Menneskesyn og verdier - utgangspunkt for selvbestemmelse? En kvalitativ studie om erfaringer fra psykisk helsearbeid i førstelinjetjenesten, sett fra et personalperspektiv

Hensikten med studien er å utforske og belyse hvordan personalet ved en institusjon i førstelinjetjenesten erfarer at mennesker med alvorlig psykisk lidelse gis mulighet til selvbestemmelse og mestring. Det er ønskelig å beskrive dagens praksis, samt å identifisere ulike faktorer som kan virke fremmende eller hemmende for selvbestemmelse. Videre er et mål å finne ut om verdiene respekt, frihet og glede er til stede i det daglige arbeidet. Ved hjelp av studien er det ønskelig å videreutvikle og forbedre arbeidet slik at beboerne ved institusjonen får optimalisert mulighetene for et autonomt liv. Med utgangspunkt i handlingsorientert forskningssamarbeid har den metodiske tilnærmingen til problemstillingen vært flersteg-fokusgruppeintervju. Studien har videre en fenomenologiskhermeneutisk tilnærming med et beskrivende og utforskende design. Tilnærmet samme gruppe har fokusert studiens forskningsspørsmål med utgangspunkt i en intervjuguide, gjennom tre intervju. Transkribering, og analyse ved hjelp av kvalitativ innholdsanalyse er foretatt av forsker. Ved å møtes i samtale for å fokusere personalets erfaringer, har man søkt bredde og nyanser mer enn entydige svar. Gjennom refleksjon og bevisstgjøring kan kunnskap for handling identifiseres. Hovedfunn i studien er et grunnleggende ønske om å ville beboerne godt. Dette kommer til uttrykk ved at personalet fokuserer en veiledende og motiverende funksjon basert på likeverdighet. Faktorer som synes å fremme og hemme selvbestemmelse er knyttet til den enkelte beboers muligheter og ønsker for sitt liv, personalets tilnærming og organisatoriske forhold. Videre viser resultatene at mennesker med alvorlig psykisk lidelse kan ha stor grad av selvbestemmelse, og at salutogenese og deler av empowerment-tenkning er relevant i forhold til mestring av eget liv innen institusjonsomsorgen i førstelinjetjenesten. Studiens funn viser at personalet i stor grad utfordres av en arbeidsform som krever at de slipper ”ekspertrollen” de tradisjonelt innehar, og videre at et bevisst verdigrunnlag vil kunne bidra til økt selvbestemmelse for mennesker med alvorlig psykisk lidelse

Blood transcriptome analysis of septic patients reveals a long non-coding Alu-RNA in the complement C5a receptor 1 gene

publishedVersio

Presence of acyl-homoserine lactones in 57 members of the Vibrionaceae family

Aims: The aim of this study was to use a sensitive method to screen and quantify 57 Vibrionaceae strains for the production of acyl-homoserine lactones (AHLs) and map the resulting AHL profiles onto a host phylogeny. Methods and Results: We used a high-performance liquid chromatography– tandem mass spectrometry (HPLC-MS/MS) protocol to measure AHLs in spent media after bacterial growth. First, the presence/absence of AHLs (qualitative analysis) was measured to choose internal standard for subsequent quantitative AHL measurements. We screened 57 strains from three genera (Aliivibrio, Photobacterium and Vibrio) of the same family (i.e. Vibrionaceae). Our results show that about half of the isolates produced multiple AHLs, typically at 25–5000 nmol l-1 . Conclusions: This work shows that production of AHL quorum sensing signals is found widespread among Vibrionaceae bacteria and that closely related strains typically produce similar AHL profiles. Significance and Impact of the Study: The AHL detection protocol presented in this study can be applied to a broad range of bacterial samples and may contribute to a wider mapping of AHL production in bacteria, for example, in clinically relevant strains

Dental and Periodontal Health in Acute Intermittent Porphyria

In the inherited metabolic disorder acute intermittent porphyria (AIP), high sugar intake prevents porphyric attacks due to the glucose effect and the following high insulin levels that may lower AIP disease activity. Insulin resistance is a known risk factor for periodontitis and sugar changes diabetogenic hormones and affects dental health. We hypothesized differences in homeostasis model assessment (HOMA) scores for insulin resistance in AIP cases vs. controls and in those with periodontitis. Our aim was to systematically study dental health in AIP as poor dental health was previously only described in case reports. Further, we aimed to examine if poor dental health and kidney failure might worsen AIP as chronic inflammation and kidney failure might increase disease activity. In 47 AIP cases and 47 matched controls, X-rays and physical examination of clinical attachment loss (CAL), probing pocket depth (PPD), and decayed missing filled teeth (DMFT) were performed. Dietary intake was evaluated through a diet logbook. Plasma cytokines and diabetogenic hormones were measured using multiplex technology and urine porphobilinogen and kidney and liver function by routine methods. An excel spreadsheet from the University of Oxford was used to estimate HOMA scores; beta cell function, HOMA%B (%B), insulin sensitivity, HOMA%S (%S), and insulin resistance HOMA-IR (IR), based on glucose and plasma (P) C-peptide. The Wilcoxon matched-pairs signed rank test, the Mann–Whitney U-test, and Spearman’s nonparametric correlation were used. Insulin (p = 0.007) and C-peptide (p = 0.006) were higher in the AIP cases with periodontitis versus those without. In AIP patients, the liver fibrosis index 4 correlated with DMFT (p < 0.001) and CAL ≥4 mm (p = 0.006); the estimated glomerular filtration rate correlated with DMFT (p < 0.001) and CAL ≥4 mm (p = 0.02). CAL ≥4 mm was correlated with chemokine ligand 11 and interleukin (IL)-13 (p = 0.04 for both), and PPD >5 mm was correlated with plasminogen activator inhibitor-1 (p = 0.003) and complement component 3 (p = 0.02). In conclusion, dental health in AIP cases was correlated with insulin resistance, inflammatory markers, and biomarkers of kidney and liver function, demonstrating that organ damage in the kidney and liver are associated with poorer dental health

Conservation and divergence of chemical defense system in the tunicate Oikopleura dioica revealed by genome wide response to two xenobiotics

<p>Abstract</p> <p>Background</p> <p>Animals have developed extensive mechanisms of response to xenobiotic chemical attacks. Although recent genome surveys have suggested a broad conservation of the chemical defensome across metazoans, global gene expression responses to xenobiotics have not been well investigated in most invertebrates. Here, we performed genome survey for key defensome genes in <it>Oikopleura dioica </it>genome, and explored genome-wide gene expression using high density tiling arrays with over 2 million probes, in response to two model xenobiotic chemicals - the carcinogenic polycyclic aromatic hydrocarbon benzo[a]pyrene (BaP) the pharmaceutical compound Clofibrate (Clo).</p> <p>Results</p> <p><it>Oikopleura </it>genome surveys for key genes of the chemical defensome suggested a reduced repertoire. Not more than 23 cytochrome P450 (CYP) genes could be identified, and neither CYP1 family genes nor their transcriptional activator AhR was detected. These two genes were present in deuterostome ancestors. As in vertebrates, the genotoxic compound BaP induced xenobiotic biotransformation and oxidative stress responsive genes. Notable exceptions were genes of the aryl hydrocarbon receptor (AhR) signaling pathway. Clo also affected the expression of many biotransformation genes and markedly repressed genes involved in energy metabolism and muscle contraction pathways.</p> <p>Conclusions</p> <p><it>Oikopleura </it>has the smallest number of CYP genes among sequenced animal genomes and lacks the AhR signaling pathway. However it appears to have basic xenobiotic inducible biotransformation genes such as a conserved genotoxic stress response gene set. Our genome survey and expression study does not support a role of AhR signaling pathway in the chemical defense of metazoans prior to the emergence of vertebrates.</p

Early and accurate detection of cholangiocarcinoma in patients with primary sclerosing cholangitis by methylation markers in bile

Background and Aims Primary sclerosing cholangitis (PSC) is associated with increased risk of cholangiocarcinoma (CCA). Early and accurate CCA detection represents an unmet clinical need as the majority of patients with PSC are diagnosed at an advanced stage of malignancy. In the present study, we aimed at establishing robust DNA methylation biomarkers in bile for early and accurate diagnosis of CCA in PSC. Approach and Results Droplet digital PCR (ddPCR) was used to analyze 344 bile samples from 273 patients with sporadic and PSC-associated CCA, PSC, and other nonmalignant liver diseases for promoter methylation of cysteine dioxygenase type 1, cannabinoid receptor interacting protein 1, septin 9, and vimentin. Receiver operating characteristic (ROC) curve analyses revealed high AUCs for all four markers (0.77-0.87) for CCA detection among patients with PSC. Including only samples from patients with PSC diagnosed with CCA 36 months) as controls, and remained high (83%) when only including patients with PSC and dysplasia as controls (n = 23). Importantly, the bile samples from the CCA-PSCPeer reviewe

DNA glycosylase Neil3 regulates vascular smooth muscle cell biology during atherosclerosis development.

BACKGROUND AND AIMS: Atherogenesis involves a complex interaction between immune cells and lipids, processes greatly influenced by the vascular smooth muscle cell (VSMC) phenotype. The DNA glycosylase NEIL3 has previously been shown to have a role in atherogenesis, though whether this is due to its ability to repair DNA damage or to other non-canonical functions is not yet clear. Hereby, we investigate the role of NEIL3 in atherogenesis, specifically in VSMC phenotypic modulation, which is critical in plaque formation and stability. METHODS: Chow diet-fed atherosclerosis-prone Apoe-/- mice deficient in Neil3, and NEIL3-abrogated human primary aortic VSMCs were characterized by qPCR, and immunohistochemical and enzymatic-based assays; moreover, single-cell RNA sequencing, mRNA sequencing, and proteomics were used to map the molecular effects of Neil3/NEIL3 deficiency in the aortic VSMC phenotype. Furthermore, BrdU-based proliferation assays and Western blot were performed to elucidate the involvement of the Akt signaling pathway in the transdifferentiation of aortic VSMCs lacking Neil3/NEIL3. RESULTS: We show that Neil3 deficiency increases atherosclerotic plaque development without affecting systemic lipids. This observation was associated with a shift in VSMC phenotype towards a proliferating, lipid-accumulating and secretory macrophage-like cell phenotype, without changes in DNA damage. VSMC transdifferentiation in Neil3-deficient mice encompassed increased activity of the Akt signaling pathway, supported by cell experiments showing Akt-dependent proliferation in NEIL3-abrogated human primary aortic VSMCs. CONCLUSIONS: Our findings show that Neil3 deficiency promotes atherosclerosis development through non-canonical mechanisms affecting VSMC phenotype involving activation of the Akt signaling pathway

Pleietjeneste til S+. En evaluering av Fransiskushjelpens pleietjeneste til kreftpasienter med kort forventet levetid

Evalueringen av Pleietjenesten i Fransiskushjelpen har vært lagt opp som en kvalitativ brukerundersøkelse hvor pårørende har beskrevet tjenesten som deres nærmeste har mottatt. Gjennom fokusgruppeintervju har flere som har hatt tjenesten i sine hjem fått komme til orde med sine personlige erfaringer, tanker og synspunkter. Til grunn for gjennomføringen ligger et ønske fra Fransiskushjelpens side om å kartlegge kritiske faktorer og forbedringspotensialer samt løfte fram kvaliteter som tjenesten kan utvikle ytterligere

Not so unconventional after all?

A quantitative study of men in care-oriented study programmes and professional occupations in Norway. Utgivelsesdata Tittel:Not so unconventional after all?Forfatter(e):Hilde KarlsenSerie:HiOA avhandlingerIssn:1893-0476Nr:2012 nr 1Utgiver:HiOAAvdeling/fakultet:SPSSider:217Pris:310,– ISBN-print:978-82-93208-08-