Hjelpen kom for sent. En studie av hvilke erfaringer fosterforeldre som har sagt opp en fosterhjemsavtale har med barneverntjenesten, og hvilke tanker de har om fremtidig fosterhjemsarbeid

Bakgrunn: Det er en stadig økning av antall barn som plasseres i fosterhjem. Dessverre opplever mange av disse å flytte fra det ene omsorgstiltaket til det andre. Det må legges til rette for en mer stabil hverdag for fosterbarna og fosterfamiliene. Formål og problemstilling: Målet med masteroppgaven er å bidra med kunnskap som kan bidra til at flere fosterforeldre blir stående i oppdraget, slik at barn og unge slipper unødvendige flyttinger. Problemstillingen er: Hvilke erfaringer har fosterforeldre som har sagt opp en fosterhjemsavtale med barneverntjenesten, og hva mener de er viktig i det fremtidige fosterhjemsarbeidet? Metode: Kvalitativ metode. Intervjudata fra 8 tidligere fosterhjem med til sammen 11 intervjupersoner. Resultat: 1) Hjelpen kom for sent. På bakgrunn av vår analyse fant vi et fellestrekk hos fosterforeldrene, nemlig en opplevelse av at hjelpen de ba om til barnet kom for sent. Vi ser en sammenheng mellom denne opplevelsen og fosterforeldrenes beslutning om å si opp fosterhjemsavtalen. 2) Fosterforeldrene i denne undersøkelsen har en opplevelse av å ikke bli anerkjent av barneverntjenesten. Vi mener at opplevelsen av at hjelpen kom for sent henger sammen med at fosterforeldrene ikke er blitt anerkjent, i den betydning at de ikke er sett, hørt eller forstått når de har bedt om hjelp. 3) Mangelfullt samarbeid. Ikke overraskende henger samarbeid med ovennevnte punkter da vi anser anerkjennelse som en del av et godt samarbeidsforhold. For å unngå at fosterforeldre opplever at hjelpen kommer for sent, må barneverntjenesten samarbeide med dem for å gi barnet riktig hjelp til rett tid. Nøkkelord: Fosterhjem, fosterhjemsarbeid, fosterforeldre, brudd i fosterhjem, barnevern, barneverntjeneste, samarbeid, oppfølgin

The Double Meaning Making of the Term Cultural Diversity in Teacher Educator Discourses

Cultural diversity is assumed to be a central component of Western education and even though it has been extensively investigated in international research on teacher education, little knowledge exists about its usage and meaning making in teacher educator discourses. This article provides insights into the usage and meaning making of the term cultural diversity based on semi-structured individual interviews with a total of twelve teacher educators from two Norwegian teacher education institutions. Drawing on the theoretical perspectives of discourse theory and critical Whiteness studies, we find that the term cultural diversity is used in a double meaning making pattern: Cultural diversity is presented as desirable and positive by teacher educators, yet it is also aligned with the notion of otherness. We discuss some possible methodological tools with which teacher educators can detect meaning making patterns and thus counter the production and reproduction of socially unjust discursive patterns

Imaging of Unstained DNA Origami Triangles with Electron Microscopy

Imaging of scaffolded DNA and DNA origami nanostructures has been dominated by atomic force microscopy of samples immobilized on bulk substrates. Less commonly used are electron microscopy techniques, typically carried out after negative staining of DNA structures or by using cryo‐transmission electron microscopy (TEM). Here, direct imaging of unstained DNA origami on common electron‐transparent substrates with utilizing high angular annular dark field scanning transmission electron microscopy (HAADF‐STEM) is reported. This approach establishes a method for depositing and imaging intact DNA triangles with mass‐thickness contrast sufficient to measure the scaffold‐to‐scaffold distances and the length of the triangle\u27s seam. The signal‐to‐noise ratio (SNR) of the DNA supported on amorphous carbon as a function of the carbon thickness is measured on three types of commercially available TEM grids. This allows for edge detection of ≈1 nm height DNA triangles on carbon substrates as thick as ≈25 nm. Observations on the effect on SNR with the imaging modes are discussed. The effect of cation concentration used for pretreating the grid on the image resolution is also explored. This work presents proof‐of‐concept results demonstrating that electron microscopy can be used to resolve key elements of the DNA origami triangle without the use of staining protocols

Repensando a interdisciplinaridade: contributos à atuação do assistente social na área da saúde

A trajetória reflexiva que segue está apoiada numa revisão de literatura. O foco da análise volta-se para o tripé Interdisciplinaridade, Formação Continuada e Serviço Social considerando queisso traz subsídios para o profissional envolvido com ações no âmbito da saúde. Entretanto, considera-se também bastante pertinente, enquanto elementos complementares à análise, a exposição de algumas ideias referentes à conceituação da palavra, resgate histórico, motivações para se refletir e agir interdisciplinarmente, reflexos destas atitudes dentro dos ambientes acadêmicos, societário, e por fim sobre os desafios que se colocam aos que desejam trilhar por este caminho

Systematic techniques for assisting recruitment to trials (START): study protocol for embedded, randomized controlled trials

BACKGROUND: Randomized controlled trials play a central role in evidence-based practice, but recruitment of participants, and retention of them once in the trial, is challenging. Moreover, there is a dearth of evidence that research teams can use to inform the development of their recruitment and retention strategies. As with other healthcare initiatives, the fairest test of the effectiveness of a recruitment strategy is a trial comparing alternatives, which for recruitment would mean embedding a recruitment trial within an ongoing host trial. Systematic reviews indicate that such studies are rare. Embedded trials are largely delivered in an ad hoc way, with interventions almost always developed in isolation and tested in the context of a single host trial, limiting their ability to contribute to a body of evidence with regard to a single recruitment intervention and to researchers working in different contexts. METHODS/DESIGN: The Systematic Techniques for Assisting Recruitment to Trials (START) program is funded by the United Kingdom Medical Research Council (MRC) Methodology Research Programme to support the routine adoption of embedded trials to test standardized recruitment interventions across ongoing host trials. To achieve this aim, the program involves three interrelated work packages: (1) methodology - to develop guidelines for the design, analysis and reporting of embedded recruitment studies; (2) interventions - to develop effective and useful recruitment interventions; and (3) implementation - to recruit host trials and test interventions through embedded studies. DISCUSSION: Successful completion of the START program will provide a model for a platform for the wider trials community to use to evaluate recruitment interventions or, potentially, other types of intervention linked to trial conduct. It will also increase the evidence base for two types of recruitment intervention. TRIAL REGISTRATION: The START protocol covers the methodology for embedded trials. Each embedded trial is registered separately or as a substudy of the host trial

Differential induction of nuclear factor-like 2 signature genes with toll-like receptors stimulation

Inflammation is associated with production of reactive oxygen species (ROS) and results in the induction of thioredoxin (TXN) and peroxiredoxins (PRDXs) and activation of nuclear factor-like 2 (Nrf2). In this study we have used the mouse RAW 264.7 macrophage and the human THP-1 monocyte cell line to investigate the pattern of expression of three Nrf2 target genes, PRDX1, TXN reductase (TXNRD1) and heme oxygenase (HMOX1), by activation of different Toll-like receptors (TLR). We found that, while the TLR4 agonist lipopolysaccharide (LPS) induces all three genes, the pattern of induction with agonists for TLR1/2, TLR3, TLR2/6 and TLR7/8 differs depending on the gene and the cell line. In all cases, the extent of induction was HMOX1>TXNRD1>PRDX1. Since LPS was a good inducer of all genes in both cell lines, we studied the mechanisms mediating LPS induction of the three genes using mouse RAW 264.7 cells. To assess the role of ROS we used the antioxidant N-acetylcysteine (NAC). Only LPS induction of HMOX1 was inhibited by NAC while that of TXNRD1 and PRDX1 was unaffected. These three genes were also induced by phorbol myristate acetate (PMA), a ROS-inducer acting by activation of protein kinase C (PKC). The protein kinase inhibitor staurosporine inhibited the induction of all three genes by PMA but only that of HMOX1 by LPS. This indicates that activation of these genes by inflammatory agents is regulated by different mechanisms involving either ROS or protein kinases, or both

Tissue-specific splicing factor gene expression signatures

The alternative splicing code that controls and coordinates the transcriptome in complex multicellular organisms remains poorly understood. It has long been argued that regulation of alternative splicing relies on combinatorial interactions between multiple proteins, and that tissue-specific splicing decisions most likely result from differences in the concentration and/or activity of these proteins. However, large-scale data to systematically address this issue have just recently started to become available. Here we show that splicing factor gene expression signatures can be identified that reflect cell type and tissue-specific patterns of alternative splicing. We used a computational approach to analyze microarray-based gene expression profiles of splicing factors from mouse, chimpanzee and human tissues. Our results show that brain and testis, the two tissues with highest levels of alternative splicing events, have the largest number of splicing factor genes that are most highly differentially expressed. We further identified SR protein kinases and small nuclear ribonucleoprotein particle (snRNP) proteins among the splicing factor genes that are most highly differentially expressed in a particular tissue. These results indicate the power of generating signature-based predictions as an initial computational approach into a global view of tissue-specific alternative splicing regulation

Analysis of the genetic phylogeny of multifocal prostate cancer identifies multiple independent clonal expansions in neoplastic and morphologically normal prostate tissue.

Genome-wide DNA sequencing was used to decrypt the phylogeny of multiple samples from distinct areas of cancer and morphologically normal tissue taken from the prostates of three men. Mutations were present at high levels in morphologically normal tissue distant from the cancer, reflecting clonal expansions, and the underlying mutational processes at work in morphologically normal tissue were also at work in cancer. Our observations demonstrate the existence of ongoing abnormal mutational processes, consistent with field effects, underlying carcinogenesis. This mechanism gives rise to extensive branching evolution and cancer clone mixing, as exemplified by the coexistence of multiple cancer lineages harboring distinct ERG fusions within a single cancer nodule. Subsets of mutations were shared either by morphologically normal and malignant tissues or between different ERG lineages, indicating earlier or separate clonal cell expansions. Our observations inform on the origin of multifocal disease and have implications for prostate cancer therapy in individual cases

Sequencing of prostate cancers identifies new cancer genes, routes of progression and drug targets

Prostate cancer represents a substantial clinical challenge because it is difficult to predict outcome and advanced disease is often fatal. We sequenced the whole genomes of 112 primary and metastatic prostate cancer samples. From joint analysis of these cancers with those from previous studies (930 cancers in total), we found evidence for 22 previously unidentified putative driver genes harboring coding mutations, as well as evidence for NEAT1 and FOXA1 acting as drivers through noncoding mutations. Through the temporal dissection of aberrations, we identified driver mutations specifically associated with steps in the progression of prostate cancer, establishing, for example, loss of CHD1 and BRCA2 as early events in cancer development of ETS fusion-negative cancers. Computational chemogenomic (canSAR) analysis of prostate cancer mutations identified 11 targets of approved drugs, 7 targets of investigational drugs, and 62 targets of compounds that may be active and should be considered candidates for future clinical trials