Miljøterapi i alderspsykiatri - Medmennesklige møter og utfordringer

Sammendrag Bakgrunn: Som vernepleier i en alderspsykiatrisk sengepost har jeg møtt utallige eldre mennesker med sammensatte psykiske og fysisk lidelser. Relasjoner og betydningen av dem i samarbeidet med pasienter er viktig for å kunne fremme bedring. Mennesker med høyere alder har ofte flere og sammensatte lidelser. Miljøterapi og det terapeutiske miljø som endringsarena skal fremme bedring for ulike mennesker på samme tid. Formål med studien: å belyse følgende problemstilling: Hvordan kan terapeutiske allianser i miljøterapi fremme bedring av psykisk helse i en alderspsykiatrisk sengepost? Metode: kvalitativ litteraturstudie Fire sentrale funn: • Forståelse av mennesker er en bevisst og ubevisst prosess. Denne prosessen styres av erfaringer, opplevelser og forestillingsevne. • Samarbeid inkluderer involvering og kontakt med andre. Kontakt skjer gjennom deling i fellesskap med endring som mål. Involvering og personlig egnethet er sentralt i samarbeidsprosesser. Gjennom læring og kontakt med andre kan bedring fremmes. • Roller handler om personlig kompetanse, fordeling og deling av ansvar. Fordeling er mangefasettert og i stadig endring. • Omgivelser er avhengige av strukturelle og relasjonelle faktorer for å kunne fremme bedring. Individuelle tilnærmende omgivelser er nødvendige og ønsket i behandling av psykiske lidelser. Konklusjon: Økt grad av individuell tilnærming i miljøterapi for eldre er nødvendig for å kunne fremme bedring av psykiske lidelser på en best mulig måte. Terapeutiske allianser er grunnstenene i endringsarbeid og er utgangspunktet for et godt samarbeid. Bedring forutsetter samarbeid mellom helsepersonell og pasienter og bør tilpasses hver pasientgruppe i den grad det er mulig.Abstract Background: As a social educator in an old-age psychiatry ward, I have met countless elderly people with complex mental and physical disorders. Relationships and their importance for collaborating with patients are important to promote improvement. Environmental therapy and the therapeutic environment as an arena for change must promote improvement for different people at the same time. Purpose of the study: to find answers to the following issue: How can therapeutic alliances in environmental therapy promote the improvement of mental health in an old-age psychiatry ward? Method used: qualitative literature study Four key findings: • Understanding people is a conscious and unconscious process. This process is governed by experiences and imagination. • Collaboration includes involvement and contact with others. Contact takes place through sharing in common with change as the goal. Involvement and personal suitability are central to the collaboration processes. Through learning and contact with others, improvement can be promoted. • Roles are about personal competence, distribution and sharing of responsibilities. Distribution is multifaceted and constantly changing. • Environment depends on structural and relational factors to promote improvement. Individual approximate environments are necessary and desired in the treatment of mental disorders. Conclusion: An increased degree of individual approach in environmental therapy for the elderly is necessary to be able to promote improvement of mental illness in the best possible way. Therapeutic alliances are the cornerstones of change work and are the starting point for collaboration. Improvement requires collaboration between healthcare professionals and health personnel and should be adapted to each patient group as much as possible

Fakta om ti innvandrergrupper i Norge

Den rapporten er en samling av statistikk om ti store innvandrergrupper med ikke-vestlig bakgrunn. Gruppene som er valgt ut er blant de største innvandrergruppene med ikke-vestlig bakgrunn i Norge; Pakistan, Vietnam, Irak, Bosnia- Hercegovina, Somalia, Iran, Tyrkia, Sri Lanka, Serbia og Montenegro og Chile. Innvandrerbefolkningen er så sammensatt at det sjelden har noe for seg å se på alle innvandrere som en gruppe under ett. Bakgrunnen for å lage disse beskrivelsene i forhold til enkeltland er en økt etterspørsel etter informasjon om hvordan det går med store enkeltgrupper. De samme ti landene skal være med i en ny levekårsundersøkelse blant ikke-vestlige innvandrere, som skal gjennomføres i 2005/2006. Beskrivelsene er laget i forbindelse med forarbeid til levekårsundersøkelsen, og som et bidrag til en ny stortingsmelding om det flerkulturelle Norge (foreløpig tittel pr. juni 2004). Beskrivelsene er basert på foreliggende og publisert statistikk og dekker demografi, inn- og utvandring, botidssammensetning, statsborgerskap, husholdssammensetning, boforhold, ekteskapsmønstre, utdanningsnivå- og utdanningsdeltakelse, arbeidsledighet og arbeidsdeltakelse, inntekt og valgdeltakelse. Vi opplever en økende etterspørsel også etter informasjon om personer som er født i Norge av to utenlandsfødte foreldre. Dette er en gruppe som øker i størrelse for hvert år, de fleste er barn, men en del begynner å bli voksne. I det siste kapittelet har vi samlet noen fakta om denne gruppen. Vi beskriver gruppens sammensetning i forhold til landbakgrunn, alder og bosetningsmønster. Benedicte Lie har hatt ansvaret for rapporten, og for å utarbeide fakta om de ulike innvandrergruppene. En særlig takk til Lars Østby for verdifulle innspill og kommentarer. Bjørn Bergskaug har bidratt med deler av teksten og tilrettleggig av en del tabeller og figurer

Ekteskapsmønstre i det flerkulturelle Norge

Denne rapporten beskriver ekteskapsmønstre i innvandrerbefolkningen, og ekteskap mellom innvandrere og personer uten innvandringsbakgrunn. Det er lagt mer vekt på å gi en utfyllende beskrivelse, enn å forklare mønsteret. Innledningsvis beskrives innvandrerbefolkningens sammensetning med hensyn til alder, kjønn, landbakgrunn og sivilstand. Deretter beskrives bestanden av ekteskap i Norge per 1.1.1990 og 1.1.2002. Samliv er mer enn ekteskap, og vi gir derfor også en kort beskrivelse av innslaget av samboerskap i forskjellige befolkningsgrupper. Ekteskapsinngåelsene som har funnet sted fra 1990 og frem til 2001 blir beskrevet i forhold til ektefellenes landbakgrunn og hjemland ved ekteskapsinngåelsen. Hvorfor lage en slik beskrivelse? En slik beskrivelse kan hjelpe oss til å forstå en del prosesser rundt selve innvandringen (kjedemigrasjon, ekteskap mellom personer som bor i Norge og utlandet), og utviklingen av et internasjonalt og flerkulturelt samfunn; Forhold som i sin tur vil representere ulike utfordringer med hensyn til integrasjon og utforming av kommunal og offentlig forvaltning. Prosjektet ble i sin tid initiert av Stine Bjertnæs. Det er gjennomført av Benedicte Lie. Oddveig Selboe har stått for en del av tabellproduksjonen, og Liv Hansen har tilrettelagt figurene. En særlig takk til Lars Østby for verdifulle innspill til prosjektet

Utredning av alternative rapporteringsløsninger for kirkelig tjenestestatistikk : Sluttrapport

Utredningsgruppen har redegjort for og vurdert følgende fem fremtidige rapporteringsløsninger for kirkelig tjenestestatistikk: 1. Dagens NSD løsning for kirkelig tjenestestatistikk 2. Web-rapportering via NSD 3. Rapportering til SSB via kommunene sitt rapporteringssystem i KOSTRA 4. Web-rapportering til SSB i KOSTRA 5. XML-rapportering til SSB i KOSTRA Alternativene 1 og 3 er etter utredningsgruppens vurdering de minst rasjonelle alternativene. Dagens NSD løsning har fungert godt i flere år, men oppfyller etter vår vurdering ikke de krav som bør settes til et helhetlig fremtidig rapporteringssystem. Dette skyldes at alternativet innebærer papirskjemarapportering, stor oppgavebyrde, lav aktualitet og mindre muligheter for integrering med KOSTRA-systemet og annen statistikk for kirkelig sektor i SSB. Rapportering til SSB via kommunene sitt KOSTRA-system ble forkastet fordi de kirkelige organer da blir avhengig av kommunene som mellomledd for å få gjennomført sin rapportering. Dermed gjenstår tre alternativer som alle er basert på elektronisk rapportering direkte fra de kirkelige organer. Vår konklusjon er derfor at vi ønsker overgang fra dagens papirskjema rapportering til elektronisk rapportering for den kirkelige tjenestestatistikken. Dette betyr samtidig at vi mener at den kirkelige tjenestestatistikken uansett bør legges om

Polymorphisms in the TP53-MDM2-MDM4-axis in patients with rheumatoid arthritis

Background In addition to being a tumour suppressor, TP53 is a suppressor of inflammation, and dysfunction of this gene has been related to autoimmune diseases. Patients with autoimmunity, such as rheumatoid arthritis (RA) have an increased risk of certain cancers, like lymphomas, indicating that some underlying mechanisms may modulate risk of both cancers and autoimmunity. Methods We genotyped 5 common genetic variants in TP53 and its main regulators MDM2 and MDM4 in a sample of 942 RA patients and 3,747 healthy controls, and mined previously published GWAS-data, to assess the potential impact of these variants on risk of RA. Results For the TP53 Arg72Pro polymorphism (rs1042522), MDM4 SNP34091 (rs4245739) and MDM2 SNP285C (rs117039649), we found no association to risk of RA. For MDM2 SNP309 (rs2279744), the minor G-allele was associated with a reduced risk of RA (OR: 0.87; CI: 0.79–0.97). This association was also seen in genotype models (OR: 0.86; CI: 0.74–0.99 and OR: 0.79; CI 0.63–0.99; dominant and recessive model, respectively), but was not validated in a large GWAS data set. For MDM2 del1518 (rs3730485), the minor del-allele was associated with an increased risk of RA in the dominant model (OR: 1.18; CI: 1.02–1.38). Stratifying RA cases and controls into phylogenetic subgroups according to the combined genotypes of all three MDM2 polymorphism, we found individuals with the del158-285–309 genotype del/ins-G/G-T/T to have an increased risk of RA as compared to those with the ins/ins-G/G-G/G genotype (OR: 1.56; CI: 1.18–2.06) indicating opposite effects of the del1518 del-allele and the SNP309 G-allele. Conclusion We find a potential association between the MDM2 del1518 variant and RA, and indications that combinatorial genotypes and haplotypes in the MDM2 locus may be related to RA.publishedVersio

No replication of previously reported association with genetic variants in the T cell receptor alpha (TRA) locus for myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS)

This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http:// creativecommons.org/licenses/by/4.0/.Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a disease with a variety of symptoms such as post-exertional malaise, fatigue, and pain, but where aetiology and pathogenesis are unknown. An increasing number of studies have implicated the involvement of the immune system in ME/CFS. Furthermore, a hereditary component is suggested by the reported increased risk for disease in relatives, and genetic association studies are being performed to identify potential risk variants. We recently reported an association with the immunologically important human leucocyte antigen (HLA) genes HLA-C and HLA-DQB1 in ME/ CFS. Furthermore, a genome-wide genetic association study in 42 ME/CFS patients reported significant association signals with two variants in the T cell receptor alpha (TRA) locus (P value.publishedVersio

Genetic association study in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) identifies several potential risk loci

This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a disease of unknown etiology and pathogenesis, which manifests in a variety of symptoms like post-exertional malaise, brain fog, fatigue and pain. Hereditability is suggested by an increased disease risk in relatives, however, genome-wide association studies in ME/CFS have been limited by small sample sizes and broad diagnostic criteria, therefore no established risk loci exist to date. In this study, we have analyzed three ME/CFS cohorts: a Norwegian discovery cohort (N = 427), a Danish replication cohort (N = 460) and a replication dataset from the UK biobank (N = 2105). To the best of our knowledge, this is the first ME/CFS genome-wide association study of this magnitude incorporating 2532 patients for the genome-wide analyses and 460 patients for a targeted analysis. Even so, we did not find any ME/ CFS risk loci displaying genome-wide significance. In the Norwegian discovery cohort, the TPPP gene region showed the most significant association (rs115523291, P = 8.5 × 10− 7 ), but we could not replicate the top SNP. However, several other SNPs in the TPPP gene identified in the Norwegian discovery cohort showed modest association signals in the self-reported UK biobank CFS cohort, which was also present in the combined analysis of the Norwegian and UK biobank cohorts, TPPP (rs139264145; P = 0.00004). Interestingly, TPPP is expressed in brain tissues, hence it will be interesting to see whether this association, with time, will be verified in even larger cohorts. Taken together our study, despite being the largest to date, could not establish any ME/CFS risk loci, but comprises data for future studies to accumulate the power needed to reach genome-wide significance.publishedVersio

Human Leukocyte Antigen alleles associated with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS)

The etiology and pathogenesis of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) are unknown, and autoimmunity is one of many proposed underlying mechanisms. Human Leukocyte Antigen (HLA) associations are hallmarks of autoimmune disease, and have not been thoroughly investigated in a large ME/CFS patient cohort. We performed high resolution HLA -A, -B, -C, -DRB1, -DQB1 and -DPB1 genotyping by next generation sequencing in 426 adult, Norwegian ME/CFS patients, diagnosed according to the Canadian Consensus Criteria. HLA associations were assessed by comparing to 4511 healthy and ethnically matched controls. Clinical information was collected through questionnaires completed by patients or relatives. We discovered two independent HLA associations, tagged by the alleles HLA-C*07:04 (OR 2.1 [95% CI 1.4–3.1]) and HLA-DQB1*03:03 (OR 1.5 [95% CI 1.1–2.0]). These alleles were carried by 7.7% and 12.7% of ME/CFS patients, respectively. The proportion of individuals carrying one or both of these alleles was 19.2% in the patient group and 12.2% in the control group (OR 1.7 [95% CI 1.3–2.2], pnc = 0.00003). ME/CFS is a complex disease, potentially with a substantial heterogeneity. We report novel HLA associations pointing toward the involvement of the immune system in ME/CFS pathogenesis.publishedVersio

A CLEC16A variant confers risk for juvenile idiopathic arthritis and anti-cyclic citrullinated peptide antibody negative rheumatoid arthritis

Objective Variants in CLEC16A have conferred susceptibility to autoimmune diseases in genome-wide association studies. The present work aimed to investigate the locus' involvements in juvenile idiopathic arthritis (JIA) and further explore the association with rheumatoid arthritis (RA), type 1 diabetes (T1D) and Addison's disease (AD) in the Norwegian population. Methods Three single nucleotide polymorphisms (SNPs) were genotyped in patients with RA (n=809), JIA (n=509), T1D (n=1211) and AD (n=414) and in healthy controls (n=2149). Results All diseases were associated with CLEC16A, but with different SNPs. The intron 22 SNP, rs6498169, was associated with RA (p=0.006) and JIA (p=0.016) and the intron 19 SNPs, rs12708716/rs12917716, with T1D (p=1×10−5) and AD (p=2×10−4). The RA association was confined to the anti-cyclic citrullinated peptide antibody (anti-CCP) negative subgroup (p=2×10−4). Conclusion This is the first report of a CLEC16A association with JIA and a split of the RA association according to anti-CCP status. Different causative variants underlie the rheumatic versus the organ specific diseases

Electrostatic Modifications of the Human Leukocyte Antigen-DR P9 Peptide-Binding Pocket and Susceptibility to Primary Sclerosing Cholangitis

The strongest genetic risk factors for primary sclerosing cholangitis (PSC) are found in the human leukocyte antigen (HLA) complex at chromosome 6p21. Genes in the HLA class II region encode molecules that present antigen to T lymphocytes. Polymorphisms in these genes are associated with most autoimmune diseases, most likely because they contribute to the specificity of immune responses. The aim of this study was to analyze the structure and electrostatic properties of the peptide-binding groove of HLA-DR in relation to PSC. Thus, four-digit resolution HLA-DRB1 genotyping was performed in 356 PSC patients and 366 healthy controls. Sequence information was used to assign which amino acids were encoded at all polymorphic positions. In stepwise logistic regressions, variations at residues 37 and 86 were independently associated with PSC (P = 1.2 × 10−32 and P = 1.8 × 10−22 in single-residue models, respectively). Three-dimensional modeling was performed to explore the effect of these key residues on the HLA-DR molecule. This analysis indicated that residue 37 was a major determinant of the electrostatic properties of pocket P9 of the peptide-binding groove. Asparagine at residue 37, which was associated with PSC, induced a positive charge in pocket P9. Tyrosine, which protected against PSC, induced a negative charge in this pocket. Consistent with the statistical observations, variation at residue 86 also indirectly influenced the electrostatic properties of this pocket. DRB1*13:01, which was PSC-associated, had a positive P9 pocket and DRB1*13:02, protective against PSC, had a negative P9 pocket. Conclusion: The results suggest that in patients with PSC, residues 37 and 86 of the HLA-DRβ chain critically influence the electrostatic properties of pocket P9 and thereby the range of peptides presented. (Hepatology 2011;53:1967-1976