This study examines whether there is a wage gap between male and female ordinary judges in the Swedish legal system in the year 2021 and what some of the possible reasons may be for the existing wage gap. The study is based on data obtained from the Swedish National Courts Administration, which includes the 1 000 ordinary judges who are active in the year 2021. The data material is then analyzed using descriptive statistics as well as a bivariate regression analysis to understand if there is an existing wage gap between male and female ordinary judges. To answer the second question, the data material is analyzed using a multiple regression analysis to give us an understanding of what may be the causes of the existing wage gap. The results show that male regular judges earn an average of 1 715 SEK more a month than their female colleagues. In addition, the results of the multiple regression analysis also show that when we use the independent variables that the data material contains, there is in 93 percentage of the cases a statistically significant guaranteed wage gap of 258 SEK per month between male and female ordinary judges in the Swedish legal system.

Concept "value-action gap" is most often mentioned in frame of behavioral studies of individial approach to ecological issues. Its meaning lies in description of a gap that opens between values claimed by respondents and their consequent actions (people act in accordance with values which are different than those pro-environmental values that they originally signed up to). There also is a concept of "knowing-doing gap" which stems from a different context and describes different situations. Its authors demonstrate how many corporations/firms/organizations employ disfunctional/ineffective management practices and ways of work organization - and all that in a situation when responsible employees and managers know about better practices. Furthermore, those employees are being continually educated about those more effective practices; corporation/firm also has plans of implementation of those done by hired consultants and all those plans would have had better results, should they be implemented. But despite this knowledge and good experiences of other organizations - managers keep on working using old inefective means. In this text I examined whether it is possible to identify a combination of those two concepts/phenomena in a frame of discourse related to expert knowledge about a state of natural...

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Master of Science / Department of Diagnostic Medicine/Pathobiology / Thu Annelise Nguyen / Colorectal cancer is one of the most common cancers in the United States with an early detection rate of only 39%. Colorectal cancer cells along with other cancer cells exhibit many deficiencies in cell-to-cell communication, particularly gap junctional intercellular communication (GJIC). GJIC has been reported to diminish as cancer cells progress. Gap junctions are intercellular channels composed of connexin proteins, which mediate the direct passage of small molecules from one cell to the next. They are involved in the regulation of the cell cycle, cell differentiation, and cell signaling. Since the regulation of gap junctions is lost in colorectal cancer cells, the goal of this study is to determine the effect of GJIC restoration in colorectal cancer cells. Overexpression of connexin 43 (Cx43) in SW480 colorectal cancer cells causes a 6-fold increase of gap junction activity compared to control un-transfected cells. This suggests that overexpressing Cx43 can restore GJIC. Furthermore, small molecule directly targeting gap junction channel was used to increase GJIC. Gap junction enhancers, PQs, at 200 nM showed a 4-fold increase of gap junction activity in SW480 cells. Using Western blot analysis, Cx43 isoform expression was seen to shift from P0 to P1 and P2 isoforms after treatment with PQ1 200 nM for 1 hour. Overall, the results show that overexpression of connexin and small molecules such as gap junction enhancers, PQs, can directly increase gap junction activity. The findings provide an important implication in which restoration of gap junction activity can be targeted for drug development.

Doctor of Philosophy / Department of Diagnostic Medicine/Pathobiology / Thu Annelise Nguyen / Gap junctional intercellular channels allow the cells to communicate with each other. A breach in gap junctional intercellular communication (GJIC) affects cell growth and proliferation. In addition, many neoplastic cells exhibit a decrease in GJIC. Many factors that decrease GJIC have been shown to potentiate cancer formation. 2,3,7,8 tetrachlorodibenzo-p-dioxin (TCDD), an environmental pollutant, is a carcinogen; however, its mechanism of carcinogenicity is unclear. Therefore, we examined the effect of TCDD on GJIC in MCF-7, a human breast cell line and normal mammary epithelial cells (HMEC). TCDD showed a decrease in GJIC in MCF-7 cells caused by increased phosphorylation of gap junctional protein, Cx43. PKCα-mediated phosphorylation of Cx43 was confirmed by inhibitor studies using calphostin C. Interestingly, TCDD affected GJIC in HMEC through a novel pathway involving redistribution of Cx43 to the perinuclear membrane. Our studies suggest that TCDD causes decrease in GJIC which could potentially lead to cancer. This also indicates that if GJIC is restored it could decrease cell growth and proliferation. Therefore, we investigated the role of substituted quinolines (PQ1), shown to bind with gap junctional proteins by computational docking. The results showed that indeed PQ1 significantly increases GJIC and exerts anti-tumor effect in human breast cancer cells compared to control without treatment or HMEC. We found an increase in GJIC, growth attenutation and increased apoptosis in T47D human breast cancer cell line. Our studies suggest that PQ1 is a novel gap junctional activator causing a decrease in tumor growth. Since PQ1 alone is effective in decreasing tumor growth in breast tumors, we proposed to test its efficacy with the current drug of choice for breast cancer, tamoxifen. The combinational treatment of tamoxifen and PQ1 showed a significant decrease in cell viability, increase in BAX (Bcl2-associated X), and, increase in caspase 3 activation compared to individual treatments. Hence, combinational treatment of PQ1 and tamoxifen can potentiate decrease in tumor growth. In conclusion, downregulation of gap junctions can potentiate tumor growth while restoration of GJIC can induce apoptosis and decrease tumor growth.

La structure du gap supraconducteur et sa modulation sont intimement liées au potentiel d'interaction responsable de l'appariement des électrons d'un supraconducteur. Ainsi, l'étude de la structure du gap-SC et de sa modulation permet de faire la lumière sur la nature du mécanisme d'appariement des électrons. À cet égard, les résultats expérimentaux des supraconducteurs à base de fer ne cadrent pas dans un seul ensemble, ce qui est en opposition au gap-SC universel des cuprates. Dans ce qui suit, nous présenterons une étude systématique du gap-SC pour plusieurs pnictides. En effet, en utilisant la conductivité thermique, une sonde directionnelle du gap-SC, nous avons été en mesure de révéler la structure du gap-SC pour les composés suivants : Ba[indice inférieur 1-x]K[indice inférieur x]Fe[indice inférieur 2]As[indice inférieur 2], Ba(Fe[indice inférieur 1-x]Co[indice inférieur x])[indice inférieur 2]As[indice inférieur 2], LiFeAs et Fe[indice inférieur 1-[delta]] Te[indice inférieur 1-x]Se[indice inférieur x]. L'étude de ces quatre composés, de trois différentes familles structurales, a pu établir un tableau partiel mais très exhaustif de la structure du gap-SC de pnictides. En effet, tel qu'illustré dans cette thèse, ces quatre composés ne possèdent aucun noeud dans leur structure du gap-SC à dopage optimal. Toutefois, à une concentration différente de celle optimale pour les composés K-Ba122 et Co-Ba122, des noeuds apparaissent sur la surface de Fermi, aux extrémités du dôme supraconducteur. Ceci suggère fortement que, pour ces composés, la présence de noeuds sur la surface de Fermi est nuisible à la phase supraconductrice.

The gap between business goals (problem domain), such as cost reduction, new business processes, increasing competitive advantage, etc., and the supporting Information Technology infrastructure (solution domain), such as the ability to implement software solutions to achieve these goals, is complex and challenging to bridge. This gap emerges for many reasons; for instance, inefficient communication, domain terminology misunderstanding or external factors, e.g. business change. As most business and software products can be described by a set of features, a promising solution would be to link both the problem and solution domains based on these features. Thus, the proposed approach aims to bridge the gap between the problem and the solution domains by using a feature-based technique in order to provide a quick and efficient means for understanding the relationships between IT solutions and business goals. The novelty of the proposed framework emanates from the three characteristics of the business-IT gap: the problem domain, the solution domain and the matching process. Besides the proposed feature-based IT-business framework, other contributions are proposed: a feature extracting method and feature matching algorithms. The proposed approach is achieved in three phases. The first phase is to decompose business needs and transform them into a feature model (presented in UML diagrams); this is represented as a top-to-middle process. The second phase is a reverse engineering process. A system program code is sliced into modules and transformed into feature-based models (again, in UML diagrams); these are represented as a bottom-to-middle process. The third phase is a model-driven engineering process. It uses model comparison techniques to match the UML feature models of the top-to-middle and bottom-to-middle phases. The presented approach in this research shows that features elicited from the business goals can be matched to features extracted from in the IT side. This proposed approach is feasible and able to provide a quick and efficient means for improving feature-based business IT matching. Two case studies are presented to demonstrate that the feature-oriented view of features from the users' perspective can be matched to the feature-oriented view of features in the IT side. This matching can serve to remove any ambiguities that may cause difficulties in the cases of system maintenance or system evolution, in particular when there are changes in requirements, which is to be expected when there is any business change.

Many within the industry, including designers, recognize the need to consider UX as the key to designing new products and services. As a consequence of this, the territory of UX has extended into many different industries and different disciplines. However, some practitioners still claim a UX project does not pay off even if they have improved UX. This way of thinking is induced from an old issue of UX. The term itself does not have a clear theoretical definition and it even makes a contradiction of itself. This phenomenon further aggravates the issue. The rapid expansion of UX territory made a gap between academia and practitioners. This research attempts to measure and examine the gap between academia and practitioners. A survey was conducted to observe how aware practitioners are of UX and their ability to recognize it as compared to the recent academia’s research.

Thesis (MAcc)--University of Stellenbosch, 2009.

As a highly versatile signal, Ca2+ operates over a wide temporal range to regulate many different cellular processes, impacting nearly every aspect of cellular life including excitability, exocytosis, motility, apoptosis, and transcription. While it has been well recognized that Ca2+ acts as both a second messenger to regulate cell-cell communication upon external stimuli and as a first messenger to integrate extracellular with intracellular signaling in various cell types. Molecular bases for such regulation and related human diseases are largely hampered by the challenges related to key membrane proteins. In the present study, we first investigated the regulatory role of intracellular Ca2+ ([Ca2+]i) on Connexin45 (Cx45) gap junction through a ubiquitous Ca2+ sensor protein-Calmodulin (CaM). Using bioluminescence resonance energy transfer assay, this study provides the first evidence of direct association of Cx45 and CaM in a Ca2+-dependent manner in cells. Complementary approaches including bioinformatics analysis and various biophysical methods identified a putative CaM-binding site in the intracellular loop of Cx45 with high Ca2+/CaM-binding affinity and Ca2+-dependent binding mode that is different from alpha family of connexins. To understand the role of extracellular calcium in regulation of gap junction hemichannels, we would like to prove a possible Ca2+-binding site predicted by our computational algorithm MUGSR in Connexin 26 (Cx26) through mutagenesis study, metal binding affinity measurement, conformational changes examination of purified Cx26 protein from Sf9; however, we failed to achieve this goal due to either the limitation of available methods or lethal effect of mutating the predicted Ca2+-binding ligand. Additionally, in this study, we identified a putative Ca2+-binding site in metabotropic glutamate receptor 5 (mGluR5) and demonstrated the importance of this Ca2+-binding site in activation of mGluR5 and modulating the actions of other orthosteric ligands on mGluR5. In addition, we successfully solved the first crystal structure of the extracellular domain of Ca2+-sensing receptor (CaSR) bound with Mg2+ and an unexpected Trp derivative. The extensive study of mechanism of CaSR function specifically through Mg2+-binding site and the unexpected ligand-binding site was done using several cell-based assays in wild type CaSR and mutants. Studies in this dissertation provides more information on how Ca2+ regulates gap junction channels, modulates mGluR5 activities and structural basis for regulation of CaSR by Mg2+ and an unexpected Trp derivative co-agonist.