NUF. Et verktøy for økonomisk kriminalitet?

Sammendrag Denne utredningen tar for seg mulighetene for økonomisk kriminalitet ved bruk av selskapsformen norskregistrert utenlandsk foretak (NUF). Selv om selskapsformen i seg selv ikke er ny, har den blitt meget populær blant nordmenn først i løpet av det siste tiåret. Populariteten skyldes hovedsakelig en dom fra EF-domstolen som sier at et hvilket som helst selskap som er lovlig etablert i et av EØS-medlemslandene fritt kan opprette filial i et annet medlemsland. Dommen har ført til en eksplosiv utvikling i antall NUF i Norge, der de aller fleste har norske eiere og det utenlandske selskapet kun er et såkalt postboksselskap eller pseudoutenlandsk selskap. Oppgavens problemstilling har vært ”på hvilke måter kan NUF benyttes til økonomisk kriminalitet?”. For å besvare denne problemstillingen har vi delt oppgaven i to deler. En teoridel som tar for seg selskapsformen og dens historie. Del to, analysedelen, forsøker å belyse metoder for økonomisk kriminalitet ved bruk av NUF. Gjennom våre analyser mener vi å ha funnet klare indikasjoner på at NUF benyttes aktivt til økonomisk kriminalitet. De mest oppsiktsvekkende funnene som er gjort er hvordan NUF benyttes til konkurskriminalitet, ikke-reell fakturering, økonomisk kriminalitet via skatteparadis samt trygdesvindel. Selv om NUF som selskapsform åpner for flere former for økonomisk kriminalitet mener vi at en innføring av revisjonsplikt for denne selskapsformen ikke vil være fordelaktig. Vi mener at en bedre håndhevelse av allerede eksisterende lovverk, da spesielt regnskapsplikten, vil bidra til å redusere de mulighetene vi har illustrert i oppgaven. I tillegg mener vi at en nektelse av filialetablering for morselskap i skatteparadis vil være fordelaktig, dersom internasjonale regler tillater dette. NUF anser vi som et godt alternativ til små aksjeselskap og enkeltpersonsforetak. Eierne har begrenset risiko som i et aksjeselskap, men slipper revisjonsplikt og kapitalkrav som ellers kreves for aksjeselskap. Vi mener at denne selskapsformen bidrar til at flere våger å starte en ny virksomhet og dermed driver norsk næringsliv fremover

Molecular Mechanisms of Androgen Action : Characterization of the Androgen Regulated Gene KLK4 and the Role of Nuclear Dynamics in Androgen Receptor-Mediated Transcription

Androgens are important for the normal development of the male sexual characteristics, but are also involved in pathological conditions such as prostate cancer. The biological effects of androgens are mediated by the androgen receptor (AR), which is a transcription factor that regulates the expression of a wide range of target genes. In this thesis, KLK4 was identified as an androgen regulated gene that is specific to the prostate for expression. Surprisingly, KLK4 has a different gene structure than the other closely related members of the kallikrein family, resulting in an intracellular protein. Analysis of KLK4 expression in prostate tissue specimens showed that KLK4 was overexpressed in malignant prostate as compared to normal prostate glands. Experiments in prostate cancer cells furthermore demonstrated that KLK4 is a proliferative factor, possibly through the alteration of cell cycle regulatory gene expression. These data suggest that KLK4 plays an important role in prostate cancer, thus having potential utility as a diagnostic marker or therapeutic target in prostate cancer therapy. Using advanced fluorescence microcopy techniques, the interaction between AR and its target genomic sites in living cell were also studied. In contrast to the traditional view, the interaction was found to be both transient and highly dynamic, and depended on the nature of ligand. Importantly, there were intramolecular interactions between the N- and C-termini of promoter-bound AR in its active state which were important for transcriptional activity. Finally, increased AR transcriptional activity, induced by histone deacetylase inhibitors, resulted in reduced mobility of AR at its target promoter. These data support the more recent view of transcription factor–chromatin interactions as a highly dynamic system in continuous change, thus providing a kinetic and mechanistic basis for regulation of gene expression by androgens and anti-androgens in living cells

Factors accounting for the association between anxiety and depression, and eczema: the Hordaland health study (HUSK)

<p>Abstract</p> <p>Background</p> <p>The association between anxiety and depression, and eczema is well known in the literature, but factors underlying this association remain unclear. Low levels of omega-3 fatty acids and female gender have been found to be associated with both depression and eczema. Somatization and health anxiety are known to be associated with anxiety and depression, further, somatization symptoms and health anxiety have also been found in several dermatological conditions. Accordingly, omega-3 fatty acid supplement, female gender, somatization and health anxiety are possible contributing factors in the association between anxiety and depression, and eczema. The aim of the study is to examine the relevance of proposed contributing factors for the association between anxiety and depression, and eczema, including, omega-3 fatty acid supplement, female gender, health anxiety and somatization.</p> <p>Methods</p> <p>Anxiety and depression was measured in the general population (n = 15715) employing the Hospital Anxiety and Depression Scale (HADS). Information on eczema, female gender, omega-3 fatty acid supplement, health anxiety and somatization was obtained by self-report.</p> <p>Results</p> <p>Somatization and health anxiety accounted for more than half of the association between anxiety/depression, and eczema, while the other factors examined were of minor relevance for the association of interest.</p> <p>Conclusions</p> <p>We found no support for female gender and omega-3 fatty acid supplement as contributing factors in the association between anxiety/depression, and eczema. Somatization and health anxiety accounted for about half of the association between anxiety/depression, and eczema, somatization contributed most. The association between anxiety/depression, and eczema was insignificant after adjustment for somatization and health anxiety. Biological mechanisms underlying the mediating effect of somatization are yet to be revealed.</p

Joining the CCS club! the economics of CO2 pipeline projects

This paper examines the conditions for a widespread adoption of Carbon Capture transport and Storage (CCS) by a group of emitters that can be connected to a common CO2 pipeline. It details a modeling framework aimed at assessing the critical value in the charge for the CO2 emissions required for each of the emitters to decide to implement capture capabilities. This model can be used to analyze how the tariff structure imposed on the CO2 pipeline operator modifies the overall cost of CO2 abatement via CCS. This framework is applied to the case of a real European CO2 pipeline project. We find that the obligation to use cross-subsidy-free pipeline tariffs has a minor impact on the minimum CO2 price required to adopt the CCS. In contrast, the obligation to charge non-discriminatory prices can either impede the adoption of CCS or significantly raise that price. Besides which, we compared two alternative regulatory frameworks for CO2 pipelines: a common European organization as opposed to a collection of national regulations. The results indicate that the institutional scope of that regulation has a limited impact on the adoption of CCS compared to the detailed design of the tariff structure imposed on pipeline operators

Role of Phospholipase A2 in Retrograde Transport of Ricin

Ricin is a protein toxin classified as a bioterror agent, for which there are no known treatment options available after intoxication. It is composed of an enzymatically active A-chain connected by a disulfide bond to a cell binding B-chain. After internalization by endocytosis, ricin is transported retrogradely to the Golgi and ER, from where the ricin A-chain is translocated to the cytosol where it inhibits protein synthesis and thus induces cell death. We have identified cytoplasmic phospholipase A2 (PLA2) as an important factor in ricin retrograde transport. Inhibition of PLA2 protects against ricin challenge, however the toxin can still be endocytosed and transported to the Golgi. Interestingly, ricin transport from the Golgi to the ER is strongly impaired in response to PLA2 inhibition. Confocal microscopy analysis shows that ricin is still colocalized with the trans-Golgi marker TGN46 in the presence of PLA2 inhibitor, but less is colocalized with the cis-Golgi marker GM130. We propose that PLA2 inhibition results in impaired ricin transport through the Golgi stack, thus preventing it from reaching the ER. Consequently, ricin cannot be translocated to the cytosol to exert its toxic action

Pax6 Represses Androgen Receptor-Mediated Transactivation by Inhibiting Recruitment of the Coactivator SPBP

The androgen receptor (AR) has a central role in development and maintenance of the male reproductive system and in the etiology of prostate cancer. The transcription factor Pax6 has recently been reported to act as a repressor of AR and to be hypermethylated in prostate cancer cells. SPBP is a transcriptional regulator that previously has been shown to enhance the activity of Pax6. In this study we have identified SPBP to act as a transcriptional coactivator of AR. We also show that Pax6 inhibits SPBP-mediated enhancement of AR activity on the AR target gene probasin promoter, a repression that was partly reversed by increased expression of SPBP. Enhanced expression of Pax6 reduced the amount of SPBP associated with the probasin promoter when assayed by ChIP in HeLa cells. We mapped the interaction between both AR and SPBP, and AR and Pax6 to the DNA-binding domains of the involved proteins. Further binding studies revealed that Pax6 and SPBP compete for binding to AR. These results suggest that Pax6 represses AR activity by displacing and/or inhibiting recruitment of coactivators to AR target promoters. Understanding the mechanism for inhibition of AR coactivators can give rise to molecular targeted drugs for treatment of prostate cancer

Activation of Estrogen Receptor-α by E2 or EGF Induces Temporally Distinct Patterns of Large-Scale Chromatin Modification and mRNA Transcription

Estrogen receptor-α (ER) transcription function is regulated in a ligand-dependent (e.g., estradiol, E2) or ligand-independent (e.g., growth factors) manner. Our laboratory seeks to understand these two modes of action. Using a cell line that contains a visible prolactin enhancer/promoter array (PRL-HeLa) regulated by ER, we analyzed ER response to E2 and EGF by quantifying image-based results. Data show differential recruitment of GFP-ER to the array, with the AF1 domain playing a vital role in EGF-mediated responsiveness. Temporal analyses of large-scale chromatin dynamics, and accumulation of array-localized reporter mRNA over 24 hours showed that the EGF response consists of a single pulse of reporter mRNA accumulation concomitant with transient increase in array decondensation. Estradiol induced a novel cyclical pattern of mRNA accumulation with a sustained increase in array decondensation. Collectively, our work shows that there is a stimuli-specific pattern of large-scale chromatin modification and transcript levels by ER

TEAD1 and c-Cbl are novel prostate basal cell markers that correlate with poor clinical outcome in prostate cancer

Prostate cancer is the most frequently diagnosed male cancer, and its clinical outcome is difficult to predict. The disease may involve the inappropriate expression of genes that normally control the proliferation of epithelial cells in the basal layer and their differentiation into luminal cells. Our aim was to identify novel basal cell markers and assess their prognostic and functional significance in prostate cancer. RNA from basal and luminal cells isolated from benign tissue by immunoguided laser-capture microdissection was subjected to expression profiling. We identified 112 and 267 genes defining basal and luminal populations, respectively. The transcription factor TEAD1 and the ubiquitin ligase c-Cbl were identified as novel basal cell markers. Knockdown of either marker using siRNA in prostate cell lines led to decreased cell growth in PC3 and disrupted acinar formation in a 3D culture system of RWPE1. Analyses of prostate cancer tissue microarray staining established that increased protein levels of either marker were associated with decreased patient survival independent of other clinicopathological metrics. These data are consistent with basal features impacting on the development and clinical course of prostate cancers