Formuesskatt på unoterte aksjer: en analyse av ulikheter i verdsettelsesgrunnlaget til børsnoterte og unoterte aksjer

Vi ønsker i denne masterutredningen å bidra til den pågående debatten om formuesskattens ulike verdsettelsesregler for fastsettelse av formue. Gjennom empirisk analyse studerer vi verdsettelsesgrunnlaget for aksjer i unoterte og børsnoterte selskaper. Dette beregnes etter henholdsvis sær- og hovedregelen. I utredningen studerer vi 133 selskaper registrert på OTC-listen. Disse selskapene er blant de mest omsatte unoterte selskapene i Norge. I tillegg til å få fastsatt ligningsmessig formuesverdi som unotert aksjeselskap, har de også en offentlig markedsverdi. De er dermed svært aktuelle å studere i lys av formuesskatten, til tross for at de utgjør en liten del av unoterte selskaper. Vår analyse viser at aksjer i selskaper verdsatt etter særregelen har en gjennomsnittlig verdsettelsesrabatt på 68,1 %. Videre finner vi at verdsettelsesrabatten øker med blant annet gjeld, alder og noen typer eiendeler. Dette er typisk eiendeler som verdsettes til lavere enn omsetningsverdien, som eiendom og immaterielle eiendeler. På den andre siden finner vi at eiendeler som verdsettes til omsetningsverdi, som bankinnskudd og markedsbaserte investeringer, har negativ sammenheng med verdsettelsesrabatten. Videre analyserer vi 61 selskaper som nylig har blitt børsnotert i løpet av perioden. Vi finner gjennom tilsvarende analyser at verdsettelsesrabatten for aksjer i nylig børsnoterte selskaper ville vært 91,4 % dersom selskapene i stedet var verdsatt etter særregelen. Med dette kan vi derfor fastslå at de ulike verdsettelsesreglene gir svært forskjellig skattegrunnlag. Aksjer i unoterte selskaper favoriseres i stor grad sammenlignet med aksjer i børsnoterte selskaper ved formuesskatteligningen. Av OTC-selskapene er det 22 selskaper som børsnoteres i perioden. Gjennom vår analyse av disse selskapene finner vi at størrelsen på verdsettelsesrabatten ikke ser ut til å påvirke beslutningen om børsnotering. Med tanke på den store verdsettelsesrabatten, er dette resultatet noe overraskende. Det må altså være noen andre fordeler ved børsnotering, som for eksempel lettere kapitaltilgang, som veier opp for den betydelig høyere formuesskatten. Vår analyse viser dermed at det ikke er grunnlag for å hevde at formuesskatten påvirker insentiver til å gå på børs.nhhma

Å være blekksprut, brannmann og vaktbikkje. En kvalitativ studie om sykepleiernes erfarte rolle og ansvar for oppfølging av legemiddelbehandling av eldre brukere i hjemmesykepleien.

Bakgrunn: Det er i dag nasjonal satsning på pasientsikkerhet i forhold til legemiddelbehandling. Legemiddelbehandling har tradisjonelt vært sett på som legemiddelhåndtering (prosessen fra legemidlet er rekvirert til det er utdelt), og er regulert i nasjonale føringer og interne retningslinjer. Oppfølgingen av legemiddelbehandlingen (observasjoner, undersøkelser og tilrettelegging av den enkeltes legemiddelbehandling) er ikke i like stor grad regulert. Sykepleierne i hjemmesykepleien har en sentral funksjon i legemiddelbehandling med nærhet til brukerne og helhetlig tilnærmingsmåte. Bakgrunnslitteraturen viser at sykepleierens rolle og ansvar i forhold til legemiddeloppfølging i liten grad er definert. Hensikt: Målet med studien var å utvikle ny innsikt i om sykepleierne i hjemmesykepleien opplever et gap mellom behovene for og forventningene til legemiddelbehandling. Mer spesifikt var målet å få frem hvordan sykepleierne forstår legemiddeloppfølging; hva de mener ligger i deres rolle og ansvar, og hva de opplever fremmer og/eller hemmer deres funksjon. Metode: Studien har et kvalitativt, eksplorerende forskningsdesign. Utvalget besto av ni sykepleiere som jobber i hjemmesykepleien i en stor kommune på Østlandet. Datasamlingen ble gjort ved to fokusgruppeintervjuer. Datamaterialet ble tatt opp på bånd, transkribert i sin helhet og videre bearbeidet gjennom en tverrgående tekstanalyse. Resultat: Sykepleierne erfarte å ha en viktig rolle og et stort personlig ansvar for oppfølgingen av legemiddelbehandlingen, men de opplevde at funksjonen ikke var definert. Sykepleiernes rolle og ansvar er påvirket av brukernes situasjon, behandlingsapparatet, arbeidsplassen, samt forhold knyttet direkte opp mot den enkelte sykepleiers kunnskaper, erfaringer og interesser. Konklusjon: Til tross for at sykepleierne erfarte å ha et stort ansvar og en sentral rolle i forhold til legemiddeloppfølgingen, opplevde de at oppfølgingen ikke dekket det reelle behovet hos brukerne for å oppnå en forsvarlig og sikker legemiddelbehandling. Erfaringene fra studien tilsier at det kan være behov for et økt fokus for avklaringer og presisering av roller og ansvar, ikke bare for sykepleierne men også opp mot fastlegene, bestillerenhetene og tjenestestedene. Nøkkelord: Pasientsikkerhet, legemiddelbehandling, legemiddeloppfølging, hjemmesykepleie, sykepleiefunksjon, kvalitetsutviklin

CREB is a critical regulator of normal hematopoiesis and leukemogenesis

The cAMP-responsive element binding protein (CREB) is a 43-kDa nuclear transcription factor that regulates cell growth, memory, and glucose homeostasis. We showed previously that CREB is amplified in myeloid leukemia blasts and expressed at higher levels in leukemia stem cells from patients with myeloid leukemia. CREB transgenic mice develop myeloproliferative disease after 1 year, but not leukemia, suggesting that CREB contributes to but is not sufficient for leukemogenesis. Here, we show that CREB is most highly expressed in lineage negative hematopoietic stem cells (HSCs). To understand the role of CREB in hematopoietic progenitors and leukemia cells, we examined the effects of RNA interference (RNAi) to knock down CREB expression in vitro and in vivo. Transduction of primary HSCs or myeloid leukemia cells with lentiviral CREB shRNAs resulted in decreased proliferation of stem cells, cell- cycle abnormalities, and inhibition of CREB transcription. Mice that received transplants of bone marrow transduced with CREB shRNA had decreased committed progenitors compared with control mice. Mice injected with Ba/F3 cells expressing either Bcr-Abl wild-type or T315I mutation with CREB shRNA had delayed leukemic infiltration by bioluminescence imaging and prolonged median survival. Our results suggest that CREB is critical for normal myelopoiesis and leukemia cell proliferation

Decidual Neutrophil Infiltration Is Not Required for Preterm Birth in a Mouse Model of Infection-Induced Preterm Labor

Parturition is associated with a leukocyte influx into the intrauterine tissues; however, the exact role these leukocytes play in the onset of labor remains unclear. Neutrophil infiltration of the uteroplacental tissues has been particularly associated with infection-associated preterm labor (PTL) in both women and mouse models. In this study, we investigated the role of neutrophils in a mouse model of infection-induced PTL. Intrauterine administration of LPS on day 17 of gestation resulted in a 7-fold increase in the number of decidual neutrophils compared with control mice receiving PBS (p < 0.01; n = 8–11). We hypothesized that neutrophil influx is necessary for PTL and that neutrophil depletion would abolish preterm birth. To test this hypothesis, mice were depleted of neutrophils by treatment with anti–Gr-1, anti–Ly-6G, or the appropriate IgG control Ab on day 16 of gestation prior to LPS on day 17 (n = 6–7). Successful neutrophil depletion was confirmed by flow cytometry and immunohistochemistry. Neutrophil depletion with Gr-1 resulted in reduced uterine and placental Il-1β expression (p < 0.05). Neutrophil depletion with Ly-6G reduced uterine Il-1β and Tnf-α expression (p < 0.05). However, neutrophil depletion with either Ab did not delay LPS-induced preterm birth. Collectively, these data show that decidual neutrophil infiltration is not essential for the induction of infection-induced PTL in the mouse, but that neutrophils contribute to the LPS-induced inflammatory response of the uteroplacental tissues

Rapid Immunomagnetic Negative Enrichment of Neutrophil Granulocytes from Murine Bone Marrow for Functional Studies In Vitro and In Vivo

Polymorphonuclear neutrophils (PMN) mediate early immunity to infection but can also cause host damage if their effector functions are not controlled. Their lack or dysfunction is associated with severe health problems and thus the analysis of PMN physiology is a central issue. One prerequisite for PMN analysis is the availability of purified cells from primary organs. While human PMN are easily isolated from peripheral blood, this approach is less suitable for mice due to limited availability of blood. Instead, bone marrow (BM) is an easily available reservoir of murine PMN, but methods to obtain pure cells from BM are limited. We have developed a novel protocol allowing the isolation of highly pure untouched PMN from murine BM by negative immunomagnetic isolation using a complex antibody cocktail. The protocol is simple and fast (∼1 h), has a high yield (5–10*106 PMN per animal) and provides a purity of cells equivalent to positive selection (>80%). Most importantly, cells obtained by this method are non-activated and remain fully functional in vitro or after adoptive transfer into recipient animals. This method should thus greatly facilitate the study of primary murine PMN in vitro and in vivo

Resistance to Mucosal Lysozyme Compensates for the Fitness Deficit of Peptidoglycan Modifications by Streptococcus pneumoniae

The abundance of lysozyme on mucosal surfaces suggests that successful colonizers must be able to evade its antimicrobial effects. Lysozyme has a muramidase activity that hydrolyzes bacterial peptidoglycan and a non-muramidase activity attributable to its function as a cationic antimicrobial peptide. Two enzymes (PgdA, a N-acetylglucosamine deacetylase, and Adr, an O-acetyl transferase) that modify different sites on the peptidoglycan of Streptococcus pneumoniae have been implicated in its resistance to lysozyme in vitro. Here we show that the antimicrobial effect of human lysozyme is due to its muramidase activity and that both peptidoglycan modifications are required for full resistance by pneumococci. To examine the contribution of lysozyme and peptidoglycan modifications during colonization of the upper respiratory tract, competition experiments were performed with wild-type and pgdAadr mutant pneumococci in lysozyme M-sufficient (LysM+/+) and -deficient (LysM−/−) mice. The wild-type strain out-competed the double mutant in LysM+/+, but not LysM−/− mice, indicating the importance of resistance to the muramidase activity of lysozyme during mucosal colonization. In contrast, strains containing single mutations in either pgdA or adr prevailed over the wild-type strain in both LysM+/+ and LysM−/− mice. Our findings demonstrate that individual peptidoglycan modifications diminish fitness during colonization. The competitive advantage of wild-type pneumococci in LysM+/+ but not LysM−/− mice suggests that the combination of peptidoglycan modifications reduces overall fitness, but that this is outweighed by the benefits of resistance to the peptidoglycan degrading activity of lysozyme

Generational distribution of a Candida glabrata population: Resilient old cells prevail, while younger cells dominate in the vulnerable host.

Similar to other yeasts, the human pathogen Candida glabrata ages when it undergoes asymmetric, finite cell divisions, which determines its replicative lifespan. We sought to investigate if and how aging changes resilience of C. glabrata populations in the host environment. Our data demonstrate that old C. glabrata are more resistant to hydrogen peroxide and neutrophil killing, whereas young cells adhere better to epithelial cell layers. Consequently, virulence of old compared to younger C. glabrata cells is enhanced in the Galleria mellonella infection model. Electron microscopy images of old C. glabrata cells indicate a marked increase in cell wall thickness. Comparison of transcriptomes of old and young C. glabrata cells reveals differential regulation of ergosterol and Hog pathway associated genes as well as adhesion proteins, and suggests that aging is accompanied by remodeling of the fungal cell wall. Biochemical analysis supports this conclusion as older cells exhibit a qualitatively different lipid composition, leading to the observed increased emergence of fluconazole resistance when grown in the presence of fluconazole selection pressure. Older C. glabrata cells accumulate during murine and human infection, which is statistically unlikely without very strong selection. Therefore, we tested the hypothesis that neutrophils constitute the predominant selection pressure in vivo. When we altered experimentally the selection pressure by antibody-mediated removal of neutrophils, we observed a significantly younger pathogen population in mice. Mathematical modeling confirmed that differential selection of older cells is sufficient to cause the observed demographic shift in the fungal population. Hence our data support the concept that pathogenesis is affected by the generational age distribution of the infecting C. glabrata population in a host. We conclude that replicative aging constitutes an emerging trait, which is selected by the host and may even play an unanticipated role in the transition from a commensal to a pathogen state.post-print10768 K