A knowledge-based framework for service management

peer-reviewedThe purpose of this paper is to investigate how information and communication technologies are used for service standardisation, customisation, and modularisation by knowledge-intensive service firms through the development and empirical validation of a knowledge-based framework. This paper uses 59 in-depth interviews, observational data, and document analysis from case studies of three service-related departments in high-technology, multinational knowledge-intensive business services (KIBSs). Prior research does not conceptualise the relationships between service customisation, standardisation and modularisation. This paper seeks to overcome this gap by integrating insights from research on the role played by both knowledge and information and communication technologies (ICTs) to construct and validate a framework to deal with this gap. It outlines the implications for service firms' use of ICT to deal with increasing knowledge intensity as well as indicating the circumstances under which service knowledge is best customised, standardised and modularised. Further testing in other industries would prove useful in extending the usefulness and applicability of the findings. The originality of the paper lies in developing and validating the first framework to outline the relationship between how service knowledge is customised, standardised or modularised and indicating the associated issues and challenges. It emphasises the role of knowledge and technology. The value of this framework increases as more firms deal with increasing knowledge intensity in the services they provide and in their use of ICTs to reap the benefits of appropriate knowledge reuse.ACCEPTEDpeer-reviewe

Adam33 polymorphisms are associated with COPD and lung function in long-term tobacco smokers

<p>Abstract</p> <p>Background</p> <p>Variation in ADAM33 has been shown to be important in the development of asthma and altered lung function. This relationship however, has not been investigated in the population susceptible to COPD; long term tobacco smokers. We evaluated the association between polymorphisms in ADAM33 gene with COPD and lung function in long term tobacco smokers.</p> <p>Methods</p> <p>Caucasian subjects, at least 50 year old, who smoked ≥ 20 pack-years (n = 880) were genotyped for 25 single nucleotide polymorphisms (SNPs) in ADAM33. COPD was defined as an FEV1/FVC ratio < 70% and percent-predicted (pp)FEV1 < 75% (n = 287). The control group had an FEV1/FVC ratio ≥ 70% and ppFEV₁≥ 80% (n = 311) despite ≥ 20 pack years of smoking. Logistic and linear regressions were used for the analysis. Age, sex, and smoking status were considered as potential confounders.</p> <p>Results</p> <p>Five SNPs in ADAM33 were associated with COPD (Q-1, intronic: p < 0.003; S1, Ile → Val: p < 0.003; S2, Gly → Gly: p < 0.04; V-1 intronic: p < 0.002; V4, in 3' untranslated region: p < 0.007). Q-1, S1 and V-1 were also associated with ppFEV1, FEV1/FVC ratio and ppFEF25–75 (p values 0.001 – 0.02). S2 was associated with FEV1/FVC ratio (p < 0.05). The association between S1 and residual volume revealed a trend toward significance (p value < 0.07). Linkage disequilibrium and haplotype analyses suggested that S1 had the strongest degree of association with COPD and pulmonary function abnormalities.</p> <p>Conclusion</p> <p>Five SNPs in ADAM33 were associated with COPD and lung function in long-term smokers. Functional studies will be needed to evaluate the biologic significance of these polymorphisms in the pathogenesis of COPD.</p

Organic or organised: An interaction analysis to identify how interactional practices influence participation in group decision meetings for residency selection

Objectives This study aims to shed light on interactional practices in real-life selection decision-making meetings. Adequate residency selection is crucial, yet currently, we have little understanding of how the decision-making process takes place in practice. Since having a wide range of perspectives on candidates is assumed to enhance decision-making, our analytical focus will lie on the possibilities for committee members to participate by contributing their perspective. Design We analysed interaction in seven recorded real-life selection group decision meetings, with explicit attention to participation. Setting Selection meetings of four different highly competitive specialties in two Dutch regions. Participants 54 participants discussed 68 candidates. Methods To unravel interactional practices, group discussions were analysed using a hybrid data-driven, iterative analytical approach. We paid explicit attention to phenomena which have effects on participation. Word counts and an inductive qualitative analysis were used to identify existing variations in the current practices. Results We found a wide variety of practices. We highlight two distinct interactional patterns, which are illustrative of a spectrum of turn-taking practices, interactional norms and conventions in the meetings. Typical for the first pattern - organised' - is a chairperson who is in control of the topic and turn-taking process, silences between turns and a slow topic development. The second pattern - organic' - can be recognised by overlapping speech, clearly voiced disagreements and negotiation about the organisation of the discussion. Both interactional patterns influence the availability of information, as they create different types of thresholds for participation. Conclusions By deconstructing group decision-making meetings concerning resident selection, we show how structure, interactional norms and conventions affect participation. We identified a spectrum ranging from organic to organised. Both ends have different effects on possibilities for committee members to participate. Awareness of this spectrum might help groups to optimise decision processes by enriching the range of perspectives shared

VII Scandinavian Copd Research Symposium, Holmenkollen, Oslo 18th-19th November 2016

Peer reviewe

Whole exome re-sequencing implicates CCDC38 and cilia structure and function in resistance to smoking related airflow obstruction

Chronic obstructive pulmonary disease (COPD) is a leading cause of global morbidity and mortality and, whilst smoking remains the single most important risk factor, COPD risk is heritable. Of 26 independent genomic regions showing association with lung function in genome-wide association studies, eleven have been reported to show association with airflow obstruction. Although the main risk factor for COPD is smoking, some individuals are observed to have a high forced expired volume in 1 second (FEV1) despite many years of heavy smoking. We # hypothesised that these ‘‘resistant smokers’’ may harbour variants which protect against lung function decline caused by smoking and provide insight into the genetic determinants of lung health. We undertook whole exome re sequencing of 100 heavy smokers who had healthy lung function given their age, sex, height and smoking history and applied three complementary approaches to explore the genetic architecture of smoking resistance. Firstly, we identified novel functional variants in the ‘‘resistant smokers’’ and looked for enrichment of these novel variants within biological pathways. Secondly, we undertook association testing of all exonic variants individually with two independent control sets. Thirdly, we undertook gene-based association testing of all exonic variants. Our strongest signal of association with smoking resistance for a non-synonymous SNP was for rs10859974 (P = 2.3461024) in CCDC38, a gene which has previously been reported to show association with FEV1/FVC, and we demonstrate moderate expression of CCDC38 in bronchial epithelial cells. We identified an enrichment of novel putatively functional variants in genes related to cilia structure and function in resistant smokers. Ciliary function abnormalities are known to be associated with both smoking and reduced mucociliary clearance in patients with COPD. We suggest that genetic influences on the development or function of cilia in the bronchial epithelium may affect growth of cilia or the extent of damage caused by tobacco smoke

Non-essential role for TLR2 and its signaling adaptor Mal/TIRAP in preserving normal lung architecture in mice

Myeloid differentiation factor 88 (MyD88) and MyD88-adaptor like (Mal)/Toll-interleukin 1 receptor domain containing adaptor protein (TIRAP) play a critical role in transducing signals downstream of the Toll-like receptor (TLR) family. While genetic ablation of the TLR4/MyD88 signaling axis in mice leads to pulmonary cell death and oxidative stress culminating in emphysema, the involvement of Mal, as well as TLR2 which like TLR4 also signals via MyD88 and Mal, in the pathogenesis of emphysema has not been studied. By employing an in vivo genetic approach, we reveal here that unlike the spontaneous pulmonary emphysema which developed in Tlr42/2 mice by 6 months of age, the lungs of Tlr22/2 mice showed no physiological or morphological signs of emphysema. A more detailed comparative analysis of the lungs from these mice confirmed that elevated oxidative protein carbonylation levels and increased numbers of alveolar cell apoptosis were only detected in Tlr42/2 mice, along with up-regulation of NADPH oxidase 3 (Nox3) mRNA expression. With respect to Mal, the architecture of the lungs of Mal2/2 mice was normal. However, despite normal oxidative protein carbonylation levels in the lungs of emphysema-free Mal2/2 mice, these mice displayed increased levels of apoptosis comparable to those observed in emphysematous Tlr42/2 mice. In conclusion, our data provide in vivo evidence for the non-essential role for TLR2, unlike the related TLR4, in maintaining the normal architecture of the lung. In addition, we reveal that Mal differentially facilitates the anti-apoptotic, but not oxidant suppressive, activities of TLR4 in the lung, both of which appear to be essential for TLR4 to prevent the onset of emphysema