Executive coaching as the differentiating patterning of power

Executive Coaching is now widely applied in organisations to bring about improvements in performance through individual focussed development. Coaches work with their clients to agree outcomes for their work together and then use their skills in a structured conversation to bring about change. The change they write of is an unfolding of the limitless human potential that resides within each of us, which is accessed by removing obstacles or interferences. The view that I present in this portfolio is significantly different to this predominant thinking and makes an important contribution to the practice of coaching, as a coach, client or line manager. I see the change that can happen in coaching, or indeed in any conversation, as occurring as movements of power. Patterns of power-relating, I argue, differentiate individual and collective identities. Coaching then, is the patterning of power-relating that has the potential for further differentiating and so transforming the identities of all those involved in the coaching process. I perceive power as ongoing patterns that paradoxically form and are formed by the processes of relating between human bodies. I argue that the complex patterning of power, that enables and constrains the actions of each person, creates identity. Identity is therefore a socially created phenomenon, simultaneously forming and being formed by the processes of relating. The differentiating patterning of power transforms identity through changes in our experience of inclusion and exclusion. From this perspective, the change that occurs in coaching assumes transformative causality instead of the dual rationalist and formative causalities that underpin the predominant approaches to executive coaching. This portfolio explores the nature of change in organisations, focussing more intensely, in each paper, on conversations as organisational change, culminating in the exploration of executive coaching as conversations initiated to create change. Through the methodology of participative inquiry, this research provides a way of understanding executive coaching that is informed by the concept of complex responsive processes and the sociology of Norbert Elias rather that the humanistic and cognitive psychologies that are at the root of the work of most executive coaching

Investigating the Photostability of Organic Photovoltaics for Indoor and Outdoor Applications

Organic photovoltaics (OPVs) show great promise for both outdoor and indoor applications. However, there remains a lack of understanding around the stability of OPVs, particularly for indoor applications. In this work, the photostability of the poly[(thiophene)-alt-(6,7-difluoro-2-(2-hexyldecyloxy)quinoxaline)]:2,2′-((2Z,2′Z)-((4,4,9,9-tetrahexyl-4,9-dihydro-s-indaceno[1,2-b:5,6-b′]dithiophene-2,7-diyl)bis(methanylylidene))bis(3-oxo-2,3-dihydro-1H-indene-2,1-diylidene))dimalononitrile blend is investigated for both outdoor and indoor applications. Photostability is found to vary drastically with illumination intensity. Devices under high-intensity white light-emitting diode (LED) illumination, with their short-circuit current density (JSC) matching JSC–EQE for AM1.5 G illumination, lose 42% of their initial performance after 30 days of illumination. Contrastingly, after almost 47 days of illumination devices under 1000 lux white LED illumination show no loss in performance. The poor photostability under 1 sun illumination is linked to the poor photostability of IDIC. Through Raman spectroscopy and mass spectrometry, IDIC is found to suffer from photoisomerization, which detrimentally impacts light absorption and carrier extraction. In this work, it is highlighted that under low light levels, the requirement of intrinsic material photostability may be less stringent

Gourds and squashes (Cucurbita spp.) adapted to megafaunal extinction and ecological anachronism through domestication.

The genus Cucurbita (squashes, pumpkins, gourds) contains numerous domesticated lineages with ancient New World origins. It was broadly distributed in the past but has declined to the point that several of the crops' progenitor species are scarce or unknown in the wild. We hypothesize that Holocene ecological shifts and megafaunal extinctions severely impacted wild Cucurbita, whereas their domestic counterparts adapted to changing conditions via symbiosis with human cultivators. First, we used high-throughput sequencing to analyze complete plastid genomes of 91 total Cucurbita samples, comprising ancient (n = 19), modern wild (n = 30), and modern domestic (n = 42) taxa. This analysis demonstrates independent domestication in eastern North America, evidence of a previously unknown pathway to domestication in northeastern Mexico, and broad archaeological distributions of taxa currently unknown in the wild. Further, sequence similarity between distant wild populations suggests recent fragmentation. Collectively, these results point to wild-type declines coinciding with widespread domestication. Second, we hypothesize that the disappearance of large herbivores struck a critical ecological blow against wild Cucurbita, and we take initial steps to consider this hypothesis through cross-mammal analyses of bitter taste receptor gene repertoires. Directly, megafauna consumed Cucurbita fruits and dispersed their seeds; wild Cucurbita were likely left without mutualistic dispersal partners in the Holocene because they are unpalatable to smaller surviving mammals with more bitter taste receptor genes. Indirectly, megafauna maintained mosaic-like landscapes ideal for Cucurbita, and vegetative changes following the megafaunal extinctions likely crowded out their disturbed-ground niche. Thus, anthropogenic landscapes provided favorable growth habitats and willing dispersal partners in the wake of ecological upheaval.Research was supported by The Pennsylvania State University Huck Institutes of the Life Sciences and College of the Liberal Arts (G.H.P.), Wenner–Gren post-PhD Research Grant 8770 and Natural Environment Research Council Independent Research Fellowship NE/L012030/1 (to L.K.), and the Smithsonian Institution (B.D.S.). Instrumentation was funded by the National Science Foundation through Grant OCI–0821527.This is the author accepted manuscript. The final version is available from PNAS via http://dx.doi.org/10.1073/pnas.151610911

Fabrication of Thin, Luminescent, Single-crystal Diamond Membranes

The formation of single-crystal diamond membranes is an important prerequisite for the fabrication of high-quality optical cavities in this material. Diamond membranes fabricated using lift-off processes involving the creation of a damaged layer through ion implantation often suffer from residual ion damage, which severely limits their usefulness for photonic structures. The current work demonstrates that strategic etch removal of the most highly defective material yields thin, single-crystal diamond membranes with strong photoluminescence and a Raman signature approaching that of single-crystal bulk diamond. These optically-active membranes can form the starting point for fabrication of high-quality optical resonators.Comment: To appear in AP

E-cadherin can limit the transforming properties of activating β-catenin mutations

Wnt pathway deregulation is a common characteristic of many cancers. But only Colorectal Cancer predominantly harbours mutations in APC, whereas other cancer types (hepatocellular carcinoma, solid pseudopapillary tumours of pancreas) have activating mutations in β-catenin (CTNNB1). We have compared the dynamics and the potency of β-catenin mutations in vivo. Within the murine small intestine (SI), an activating mutation of β-catenin took much longer to achieve a Wnt deregulation and acquire a crypt-progenitor-cell (CPC) phenotype than Apc or Gsk3 loss. Within the colon, a single activating mutation of β-catenin was unable to drive Wnt deregulation or induce the CPC phenotype. This ability of β-catenin mutation to differentially transform the SI versus the colon correlated with significantly higher expression of the β-catenin binding partner E-cadherin. This increased expression is associated with a higher number of E-cadherin:β-catenin complexes at the membrane. Reduction of E-cadherin synergised with an activating mutation of β-catenin so there was now a rapid CPC phenotype within the colon and SI. Thus there is a threshold of β-catenin that is required to drive transformation and E-cadherin can act as a buffer to prevent β-catenin accumulation

Nitrate enhances skeletal muscle fatty acid oxidation via a nitric oxide-cGMP-PPAR-mediated mechanism.

BACKGROUND: Insulin sensitivity in skeletal muscle is associated with metabolic flexibility, including a high capacity to increase fatty acid (FA) oxidation in response to increased lipid supply. Lipid overload, however, can result in incomplete FA oxidation and accumulation of potentially harmful intermediates where mitochondrial tricarboxylic acid cycle capacity cannot keep pace with rates of β-oxidation. Enhancement of muscle FA oxidation in combination with mitochondrial biogenesis is therefore emerging as a strategy to treat metabolic disease. Dietary inorganic nitrate was recently shown to reverse aspects of the metabolic syndrome in rodents by as yet incompletely defined mechanisms. RESULTS: Herein, we report that nitrate enhances skeletal muscle FA oxidation in rodents in a dose-dependent manner. We show that nitrate induces FA oxidation through a soluble guanylate cyclase (sGC)/cGMP-mediated PPARβ/δ- and PPARα-dependent mechanism. Enhanced PPARβ/δ and PPARα expression and DNA binding induces expression of FA oxidation enzymes, increasing muscle carnitine and lowering tissue malonyl-CoA concentrations, thereby supporting intra-mitochondrial pathways of FA oxidation and enhancing mitochondrial respiration. At higher doses, nitrate induces mitochondrial biogenesis, further increasing FA oxidation and lowering long-chain FA concentrations. Meanwhile, nitrate did not affect mitochondrial FA oxidation in PPARα(-/-) mice. In C2C12 myotubes, nitrate increased expression of the PPARα targets Cpt1b, Acadl, Hadh and Ucp3, and enhanced oxidative phosphorylation rates with palmitoyl-carnitine; however, these changes in gene expression and respiration were prevented by inhibition of either sGC or protein kinase G. Elevation of cGMP, via the inhibition of phosphodiesterase 5 by sildenafil, also increased expression of Cpt1b, Acadl and Ucp3, as well as CPT1B protein levels, and further enhanced the effect of nitrate supplementation. CONCLUSIONS: Nitrate may therefore be effective in the treatment of metabolic disease by inducing FA oxidation in muscle.This work was kindly supported by a British Heart Foundation studentship to TA (FS/09/050). AJMu thanks the Research Councils UK for supporting his academic fellowship. LDR is supported by the Medical Research Council-Human Nutrition Research Elsie Widdowson Fellowship. AJMo thanks the Natural Sciences and Engineering Research Council for supporting her postdoctoral fellowship. MF acknowledges support from the Medical Research Council (G1001536). JLG thanks the Medical Research Council (MC_UP_A090_1006), the Biotechnology and Biological Sciences Research Council (BB/H013539/2) and British Heart Foundation for supporting work in his laboratory

PATH-38. ROSETTE-FORMING GLIONEURONAL TUMOR IS DEFINED BY FGFR1 ACTIVATING ALTERATIONS WITH FREQUENT ACCOMPANYING PI3K AND MAPK PATHWAY MUTATIONS

Abstract BACKGROUND Rosette-forming glioneuronal tumor (RGNT) is an uncommon CNS tumor originally described in the fourth ventricle characterized by a low-grade glial neoplasm admixed with a rosette-forming neurocytic component. METHODS We reviewed clinicopathologic features of 42 patients with RGNT. Targeted next-generation sequencing was performed, and genome-wide methylation profiling is underway. RESULTS The 20 male and 22 female patients had a mean age of 25 years (range 3–47) at time of diagnosis. Tumors were located within or adjacent to the lateral ventricle (n=16), fourth ventricle (15), third ventricle (9), and spinal cord (2). All 31 tumors assessed to date contained FGFR1 activating alterations, either in-frame gene fusion, kinase domain tandem duplication, or hotspot missense mutation in the kinase domain (p.N546 or p.K656). While 7 of these 31 tumors harbored FGFR1 alterations as the solitary pathogenic event, 24 contained additional pathogenic alterations within PI3-kinase or MAP kinase pathway genes: 5 with additional PIK3CA and NF1 mutations, 4 with PIK3CA mutation, 3 with PIK3R1 mutation (one of which also contained focal RAF1 amplification), 5 with PTPN11 mutation (one with additional PIK3R1 mutation), and 2 with NF1 deletion. The other 5 cases demonstrated anaplastic features including hypercellularity and increased mitotic activity. Among these anaplastic cases, 3 harbored inactivating ATRX mutations and two harbored CDKN2A homozygous deletion, in addition to the FGFR1 alterations plus other PI3-kinase and MAP kinase gene mutations seen in those RGNT without anaplasia. CONCLUSION Independent of ventricular location, RGNT is defined by FGFR1 activating mutations or rearrangements, which are frequently accompanied by mutations involving PIK3CA, PIK3R1, PTPN11, NF1, and KRAS. Whereas pilocytic astrocytoma and ganglioglioma are characterized by solitary activating MAP kinase pathway alterations (e.g. BRAF fusion or mutation), RGNT are genetically more complex with dual PI3K-Akt-mTOR and Ras-Raf-MAPK pathway activation. Rare anaplastic examples may show additional ATRX and/or CDKN2A inactivation

Toward Improved Environmental Stability of Polymer:Fullerene and Polymer:Nonfullerene Organic Solar Cells: A Common Energetic Origin of Light- and Oxygen-Induced Degradation

With the emergence of nonfullerene electron acceptors resulting in further breakthroughs in the performance of organic solar cells, there is now an urgent need to understand their degradation mechanisms in order to improve their intrinsic stability through better material design. In this study, we present quantitative evidence for a common root cause of light-induced degradation of polymer:nonfullerene and polymer:fullerene organic solar cells in air, namely, a fast photo-oxidation process of the photoactive materials mediated by the formation of superoxide radical ions, whose yield is found to be strongly controlled by the lowest unoccupied molecular orbital (LUMO) levels of the electron acceptors used. Our results elucidate the general relevance of this degradation mechanism to both polymer:fullerene and polymer:nonfullerene blends and highlight the necessity of designing electron acceptor materials with sufficient electron affinities to overcome this challenge, thereby paving the way toward achieving long-term solar cell stability with minimal device encapsulation