Statlige pensjonsfond og offentlige realinvesteringer : hvordan bør store nasjonale finansformuer forvaltes?

I denne oppgaven ser jeg på optimal bruk av statlige finansformuer gjennom en teoretisk økonomisk modell med flere generasjoner. Fremtidig produktivitet påvirkes av learning by doing og offentlige investeringer, og en samfunnsplanlegger ønsker å maksimere dagens og fremtidige generasjoners nytte. Finansformuen kan brukes på pengeoverføringer og realinvesteringer. Modellen finner at optimal bruk av finansformue i periode 1 er større når myndighetene åpner for å gjøre realinvesteringer. Når realinvesteringer gjøres med varer/tjenester fra konkurranseutsatt sektor får vi det høyeste nivået av forbruk og nytte for dagens og fremtidige generasjoner

TGF beta 1 attenuates expression of prolactin and IGFBP-1 in decidualized endometrial stromal cells by both SMAD-dependent and SMAD-independent pathways

Background: Decidualization (differentiation) of the endometrial stromal cells during the secretory phase of the menstrual cycle is essential for successful implantation. Transforming Growth Factor beta 1 (TGF beta 1) canonically propagates its actions via SMAD signalling. A role for TGF beta 1 in decidualization remains to be established and published data concerning effects of TGF beta 1 on markers of endometrial decidualization are inconsistent. Methodology/Principal Findings: Non-pregnant endometrial stromal cells (ESC) and first trimester decidual stromal cells (DSC) were cultured in the presence or absence of a decidualizing stimulus. Incubation of ESCs with TGF beta 1 (10 ng/ml) down-regulated the expression of transcripts encoding the decidual marker proteins prolactin (PRL), insulin-like growth factor binding protein-1 (IGFBP-1) and tissue factor (TF). TGF beta 1 also inhibited secretion of PRL and IGFBP-1 proteins by ESCs and surprisingly this response preceded down-regulation of their mRNAs. In contrast, DSCs were more refractory to the actions of TGF beta 1, characterized by blunted and delayed down-regulation of PRL, IGFBP-1, and TF transcripts, which was not associated with a significant reduction in secretion of PRL or IGFBP-1 proteins. Addition of an antibody directed against TGF beta 1 increased expression of IGFBP-1 mRNA in decidualised cells. Knockdown of SMAD 4 using siRNAs abrogated the effect of TGF beta 1 on expression of PRL in ESCs but did not fully restore expression of IGFBP-1 mRNA and protein. Conclusions/Significance: TGF beta 1 inhibits the expression and secretion of decidual marker proteins. The impact of TGF beta 1 on PRL is SMAD-dependent but the impact on IGFBP1 is via an alternative mechanism. In early pregnancy, resistance of DSC to the impact of TGF beta 1 may be important to ensure tissue homeostasis

Caught in the cosmic web:Environmental effect on halo concentrations, shape, and spin

Using a set of high-resolution simulations we study the statistical correlation of dark matter halo properties with the large-scale environment. We consider halo populations split into four Cosmic Web (CW) elements: voids, walls, filaments, and nodes. For the first time we present a study of CW effects for halos covering six decades in mass: $10^{8}-10^{14}{h^{-1}{\rm M}_{\odot}}$. We find that the fraction of halos living in various web components is a strong function of mass, with the majority of $M>10^{12}{h^{-1}{\rm M}_{\odot}}$ halos living in filaments and nodes. Low mass halos are more equitably distributed in filaments, walls, and voids. For halo density profiles and formation times we find a universal mass threshold of $M_{th}\sim6\times10^{10}{h^{-1}{\rm M}_{\odot}}$ below which these properties vary with environment. Here, filament halos have the steepest concentration-mass relation, walls are close to the overall mean, and void halos have the flattest relation. This amounts to $c_{200}$ for filament and void halos that are respectively $14\%$ higher and $7\%$ lower than the mean at $M=2\times10^8{h^{-1}{\rm M}_{\odot}}$, with low-mass node halos being most likely splashed-back. We find double power-law fits that very well describe $c(M)$ for the four environments in the whole probed mass range. A complementary picture is found for the average formation times, with the mass-formation time relations following trends shown for the concentrations: the nodes halos being the oldest and void halo the youngest. The CW environmental effect is much weaker when studying the halo spin and shapes. The trends with halo mass is reversed: the small halos with $M<10^{10}{h^{-1}{\rm M}_{\odot}}$ seem to be unaffected by the CW environment. Some weak trends are visible for more massive void and walls halos, which, on average, are characterized by lower spin and higher triaxiality parameters.Comment: 18 pages, 9 figures, match the published version in Physical Review D eid. 06351

Feedback modulation of cholesterol metabolism by the lipid-responsive non-coding RNA LeXis.

Liver X receptors (LXRs) are transcriptional regulators of cellular and systemic cholesterol homeostasis. Under conditions of excess cholesterol, LXR activation induces the expression of several genes involved in cholesterol efflux, facilitates cholesterol esterification by promoting fatty acid synthesis, and inhibits cholesterol uptake by the low-density lipoprotein receptor. The fact that sterol content is maintained in a narrow range in most cell types and in the organism as a whole suggests that extensive crosstalk between regulatory pathways must exist. However, the molecular mechanisms that integrate LXRs with other lipid metabolic pathways are incompletely understood. Here we show that ligand activation of LXRs in mouse liver not only promotes cholesterol efflux, but also simultaneously inhibits cholesterol biosynthesis. We further identify the long non-coding RNA LeXis as a mediator of this effect. Hepatic LeXis expression is robustly induced in response to a Western diet (high in fat and cholesterol) or to pharmacological LXR activation. Raising or lowering LeXis levels in the liver affects the expression of genes involved in cholesterol biosynthesis and alters the cholesterol levels in the liver and plasma. LeXis interacts with and affects the DNA interactions of RALY, a heterogeneous ribonucleoprotein that acts as a transcriptional cofactor for cholesterol biosynthetic genes in the mouse liver. These findings outline a regulatory role for a non-coding RNA in lipid metabolism and advance our understanding of the mechanisms that coordinate sterol homeostasis

De Novo Sequencing, Assembly, and Annotation of Four Threespine Stickleback Genomes Based on Microfluidic Partitioned DNA Libraries

The threespine stickleback is a geographically widespread and ecologically highly diverse fish that has emerged as a powerful model system for evolutionary genomics and developmental biology. Investigations in this species currently rely on a single high-quality reference genome, but would benefit from the availability of additional, independently sequenced and assembled genomes. We present here the assembly of four new stickleback genomes, based on the sequencing of microfluidic partitioned DNA libraries. The base pair lengths of the four genomes reach 92–101% of the standard reference genome length. Together with their de novo gene annotation, these assemblies offer a resource enhancing genomic investigations in stickleback. The genomes and their annotations are available from the Dryad Digital Repository (https://doi.org/10.5061/dryad.113j3h7)

A high-valent non heme μ-oxo MnIV dimer generated from a thiolate-bound MnII complex and O2

International audienceThis study deals with the unprecedented reactivity of dinuclear non-heme MnII -thiolate complexes with O2 , which dependent on the protonation state of the initial MnII dimer selectively generates either a di-μ-oxo or μ-oxo-μ-hydroxo MnIV complex. Both dimers have been characterized by different techniques including single-crystal X-ray diffraction and mass spectrometry. Oxygenation reactions carried out with labeled 18 O2 unambiguously show that the oxygen atoms present in the MnIV dimers originate from O2 . Based on experimental observations and DFT calculations, evidence is provided that these MnIV species comproportionate with a MnII precursor to yield μ-oxo and/or μ-hydroxo MnIII dimers. Our work highlights the delicate balance of reaction conditions to control the synthesis of non-heme high-valent μ-oxo and μ-hydroxo Mn species from MnII precursors and O2

Phenotypic variability of the kyphoscoliotic type of Ehlers-Danlos syndrome (EDS VIA): clinical, molecular and biochemical delineation

BACKGROUND: The kyphoscoliotic type of Ehlers-Danlos syndrome (EDS VIA) (OMIM 225400) is a rare inheritable connective tissue disorder characterized by a deficiency of collagen lysyl hydroxylase 1 (LH1; EC 1.14.11.4) due to mutations in PLOD1. Biochemically this results in underhydroxylation of collagen lysyl residues and, hence, an abnormal pattern of lysyl pyridinoline (LP) and hydroxylysyl pyridinoline (HP) crosslinks excreted in the urine. Clinically the disorder is characterized by hypotonia and kyphoscoliosis at birth, joint hypermobility, and skin hyperelasticity and fragility. Severe hypotonia usually leads to delay in gross motor development, whereas cognitive development is reported to be normal. METHODS: We describe the clinical, biochemical and molecular characterisation, as well as electron microscopy findings of skin, in 15 patients newly diagnosed with this rare type of Ehlers-Danlos syndrome. RESULTS: Age at diagnosis ranged from 5 months to 27 years, with only 1/3 of the patients been diagnosed correctly in the first year of life. A similar disease frequency was found in females and males, however a broad disease severity spectrum (intra- and interfamilial), independent of molecular background or biochemical phenotype, was observed. Kyphoscoliosis, one of the main clinical features was not present at birth in 4 patients. Importantly we also noted the occurrence of vascular rupture antenatally and postnatally, as well as developmental delay in 5 patients. CONCLUSION: In view of these findings we propose that EDS VIA is a highly variable clinical entity, presenting with a broad clinical spectrum, which may also be associated with cognitive delay and an increased risk for vascular events. Genotype/phenotype association studies and additional molecular investigations in more extended EDS VIA populations will be necessary to further elucidate the cause of the variability of the disease severity