-band gap semiconductors as well as in carbon-based materials when specific defects are introduced. It is thus desirable to establish a direct relation between the defects and the resulting ferromagnetism. Here, we contribute to revealing the origin of defect-induced ferromagnetism using SiC as a prototypical example. We show that the long-range ferromagnetic coupling can be attributed to the p electrons of the nearest-neighbor carbon atoms around the VSiVC divacancies. Thus, the ferromagnetism is traced down to its microscopic electronic origin.
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http://dx.doi.org/10.1038/srep08999DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4355737PMC
March 2015

Targeting transcription regulation in cancer with a covalent CDK7 inhibitor.

Nature 2014 Jul 22;511(7511):616-20. Epub 2014 Jun 22.

1] Department of Cancer Biology, Dana-Farber Cancer Institute, Boston, Massachusetts 02115, USA [2] Department of Biological Chemistry and Molecular Pharmacology, Harvard Medical School, Boston, Massachusetts 02115, USA.

Tumour oncogenes include transcription factors that co-opt the general transcriptional machinery to sustain the oncogenic state, but direct pharmacological inhibition of transcription factors has so far proven difficult. However, the transcriptional machinery contains various enzymatic cofactors that can be targeted for the development of new therapeutic candidates, including cyclin-dependent kinases (CDKs). Here we present the discovery and characterization of a covalent CDK7 inhibitor, THZ1, which has the unprecedented ability to target a remote cysteine residue located outside of the canonical kinase domain, providing an unanticipated means of achieving selectivity for CDK7. Cancer cell-line profiling indicates that a subset of cancer cell lines, including human T-cell acute lymphoblastic leukaemia (T-ALL), have exceptional sensitivity to THZ1. Genome-wide analysis in Jurkat T-ALL cells shows that THZ1 disproportionally affects transcription of RUNX1 and suggests that sensitivity to THZ1 may be due to vulnerability conferred by the RUNX1 super-enhancer and the key role of RUNX1 in the core transcriptional regulatory circuitry of these tumour cells. Pharmacological modulation of CDK7 kinase activity may thus provide an approach to identify and treat tumour types that are dependent on transcription for maintenance of the oncogenic state.
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http://dx.doi.org/10.1038/nature13393DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4244910PMC
July 2014

Oxygen spectroscopy and polarization-dependent imaging contrast (PIC)-mapping of calcium carbonate minerals and biominerals.

J Phys Chem B 2014 Jul 10;118(28):8449-57. Epub 2014 Jun 10.

Department of Physics, University of Wisconsin-Madison , 1150 University Avenue, Madison, Wisconsin 53706, United States.

X-ray absorption near-edge structure (XANES) spectroscopy and spectromicroscopy have been extensively used to characterize biominerals. Using either Ca or C spectra, unique information has been obtained regarding amorphous biominerals and nanocrystal orientations. Building on these results, we demonstrate that recording XANES spectra of calcium carbonate at the oxygen K-edge enables polarization-dependent imaging contrast (PIC) mapping with unprecedented contrast, signal-to-noise ratio, and magnification. O and Ca spectra are presented for six calcium carbonate minerals: aragonite, calcite, vaterite, monohydrocalcite, and both hydrated and anhydrous amorphous calcium carbonate. The crystalline minerals reveal excellent agreement of the extent and direction of polarization dependences in simulated and experimental XANES spectra due to X-ray linear dichroism. This effect is particularly strong for aragonite, calcite, and vaterite. In natural biominerals, oxygen PIC-mapping generated high-magnification maps of unprecedented clarity from nacre and prismatic structures and their interface in Mytilus californianus shells. These maps revealed blocky aragonite crystals at the nacre-prismatic boundary and the narrowest calcite needle-prisms. In the tunic spicules of Herdmania momus, O PIC-mapping revealed the size and arrangement of some of the largest vaterite single crystals known. O spectroscopy therefore enables the simultaneous measurement of chemical and orientational information in CaCO3 biominerals and is thus a powerful means for analyzing these and other complex materials. As described here, PIC-mapping and spectroscopy at the O K-edge are methods for gathering valuable data that can be carried out using spectromicroscopy beamlines at most synchrotrons without the expense of additional equipment.
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http://dx.doi.org/10.1021/jp503700gDOI Listing
July 2014

Anisotropic charge-transfer effects in the asymmetric Fe(CN)5NO octahedron of sodium nitroprusside: a soft X-ray absorption spectroscopy study.

Phys Chem Chem Phys 2014 Apr 7;16(15):7031-6. Epub 2014 Mar 7.

Energy Technology Research Institute, National Institute of Advanced Industrial Science and Technology, Tsukuba, Ibaraki 305-8568, Japan.

The electronic structure of Na2[Fe(CN)5NO]·2H2O (sodium nitroprusside: SNP) was investigated by using soft X-ray absorption (XA) spectroscopy. The Fe L2,3-edge XA spectrum of SNP exhibited distinct and very large satellite peaks for L3 and L2 regions, which is different from the spectra of hexacyanoferrates and the other iron compounds. A configuration-interaction full-multiplet calculation, in which the ligand molecular orbitals for the C4v symmetry were taken into account, revealed the Fe(2+) low-spin state with very strong effects of metal-to-ligand charge-transfer from the Fe 3d to NO 2p orbitals.
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http://dx.doi.org/10.1039/c3cp55471fDOI Listing
April 2014

Evidence of redox-active iron formation following aggregation of ferrihydrite and the Alzheimer's disease peptide β-amyloid.

Inorg Chem 2014 Mar 21;53(6):2803-9. Epub 2014 Feb 21.

Institute for Science and Technology in Medicine, Keele University , Stoke-on-Trent, Staffordshire ST4 7QB, United Kingdom.

Recent work has demonstrated increased levels of redox-active iron biominerals in Alzheimer's disease (AD) tissue. However, the origin, nature, and role of iron in AD pathology remains unclear. Using X-ray absorption, X-ray microspectroscopy, and electron microscopy techniques, we examined interactions between the AD peptide β-amyloid (Aβ) and ferrihydrite, which is the ferric form taken when iron is stored in humans. We report that Aβ is capable of reducing ferrihydrite to a pure iron(II) mineral where antiferromagnetically ordered Fe(2+) cations occupy two nonequivalent crystal symmetry sites. Examination of these iron(II) phases following air exposure revealed a material consistent with the iron(II)-rich mineral magnetite. These results demonstrate the capability of Aβ to induce the redox-active biominerals reported in AD tissue from natural iron precursors. Such interactions between Aβ and ferrihydrite shed light upon the processes of AD pathogenesis, while providing potential targets for future therapies.
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http://dx.doi.org/10.1021/ic402406gDOI Listing
March 2014

How does change occur following a theoretically based self-management intervention for type 2 diabetes.

Psychol Health Med 2014 10;19(5):536-46. Epub 2013 Oct 10.

a Centre for Primary Care and Public Health , Barts and the London School of Medicine and Dentistry, Queen Mary University of London , London , UK.

The purpose of this study was to test the extent that constructs from two theoretical models (self-regulatory theory and social cognitive theory) mediated change in outcomes following a self-management intervention. One hundred and twenty four individuals with type 2 diabetes who had participated in a randomised controlled trial of a diabetes self-management programme were analysed for the extent that illness beliefs and self-efficacy mediated change in self-management behaviours and illness specific quality of life. Exercise specific self-efficacy significantly mediated change in exercise at three months (B = .03; .01, p < .05) while monitoring specific self-efficacy mediated change in monitoring behaviour at both three (B = .04; .01, p < .01) and nine months follow-up (B = 5.97; 1.01, p < .01). Belief in control over diabetes mediated change in illness specific quality of life at three months (B = -.07; .28, p < .05) and nine months (B = .79; .28, p < .01) follow-ups, as well as change in exercise behaviour at immediately post-intervention (B = -.12; .17, p < .05). Behaviour-specific self-efficacy may have a stronger role in mediating self-management behaviours than illness beliefs; however, belief in control over diabetes may be important to manipulate for change in quality of life. This suggests different theoretical constructs may mediate change dependent on outcome.
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http://dx.doi.org/10.1080/13548506.2013.845301DOI Listing
May 2015

Experimental evidence for oxygen sublattice control in polar infinite layer SrCuO2.

Phys Rev Lett 2013 Aug 27;111(9):096102. Epub 2013 Aug 27.

MESA+ Institute for Nanotechnology, University of Twente, Post Office Box 217, 7500AE Enschede, The Netherlands.

A recent theoretical study [Phys. Rev. B 85, 121411(R) (2012)] predicted a thickness limit below which ideal polar cuprates turn nonpolar driven by the associated electrostatic instability. Here we demonstrate this possibility by inducing a structural transformation from the bulk planar to chainlike structure upon reducing the SrCuO2 repeat thickness in SrCuO2/SrTiO3 superlattices with unit-cell precision. Our results, based on structural investigation by x-ray diffraction and high resolution scanning transmission electron microscopy, demonstrate that the oxygen sublattice can essentially be built by design. In addition, the electronic structure of the chainlike structure, as studied by x-ray absorption spectroscopy, shows the signature for preferential hole occupation in the Cu 3d(3z2-r2) orbital, which is different from the planar case.
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http://dx.doi.org/10.1103/PhysRevLett.111.096102DOI Listing
August 2013

Design scheme of new tetragonal Heusler compounds for spin-transfer torque applications and its experimental realization.

Adv Mater 2012 Dec 11;24(47):6283-7. Epub 2012 Sep 11.

Institut für Anorganische und Analytische Chemie, Johannes Gutenberg-Universität, Mainz, Germany.

Band Jahn-Teller type structural instabilities of cubic Mn(2)YZ Heusler compounds causing tetragonal distortions can be predicted by ab initio band-structure calculations. This allows for identification of new Heusler materials with tunable magnetic and structural properties that can satisfy the demands for spintronic applications, such as in spin-transfer torque-based devices.
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http://dx.doi.org/10.1002/adma.201201879DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3546386PMC
December 2012

Challenge of magnetism in strongly correlated open-shell 2p systems.

Phys Rev Lett 2009 Jan 5;102(1):016401. Epub 2009 Jan 5.

Institut für Anorganische und Analytische Chemie, Johannes Gutenberg-Universität, D-55099 Mainz, Germany.

We report on theoretical investigations of the exotic magnetism in rubidium sesquioxide Rb4O6, a model correlated system with an open 2p shell. Experimental investigations indicated that Rb4O6 is a magnetically frustrated insulator. The frustration is explained here by electronic structure calculations that incorporate the correlation between the oxygen 2p electrons and deal with the mixed-valent oxygen. This leads to a physical picture where the symmetry is reduced because one third of the oxygen in Rb4O6 is nonmagnetic while the remaining two thirds assemble in antiferromagnetic arrangements. A degenerate, insulating ground state with a large number of frustrated noncollinear magnetic configurations is confidently deduced from the theoretical point of view. These findings demonstrate in general the importance of electron-electron correlations in open-shell p-electron systems.
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http://dx.doi.org/10.1103/PhysRevLett.102.016401DOI Listing
January 2009

Ethical international recruitment.

Int Psychiatry 2004 Oct 1;1(6):18-19. Epub 2004 Oct 1.

NHS International Fellowships Project Manager, Department of Health, email

Right from the start of our international recruitment campaign the Department of Health was determined to ensure that international recruitment takes place using a planned and managed approach. Now, the UK leads the way in developing and implementing the types of international recruitment policies called for by the World Health Assembly.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC6733087PMC
October 2004