Personal knowledge development in online learning:a model for measuring externalisation, combination and internalisation

This paper presents a model for measuring personal knowledge development in online learning environments. It is based on Nonaka‘s SECI model of organisational knowledge creation. It is argued that Socialisation is not a relevant mode in the context of online learning and was therefore not covered in the measurement instrument. Therefore, the remaining three of SECI‘s knowledge conversion modes, namely Externalisation, Combination, and Internalisation were used and a measurement instrument was created which also examines the interrelationships between the three modes. Data was collected using an online survey, in which online learners report on their experiences of personal knowledge development in online learning environments. In other words, the instrument measures the magnitude of online learners‘ Externalisation and combination activities as well as their level of internalisation, which is the outcome of their personal knowledge development in online learning.

A template for externalisation-internalisation decisions in virtual enterprises

Recognising the importance of alliance decision making in a virtual enterprise (VE), this paper proposes an analysis template to facilitate this process. The existing transaction-cost and resource-based theories in the literature are first reviewed, showing some deficiencies in both type of theories, and the potential of the resource based explanations. The paper then goes on to propose a resource-based analysis template, integrating both the motives of using certain business forms and the factors why different forms help achieve different objectives, Resource-combination effectiveness, management complexity and flexibility are identified as the three factors providing fundamental explanations of an organization's alliance making decision process. The template provides a comprehensive and generic approach for analysing alliance decisions.

Shifting borders of European Union internal security:technology, externalisation and accountability

This edited volume analyzes recent key developments in EU border management. In light of the refugee crises in the Mediterranean and the responses on the part of EU member states, this volume presents an in-depth reflection on European border practices and their political, social and economic consequences. Approaching borders as concepts in flux, the authors identify three main trends: the rise of security technologies such as the EUROSUR system, the continued externalization of EU security governance such as border mission training in third states, and the unfolding dynamics of accountability. The contributions show that internal security cooperation in Europe is far from consolidated, since both political oversight mechanisms and the definition of borders remain in flux. This edited volume makes a timely and interdisciplinary contribution to the ongoing academic and political debate on the future of open borders and legitimate security governance in Europe. It offers a valuable resource for scholars in the fields of international security and migration studies, as well as for practitioners dealing with border management mechanisms.

Factors important to the secretion and matrix deposition of tissue transglutaminase

Data suggest that for TG2 to be secreted, an intact N-terminal FN binding site (for which TG2 has high affinity) is required, however interaction of TG2 with its high affinity binding partners presents both in the intracellular and extracellular space as well as with specific cell surface receptors may also be involved in this process. Using a site-directed mutagenesis approach, the effects of specific mutations of TG2 on its translocation to the cell surface and secretion into the ECM have been investigated. Mutations include those affecting FN binding (FN1), HSPGs binding (HS1, HS2) GTP/GDP binding site (GTP1, 2) as well as N-terminal and C-terminal domains (TG2 deletion mutants N, and C). By performing transglutaminase activity assays, cell surface protein biotinylation and verifying distribution of TG2 mutants in the ECM we demonstrated that one of the potential heparan sulfate binding site mutants (HS2 mutant) is secreted at the cell surface in a much reduced manner and is less deposited into the ECM than the HS1 mutant. The HS2 mutant showed a low affinity for binding to a heparin sepharose column demonstrating this mutation site may be a potential heparan binding site of TG2. Analogous peptides to this site were shown to have some efficiency in the inhibition of the binding of the FN-TG2 complex to cell surface heparan sulfates in a cell adhesion assay indicating the peptide to be representative of the novel heparin binding site within TG2. The GTP binding site mutants GTP1 and GTP2 exhibited low specific activity however, GTP2 showed more secretion to the cell surface in comparison to GTP1. The FN1 binding mutant did not greatly affect TG2 activity nor did it alter TG2 secretion at the cell surface and deposition into the ECM indicating that fibronectin binding at this site on the enzyme is not an important factor. Interestingly an intact N-terminus (?1-15) appeared to be essential for enzyme externalisation. Removal of the first 15 amino acids (N-terminal mutant) abolished TG2 secretion to the cell surface as well as deposition into the ECM. In addition it reduced the enzymes affinity for binding to heparin. In contrast, deletion of the C-terminal TG2 domain (?594-687) increased enzyme secretion to the cell surface. Consistent with the data presented in this thesis we speculate that TG2 must fulfill two requirements to be successfully secreted from cells. The findings indicate that the closed conformation of the enzyme as well as intact N-terminal tail and a novel HS binding site within the TG2 molecule are key elements for the enzyme’s localisation at the cell surface and its deposition into the extracellular matrix. The importance of understanding the interactions between TG2, heparan sulfates and other TG2 binding partners at the cell surface could have an impact on the design of novel strategies for enzyme inhibition which could be important in the control of extracellular TG2 related diseases.

Cellular and molecular consequences of S100A4-induced motility in rat breast tumour Rama 37 cells

Since the first discovery of S100 members in 1965, their expressions have been affiliated with numerous biological functions in all cells of the body. However, in the recent years, S100A4, a member of this superfamily has emerged as the central target in generating new avenue for cancer therapy as its overexpression has been correlated with cancer patients’ mortality as well as established roles as motility and metastasis promoter. As it has no catalytic activity, S100A4 has to interact with its target proteins to regulate such effects. Up to date, more than 10 S100A4 target proteins have been identified but the mechanical process regulated by S100A4 to induce motility remains vague. In this work, we demonstrated that S100A4 overexpression resulted in actin filaments disorganisation, reduction in focal adhesions, instability of filopodia as well as exhibiting polarised morphology. However, such effects were not observed in truncated versions of S100A4 possibly highlighting the importance of C terminus of S100A4 target recognition. In order to assess some of the intracellular mechanisms that may be involved in promoting migrations, different strategies were used, including active pharmaceutical agents, inhibitors and knockdown experiments. Treatment of S100A4 overexpressing cells with blebbistatin and Y-27632, non muscle myosin IIA (NMMIIA) inhibitors, as well as knockdown of NMMIIA, resulted in motility enhancement and focal adhesions reduction proposing that NMMIIA assisted S100A4 in regulating cell motility but its presence is not essential. Further work done using Cos 7 cell lines, naturally lacking NMMIIA, further demonstrated that S100A4 is capable of regulating cell motility independent of NMMIIA, possibly through poor maturation of focal adhesion. Given that all these experiments highlighted the independency of NMMIIA towards migration, a protein that has been put at the forefront of S100A4-induced motility, we aimed to gather further understanding regarding the other molecular mechanisms that may be at play for motility. Using high throughput imaging (HCI), 3 compounds were identified to be capable of inhibiting S100A4-mediated migration. Although we have yet to investigate the underlying mechanism for their effects, these compounds have been shown to target membrane proteins and the externalisation of S100 proteins, for at least one of the compounds, leading us to speculate that preventing externalisation of S100A4 could potentially regulate cell motility.

The external dimension of the EU’s fight against organized crime:the search for coherence between rhetoric and practice

SSince the external dimension of the European Union’s Justice and Home Affairs (JHA) began to be considered, a substantial amount of literature has been dedicated to discussing how the EU is cooperating with non-member states in order to counter problems such as terrorism, organized crime and illegal migration. According to the EU, the degree of security interconnectedness has become so relevant that threats can only be adequately controlled if there is effective concerted regional action. This reasoning has led the EU to develop a number of instruments, which have resulted in the exporting of certain elements of its JHA policies, either through negotiation or socialization. Although the literature has explored how this transfer has been applied to the field of terrorism and immigration, very little has been written on the externalisation of knowledge, practice and norms in the area of organized crime. This article proposes to bridge this gap by looking at EU practice in the development of the external dimension of organized crime policies, through the theoretical lens of the EU governance framework.