Understanding the Emergent Structure of Competency Centers in Post-implementation Enterprise Systems

Part 3: Structures and NetworksInternational audiencePrior research provides conflicting insights about the link between investment in enterprise systems and firm value and in the ES governance mechanisms. The literature generally suggests that management should cultivate its technical and organizational expertise to derive value from currently deployed Enterprise Systems (ES) [8]. In the realm of practice, ERP vendors and configuration/integration partners strongly recommend the creation of an organizational structure to govern the ERP implementation and post-implementation process to improve project success and extract greater value from the ES investment. The ES literature, while unclear on the formation, and functioning of ES governance units, suggests the need for formal and fixed governance structures. This research utilizes Deleuze’s assemblage theory and emergence theory to explain the genesis and evolution of the governing ‘structure’ known as the Competency Center (CC). Our results illustrate the business needs driving the structuring processes behind the CC, are also those that lead to unintended and destabilizing outcomes. Whether the CC ‘assemblage’ survives to provide value depends on how the emergent issues are handled and how the assemblages are “positioned”. This research suggests effective ES governance is not derived from a prescribed step-wise process yielding formal structures, but rather form an organic process of assemblage

Sporting embodiment: sports studies and the (continuing) promise of phenomenology

Whilst in recent years sports studies have addressed the calls ‘to bring the body back in’ to theorisations of sport and physical activity, the ‘promise of phenomenology’ remains largely under-realised with regard to sporting embodiment. Relatively few accounts are grounded in the ‘flesh’ of the lived sporting body, and phenomenology offers a powerful framework for such analysis. A wide-ranging, multi-stranded, and interpretatively contested perspective, phenomenology in general has been taken up and utilised in very different ways within different disciplinary fields. The purpose of this article is to consider some selected phenomenological threads, key qualities of the phenomenological method, and the potential for existentialist phenomenology in particular to contribute fresh perspectives to the sociological study of embodiment in sport and exercise. It offers one way to convey the ‘essences’, corporeal immediacy and textured sensuosity of the lived sporting body. The use of Interpretative Phenomenological Analysis (IPA) is also critically addressed. Key words: phenomenology; existentialist phenomenology; interpretative phenomenological analysis (IPA); sporting embodiment; the lived-body; Merleau-Pont

Professional closure by proxy: the impact of changing educational requirements on class mobility for a cohort of Big 8 partners

Closure events impacting on class mobility may include mechanisms initiated by bodies other than the professional body. The research examines if the introduction of full-time study requirements at universities for aspiring accountants effectively introduced a closure mechanism in the accounting profession. Data was derived from an Oral History study of partners in large firms. The younger partners (born after the Second World War) completed full-time degree study at university, but did not provide evidence of class mobility into the profession. The older cohort, born between 1928 and 1946, completed part-time studies only, few completed a degree, and, in contrast to the younger cohort, shows a perceptible upward movement from lower socio-economic classes into the professional class. This suggests that changing the preferred educational routes for new accountants entering the large chartered accounting (CA) firms compromised the "stepping stone" function of accounting as a portal into the professional class

Prediction and clinical utility of a contralateral breast cancer risk model

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Non-crossing dependencies: Least effort, not grammar

The use of null hypotheses (in a statistical sense) is common in hard sciences but not in theoretical linguistics. Here the null hypothesis that the low frequency of syntactic dependency crossings is expected by an arbitrary ordering of words is rejected. It is shown that this would require star dependency structures, which are both unrealistic and too restrictive. The hypothesis of the limited resources of the human brain is revisited. Stronger null hypotheses taking into account actual dependency lengths for the likelihood of crossings are presented. Those hypotheses suggests that crossings are likely to reduce when dependencies are shortened. A hypothesis based on pressure to reduce dependency lengths is more parsimonious than a principle of minimization of crossings or a grammatical ban that is totally dissociated from the general and non-linguistic principle of economy.Postprint (author's final draft

Mendelian randomisation study of height and body mass index as modifiers of ovarian cancer risk in 22,588 BRCA1 and BRCA2 mutation carriers

Item does not contain fulltextBACKGROUND: Height and body mass index (BMI) are associated with higher ovarian cancer risk in the general population, but whether such associations exist among BRCA1/2 mutation carriers is unknown. METHODS: We applied a Mendelian randomisation approach to examine height/BMI with ovarian cancer risk using the Consortium of Investigators for the Modifiers of BRCA1/2 (CIMBA) data set, comprising 14,676 BRCA1 and 7912 BRCA2 mutation carriers, with 2923 ovarian cancer cases. We created a height genetic score (height-GS) using 586 height-associated variants and a BMI genetic score (BMI-GS) using 93 BMI-associated variants. Associations were assessed using weighted Cox models. RESULTS: Observed height was not associated with ovarian cancer risk (hazard ratio [HR]: 1.07 per 10-cm increase in height, 95% confidence interval [CI]: 0.94-1.23). Height-GS showed similar results (HR = 1.02, 95% CI: 0.85-1.23). Higher BMI was significantly associated with increased risk in premenopausal women with HR = 1.25 (95% CI: 1.06-1.48) and HR = 1.59 (95% CI: 1.08-2.33) per 5-kg/m(2) increase in observed and genetically determined BMI, respectively. No association was found for postmenopausal women. Interaction between menopausal status and BMI was significant (Pinteraction < 0.05). CONCLUSION: Our observation of a positive association between BMI and ovarian cancer risk in premenopausal BRCA1/2 mutation carriers is consistent with findings in the general population

Identification of independent association signals and putative functional variants for breast cancer risk through fine-scale mapping of the 12p11 locus.

BACKGROUND: Multiple recent genome-wide association studies (GWAS) have identified a single nucleotide polymorphism (SNP), rs10771399, at 12p11 that is associated with breast cancer risk. METHOD: We performed a fine-scale mapping study of a 700 kb region including 441 genotyped and more than 1300 imputed genetic variants in 48,155 cases and 43,612 controls of European descent, 6269 cases and 6624 controls of East Asian descent and 1116 cases and 932 controls of African descent in the Breast Cancer Association Consortium (BCAC; http://bcac.ccge.medschl.cam.ac.uk/ ), and in 15,252 BRCA1 mutation carriers in the Consortium of Investigators of Modifiers of BRCA1/2 (CIMBA). Stepwise regression analyses were performed to identify independent association signals. Data from the Encyclopedia of DNA Elements project (ENCODE) and the Cancer Genome Atlas (TCGA) were used for functional annotation. RESULTS: Analysis of data from European descendants found evidence for four independent association signals at 12p11, represented by rs7297051 (odds ratio (OR) = 1.09, 95 % confidence interval (CI) = 1.06-1.12; P = 3 × 10(-9)), rs805510 (OR = 1.08, 95 % CI = 1.04-1.12, P = 2 × 10(-5)), and rs1871152 (OR = 1.04, 95 % CI = 1.02-1.06; P = 2 × 10(-4)) identified in the general populations, and rs113824616 (P = 7 × 10(-5)) identified in the meta-analysis of BCAC ER-negative cases and BRCA1 mutation carriers. SNPs rs7297051, rs805510 and rs113824616 were also associated with breast cancer risk at P < 0.05 in East Asians, but none of the associations were statistically significant in African descendants. Multiple candidate functional variants are located in putative enhancer sequences. Chromatin interaction data suggested that PTHLH was the likely target gene of these enhancers. Of the six variants with the strongest evidence of potential functionality, rs11049453 was statistically significantly associated with the expression of PTHLH and its nearby gene CCDC91 at P < 0.05. CONCLUSION: This study identified four independent association signals at 12p11 and revealed potentially functional variants, providing additional insights into the underlying biological mechanism(s) for the association observed between variants at 12p11 and breast cancer risk.UK funding includes Cancer Research UK and NIH.This is the final version of the article. It first appeared from BioMed Central via http://dx.doi.org/10.1186/s13058-016-0718-

Functional mechanisms underlying pleiotropic risk alleles at the 19p13.1 breast-ovarian cancer susceptibility locus

A locus at 19p13 is associated with breast cancer (BC) and ovarian cancer (OC) risk. Here we analyse 438 SNPs in this region in 46,451 BC and 15,438 OC cases, 15,252 BRCA1 mutation carriers and 73,444 controls and identify 13 candidate causal SNPs associated with serous OC (P=9.2 × 10-20), ER-negative BC (P=1.1 × 10-13), BRCA1-associated BC (P=7.7 × 10-16) and triple negative BC (P-diff=2 × 10-5). Genotype-gene expression associations are identified for candidate target genes ANKLE1 (P=2 × 10-3) and ABHD8 (P<2 × 10-3). Chromosome conformation capture identifies interactions between four candidate SNPs and ABHD8, and luciferase assays indicate six risk alleles increased transactivation of the ADHD8 promoter. Targeted deletion of a region containing risk SNP rs56069439 in a putative enhancer induces ANKLE1 downregulation; and mRNA stability assays indicate functional effects for an ANKLE1 3′-UTR SNP. Altogether, these data suggest that multiple SNPs at 19p13 regulate ABHD8 and perhaps ANKLE1 expression, and indicate common mechanisms underlying breast and ovarian cancer risk

Fine-mapping of prostate cancer susceptibility loci in a large meta-analysis identifies candidate causal variants

Prostate cancer is a polygenic disease with a large heritable component. A number of common, low-penetrance prostate cancer risk loci have been identified through GWAS. Here we apply the Bayesian multivariate variable selection algorithm JAM to fine-map 84 prostate cancer susceptibility loci, using summary data from a large European ancestry meta-analysis. We observe evidence for multiple independent signals at 12 regions and 99 risk signals overall. Only 15 original GWAS tag SNPs remain among the catalogue of candidate variants identified; the remainder are replaced by more likely candidates. Biological annotation of our credible set of variants indicates significant enrichment within promoter and enhancer elements, and transcription factor-binding sites, including AR, ERG and FOXA1. In 40 regions at least one variant is colocalised with an eQTL in prostate cancer tissue. The refined set of candidate variants substantially increase the proportion of familial relative risk explained by these known susceptibility regions, which highlights the importance of fine-mapping studies and has implications for clinical risk profiling. © 2018 The Author(s).Prostate cancer is a polygenic disease with a large heritable component. A number of common, low-penetrance prostate cancer risk loci have been identified through GWAS. Here we apply the Bayesian multivariate variable selection algorithm JAM to fine-map 84 prostate cancer susceptibility loci, using summary data from a large European ancestry meta-analysis. We observe evidence for multiple independent signals at 12 regions and 99 risk signals overall. Only 15 original GWAS tag SNPs remain among the catalogue of candidate variants identified; the remainder are replaced by more likely candidates. Biological annotation of our credible set of variants indicates significant enrichment within promoter and enhancer elements, and transcription factor-binding sites, including AR, ERG and FOXA1. In 40 regions at least one variant is colocalised with an eQTL in prostate cancer tissue. The refined set of candidate variants substantially increase the proportion of familial relative risk explained by these known susceptibility regions, which highlights the importance of fine-mapping studies and has implications for clinical risk profiling. © 2018 The Author(s).Peer reviewe