Manager ambidexterity in healthcare: the effect of paradoxical thinking, reflective learning, and context responsiveness

Manager ambidexterity is the capability to demonstrate equally well exploiting and exploring behaviour. Managers vary in ambidexterity capability therefore there is need for further scholarly work to examine the factors which explain this variation. The purpose of the current study was to explore and develop hypotheses on the influence of paradoxical thinking, leader role behaviour, and contextual factors on managerial ambidexterity. A self-report questionnaire was distributed to 152 managers of a public healthcare organisation. Findings of the study indicated although paradoxical thinking did not significantly predict manager ambidexterity, leader role behaviours characterising reflective learning and context responsiveness accounted for higher levels of exploiting and exploring behaviour. These findings suggest manager ambidexterity could be developed and enhanced through the development of skills and competencies for reflective learning and context responsiveness

Identifying Candida albicans Gene Networks Involved in Pathogenicity

Acknowledgments This is a short text to acknowledge the contributions of specific colleagues, institutions, or agencies that aided the efforts of the authors. Funding RA was generously supported by a Wellcome Trust Institutional Strategic Support Award [WT105618MA], a Microbiology Research Visit Grant [RVG16/18], and a EPSRC/BBSRC Innovation Fellowship [EP/S001352/1]. AB was supported by a programme grant from the UK Medical Research Council [MR/M026663/1] and by the Medical Research Council Centre for Medical Mycology at the University of Aberdeen [MR/N006364/1]. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.Peer reviewedPublisher PD

The Evolutionary Rewiring of Ubiquitination Targets Has Reprogrammed the Regulation of Carbon Assimilation in the Pathogenic Yeast \u3ci\u3eCandida albicans\u3c/i\u3e

Microbes must assimilate carbon to grow and colonize their niches. Transcript profiling has suggested that Candida albicans, a major pathogen of humans, regulates its carbon assimilation in an analogous fashion to the model yeast Saccharomyces cerevisiae, repressing metabolic pathways required for the use of alterative nonpreferred carbon sources when sugars are available. However, we show that there is significant dislocation between the proteome and transcriptome in C. albicans. Glucose triggers the degradation of the ICL1 and PCK1 transcripts in C. albicans, yet isocitrate lyase (Icl1) and phosphoenolpyruvate carboxykinase (Pck1) are stable and are retained. Indeed, numerous enzymes required for the assimilation of carboxylic and fatty acids are not degraded in response to glucose. However, when expressed in C. albicans, S. cerevisiae Icl1 (ScIcl1) is subjected to glucose-accelerated degradation, indicating that like S. cerevisiae, this pathogen has the molecular apparatus required to execute ubiquitin-dependent catabolite inactivation. C. albicans Icl1 (CaIcl1) lacks analogous ubiquitination sites and is stable under these conditions, but the addition of a ubiquitination site programs glucose-accelerated degradation of CaIcl1. Also, catabolite inactivation is slowed in C. albicans ubi4 cells. Ubiquitination sites are present in gluconeogenic and glyoxylate cycle enzymes from S. cerevisiae but absent from their C. albicans homologues. We conclude that evolutionary rewiring of ubiquitination targets has meant that following glucose exposure, C. albicans retains key metabolic functions, allowing it to continue to assimilate alternative carbon sources. This metabolic flexibility may be critical during infection, facilitating the rapid colonization of dynamic host niches containing complex arrays of nutrients

Stress adaptation in a pathogenic fungus

Funding We are grateful to our funding bodies for their support. This work was supported by the European Commission [FINSysB, PITN-GA-2008-214004; STRIFE, ERC-2009-AdG-249793], by the UK Biotechnology and Biological Research Council [grant numbers BBS/B/06679; BB/C510391/1; BB/D009308/1; BB/F000111/1; BB/F010826/1; BB/F00513X/1], and by the Wellcome Trust [grant numbers 080088, 097377]. M.D.L. was also supported by a Carnegie/Caledonian Scholarship and a Sir Henry Wellcome Postdoctoral Fellowship from the Wellcome Trust [grant number 096072]. Deposited in PMC for immediate release.Peer reviewedPublisher PD

Elevated catalase expression in a fungal pathogen is a double-edged sword of iron

We thank our colleagues in the Aberdeen Fungal Group, Lloyd Peck (British Antarctic Survey) and John Helmann (Cornell University) for insightful discussions. We thank Christophe d’Enfert and Melanie Legrand (Institut Pasteur) for help with the design of barcodes and provision of the CIp10-PTET-GTw overexpression vector and CEC2908 strain. We are grateful to the following Core Facilities at the University of Aberdeen for their excellent technical assistance, advice and support: the Medical Research Facility; the Centre for Genome Enabled Biology and Medicine; the Iain Fraser Cytometry Centre; the Microscopy and Histology Facility; Aberdeen Proteomics; and the qPCR Facility.Peer reviewedPublisher PD

The Rewiring of Ubiquitination Targets in a Pathogenic Yeast Promotes Metabolic Flexibility, Host Colonization and Virulence

Funding: This work was funded by the European Research Council [http://erc.europa.eu/], AJPB (STRIFE Advanced Grant; C-2009-AdG-249793). The work was also supported by: the Wellcome Trust [www.wellcome.ac.uk], AJPB (080088, 097377); the UK Biotechnology and Biological Research Council [www.bbsrc.ac.uk], AJPB (BB/F00513X/1, BB/K017365/1); the CNPq-Brazil [http://cnpq.br], GMA (Science without Borders fellowship 202976/2014-9); and the National Centre for the Replacement, Refinement and Reduction of Animals in Research [www.nc3rs.org.uk], DMM (NC/K000306/1). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. Acknowledgments We thank Dr. Elizabeth Johnson (Mycology Reference Laboratory, Bristol) for providing strains, and the Aberdeen Proteomics facility for the biotyping of S. cerevisiae clinical isolates, and to Euroscarf for providing S. cerevisiae strains and plasmids. We are grateful to our Microscopy Facility in the Institute of Medical Sciences for their expert help with the electron microscopy, and to our friends in the Aberdeen Fungal Group for insightful discussions.Peer reviewedPublisher PD

Hsp90 orchestrates transcriptional regulation by Hsf1 and cell wall remodelling by MAPK signalling during thermal adaptation in a pathogenic yeast

Acknowledgments We thank Rebecca Shapiro for creating CaLC1819, CaLC1855 and CaLC1875, Gillian Milne for help with EM, Aaron Mitchell for generously providing the transposon insertion mutant library, Jesus Pla for generously providing the hog1 hst7 mutant, and Cathy Collins for technical assistance.Peer reviewedPublisher PD

Abstract Maximum Availability Models for Selecting Ambulance Station and Vehicle Locations: A Critique

Several researchers have employed the notion of reliability of coverage to extend the set covering and maximal coverage models. We discuss the suitability of these models in general for choosing ambulance station or vehicle locations. Then, we discuss one particular model (the queueing maximum availability location problem) in greater detail and describe difficulties encountered in applying it using realistic data. Acknowledgments This work has been partly supported by Discovery grants 25481 and 203534 from the Natura