An analysis of schema change intervention

Successful organizational transformation relies on being able to achieve paradigm or collective schema change, and more particularly, the ability to manage the interplay between pre-existing schemas and alternative schemas required for new environments. This conceptual paper presents an analysis and critique of collective schema change dynamics. Two schema change pathways are reflected in the literature: frame-juxtapose-transition and frame-disengage-learning. Research findings in each pathway are limited and/or contradictory. Moreover, research on schema change focuses primarily on social dynamics and less on the relationship between social schema change dynamics and individual schema change dynamics. One implication of this lack of focus on individual schema change dynamics is the masking of the high level of cognitive processing and cognitive effort required by individuals to effect schema change. The capacity to achieve organizational transformation requires that more attention is given to managing these dynamics, which, in turn, requires significant investment in developing the change leadership capabilities of managers and the organizations they manage.

The contribution of leadership attributes to large scale, complex project success

Mismanagement of large-scale, complex projects has resulted in spectacular failures, cost overruns, time blowouts, and stakeholder dissatisfaction. We focus discussion on the interaction of key management and leadership attributes which facilitate leaders’ adaptive behaviors. These behaviors should in turn influence adaptive team member behavior, stakeholder engagement and successful project outcomes, outputs and impacts. An understanding of this type of management will benefit from a perspective based in managerial and organizational cognition. The research question we explore is whether successful leaders of large-scale complex projects have an internal process leading to a display of administrative, adaptive, and enabling behaviors that foster adaptive processes and enabling behaviors within their teams and with external stakeholders. At the core of the model we propose interactions of key attributes, namely cognitive flexibility, affect, and emotional intelligence. The result of these cognitive-affective attribute interactions is leadership leading to enhanced likelihood of complex project success.

A multi-level model of leadership in complex project management

Management (or perceived mismanagement) of large-scale, complex projects poses special problems and often results in spectacular failures, cost overruns, time blowouts and stakeholder dissatisfaction. While traditional project management responds with increasingly administrative constraints, we argue that leaders of such projects also need to display adaptive and enabling behaviours to foster adaptive processes, such as opportunity recognition, which requires an interaction of cognitive and affective processes of individual, project, and team leader attributes and behaviours. At the core of this model we propose is an interaction of cognitive flexibility, affect and emotional intelligence. The result of this interaction is enhanced leader opportunity recognition that, in turn, facilitates multilevel outcomes.

Person-environment fit: project leader-stakeholder relationships in a complex project environment

In this paper, we develop a conceptual model to explore the perceived complementary congruence between complex project leaders and the demands of the complex project environment to understand how leaders’ affective and behavioural performance at work might be impacted by this fit. We propose that complex project leaders high in emotional intelligence and cognitive flexibility should report a higher level of fit between themselves and the complex project environment. This abilities-demands measure of fit should then relate to affective and behavioural performance outcomes, such that leaders who perceive a higher level of fit should establish and maintain more effective, higher quality project stakeholder relationships than leaders who perceive a lower level of fit.

Cyclin-dependent kinase-mediated phosphorylation of RBP1 and pRb promotes their dissociation to mediate release of the SAP30·mSin3·HDAC transcriptional repressor complex

Eukaryotic cell cycle progression is mediated by phosphorylation of protein substrates by cyclin-dependent kinases (CDKs). A critical substrate of CDKs is the product of the retinoblastoma tumor suppressor gene, pRb, which inhibits G1-S phase cell cycle progression by binding and repressing E2F transcription factors. CDK-mediated phosphorylation of pRb alleviates this inhibitory effect to promote G1-S phase cell cycle progression. pRb represses transcription by binding to the E2F transactivation domain and recruiting the mSin3·histone deacetylase (HDAC) transcriptional repressor complex via the retinoblastoma-binding protein 1 (RBP1). RBP1 binds to the pocket region of pRb via an LXCXE motif and to the SAP30 subunit of the mSin3·HDAC complex and, thus, acts as a bridging protein in this multisubunit complex. In the present study we identified RBP1 as a novel CDK substrate. RBP1 is phosphorylated by CDK2 on serines 864 and 1007, which are N- and C-terminal to the LXCXE motif, respectively. CDK2-mediated phosphorylation of RBP1 or pRb destabilizes their interaction in vitro, with concurrent phosphorylation of both proteins leading to their dissociation. Consistent with these findings, RBP1 phosphorylation is increased during progression from G 1 into S-phase, with a concurrent decrease in its association with pRb in MCF-7 breast cancer cells. These studies provide new mechanistic insights into CDK-mediated regulation of the pRb tumor suppressor during cell cycle progression, demonstrating that CDK-mediated phosphorylation of both RBP1 and pRb induces their dissociation to mediate release of the mSin3·HDAC transcriptional repressor complex from pRb to alleviate transcriptional repression of E2F.

Informed learning in online environments : supporting the higher education curriculum beyond Web 2.0

As boundaries between physical and online learning spaces become increasingly blurred in higher education, how can students gain full benefit of Web 2.0 social media and mobile technologies for learning? How can we, as information professionals and educators, best support the information literacy learning needs of students who are universally mobile and Google-focused? This chapter presents informed learning (Bruce, 2008) as a pedagogical construct with potential to support learning across the higher education curriculum, for Web 2.0 and beyond. After outlining the principles of informed learning and how they may enrich the higher education curriculum, we explain the role of library and information professionals in promoting informed learning for Web 2.0 and beyond. Then, by way of illustration, we describe recent experience at an American university where librarians simultaneously learned about and applied informed learning principles in reshaping the information literacy program.

Informed cyberlearning : a case study

This cyberlearning case study demonstrates the application of Web 2.0 in mainstream higher education curriculum, whilst providing an in-practice example of informed learning (Bruce, 2008. The case study features the learning experiences and creative outcomes of postgraduate Cyberlearning students at Queensland University of Technology in 2011. As informed learners, the students learned simultaneously about the theory and practice of Cyberlearning by carrying out a virtual team project. This involved collaboratively researching a topical issue, as well as exploring and applying Web 2.0 media. To support the informed learning of their peers, they created online resources which both convey disciplinary knowledge and showcase the educational potential of Web 2.0.

Association between prostinogen (KLK15) genetic variants and prostate cancer risk and aggressiveness in Australia and a meta-analysis of GWAS data

Background: Kallikrein 15 (KLK15)/Prostinogen is a plausible candidate for prostate cancer susceptibility. Elevated KLK15 expression has been reported in prostate cancer and it has been described as an unfavorable prognostic marker for the disease. Objectives: We performed a comprehensive analysis of association of variants in the KLK15 gene with prostate cancer risk and aggressiveness by genotyping tagSNPs, as well as putative functional SNPs identified by extensive bioinformatics analysis. Methods and Data Sources: Twelve out of 22 SNPs, selected on the basis of linkage disequilibrium pattern, were analyzed in an Australian sample of 1,011 histologically verified prostate cancer cases and 1,405 ethnically matched controls. Replication was sought from two existing genome wide association studies (GWAS): the Cancer Genetic Markers of Susceptibility (CGEMS) project and a UK GWAS study. Results: Two KLK15 SNPs, rs2659053 and rs3745522, showed evidence of association (p, 0.05) but were not present on the GWAS platforms. KLK15 SNP rs2659056 was found to be associated with prostate cancer aggressiveness and showed evidence of association in a replication cohort of 5,051 patients from the UK, Australia, and the CGEMS dataset of US samples. A highly significant association with Gleason score was observed when the data was combined from these three studies with an Odds Ratio (OR) of 0.85 (95% CI = 0.77-0.93; p = 2.7610 24). The rs2659056 SNP is predicted to alter binding of the RORalpha transcription factor, which has a role in the control of cell growth and differentiation and has been suggested to control the metastatic behavior of prostate cancer cells. Conclusions: Our findings suggest a role for KLK15 genetic variation in the etiology of prostate cancer among men of European ancestry, although further studies in very large sample sets are necessary to confirm effect sizes.

Identification of a novel prostate cancer susceptibility variant in the KLK3 gene transcript

Abstract Genome-wide association studies (GWAS) have identified more than 30 prostate cancer (PrCa) susceptibility loci. One of these (rs2735839) is located close to a plausible candidate susceptibility gene, KLK3, which encodes prostate-specific antigen (PSA). PSA is widely used as a biomarker for PrCa detection and disease monitoring. To refine the association between PrCa and variants in this region, we used genotyping data from a two-stage GWAS using samples from the UK and Australia, and the Cancer Genetic Markers of Susceptibility (CGEMS) study. Genotypes were imputed for 197 and 312 single nucleotide polymorphisms (SNPs) from HapMap2 and the 1000 Genome Project, respectively. The most significant association with PrCa was with a previously unidentified SNP, rs17632542 (combined P = 3.9 × 10−22). This association was confirmed by direct genotyping in three stages of the UK/Australian GWAS, involving 10,405 cases and 10,681 controls (combined P = 1.9 × 10−34). rs17632542 is also shown to be associated with PSA levels and it is a non-synonymous coding SNP (Ile179Thr) in KLK3. Using molecular dynamic simulation, we showed evidence that this variant has the potential to introduce alterations in the protein or affect RNA splicing. We propose that rs17632542 may directly influence PrCa risk.

It’s about time : investing in transportation to keep Texas economically competitive : Appendices

APPENDIX A : PAVEMENT QUALITY (Zhanmin Zhang, Michael R. Murphy, Robert Harrison), 7 pages -- APPENDIX B : BRIDGE QUALITY (Jose Weissmann, Angela J. Weissmann), 6 pages -- APPENDIX C : URBAN TRAFFIC CONGESTION (Tim Lomax, David Schrank), 32 pages -- APPENDIX D: RURAL CORRIDORS (Tim Lomax, David Schrank), 6 pages -- APPENDIX E: ADDITIONAL REVENUE SOURCE OPTIONS FOR PAVEMENT AND BRIDGE MAINTENANCE (Mike Murphy, Seokho Chi, Randy Machemehl, Khali Persad, Robert Harrison, Zhanmin Zhang), 81 pages -- APPENDIX F: FUNDING TRANSPORTATION IMPROVEMENTS (David Ellis, Brianne Glover, Nick Norboge, Wally Crittenden), 19 pages -- APPENDIX G: ESTIMATING VEHICLE OPERATING COSTS AND PAVEMENT DETERIORATION (by Robert Harrison), 4 pages

Transforming organizational leadership : a schema change perspective

Successful organizational transformation typically requires transformed leadership; that is, fundamental changes in the implicit leadership schema that underpin observed organizational leadership practice. The purpose of this study is to elaborate leadership schema change theory by investigating a case study in which the CEO of a public infrastructure organization sought to transform traditional organizational leadership to facilitate wider organization transformation. Data were generated through focus groups and semi-structured interviews at four points over a three-year period. Our findings suggest that (a) change leader initiatives do not necessarily activate the cognitive processing required to achieve leadership schema change, (b) collective schema change, defined in terms of the system of beliefs and values underlying the new leading-managing schema did not occur, however, (c) sub-schema change did occur. The research contributes to existing literature on implicit leadership schema change in three main ways. First, we provide a schema change framework to guide current and future research on schema change. Second, we highlight the role that both change leader initiatives and individual and social processing play in schema change. Finally, we stress the role of teleological processes in leadership schema change.

Protein monoubiquitination and polyubiquitination generate structural diversity to control distinct biological processes

Ubiquitination involves the attachment of ubiquitin (Ub) to lysine residues on substrate proteins or itself, which can result in protein monoubiquitination or polyubiquitination. Polyubiquitination through different lysines (seven) or the N-terminus of Ub can generate different protein-Ub structures. These include monoubiquitinated proteins, polyubiqutinated proteins with homotypic chains through a particular lysine on Ub or mixed polyubiquitin chains generated by polymerization through different Ub lysines. The ability of the ubiquitination pathway to generate different protein-Ub structures provides versatility of this pathway to target proteins to different fates. Protein ubiquitination is catalyzed by Ub-conjugating and Ub-ligase enzymes, with different combinations of these enzymes specifying the type of Ub modification on protein substrates. How Ub-conjugating and Ub-ligase enzymes generate this structural diversity is not clearly understood. In the current review, we discuss mechanisms utilized by the Ub-conjugating and Ub-ligase enzymes to generate structural diversity during protein ubiquitination, with a focus on recent mechanistic insights into protein monoubiquitination and polyubiquitination.