Predictors of length of stay in forensic psychiatry: The influence of perceived risk of violence.

This study describes the prevalence of adverse events and length of stay in forensic psychiatric patients with and without a restriction order. Detailed clinical and administrative information from medical records and written court decisions was gathered retrospectively from admission until discharge for a Swedish population-based, consecutive cohort of forensic psychiatric patients (n=125). The median length of stay for the whole cohort was 951days, but patients with a restriction order stayed in hospital almost five times as long as patients without. Restriction orders were related to convictions for violent crime, but not for any other differences in demographic or clinical variables. The majority of the patients (60%) were involved in adverse events (violence, threats, substance abuse, or absconding) at some time during their treatment. Patients with restriction orders were overrepresented in violent and threat events. Previous contact with child and adolescence psychiatric services, current violent index crime, psychotic disorders, a history of substance, and absconding during treatment predicted longer length of stay. Being a parent, high current Global Assessment of Functioning scores, and mood disorders were all significantly related to earlier discharge. In a stepwise Cox regression analysis current violent index crime and absconding remained risk factors for a longer hospital stay, while a diagnosis of mood disorder was significantly related to a shorter length of stay

A cluster of genes located in 1p36 are down-regulated in neuroblastomas with poor prognosis, but not due to CpG island methylation

BACKGROUND: A common feature of neuroblastoma tumours are partial deletions of the short arm of chromosome 1 (1p-deletions). This is indicative of a neuroblastoma tumour suppressor gene being located in the region. Several groups including our have been studying candidate neuroblastoma genes in the region, but no gene/genes have yet been found that fulfil the criteria for being a neuroblastoma tumour suppressor. Since frequent mutations have not been detected, we have now analyzed the expression and promoter CpG island methylation status of the genes UBE4B, KIF1B, PGD, APITD1, DFFA and PEX14 in the 1p36.22 region in order to find an explanation for a possible down-regulation of this region. RESULTS: The current study shows that gene transcripts in high stage neuroblastoma tumours are significantly down-regulated compared to those in low stage tumours in the 1p36.22 region. CpG island methylation does not seem to be the mechanism of down-regulation for most of the genes tested, since no methylation was detected in the fragments analyzed. One exception is the CpG island of APITD1. Methylation of this gene is also seen in blood from control individuals and is therefore not believed to participate in tumour development. CONCLUSION: The genes UBE4B, KIF1B, PGD, APITD1, DFFA and PEX14 are down-regulated in high stage NB tumours, a feature that can not be explained by CpG island methylation

Vad kan evidensbaserad praktik vara? : Några socialarbetare talar om evidensbaserat arbete

Denna kvalitativa studie belyser hur socialarbetare inom missbruksvården uttalade sig om evidensbaserad praktik. Syftet var även att få en förståelse i vad som kan hindra eller främja ett evidensbaserat arbetssätt. Studien utgick ifrån en socialkonstruktivistisk ansats genom Berger och Luckmanns tresidiga modell där även studiens resultat är tolkat i samma anda. Studien gjordes utefter semistrukturerad utgångspunkt med fem socialarbetare inom missbruksvården i sammanlagt tre kommuner. Resultatet visar att evidensbaserad praktik ses som något som är beforskat och beprövat. I övrigt ligger delade meningar i begreppets innebörd. Vad som kan ses som ett hinder i implementeringen av evidenbaserad praktik är att hamna i ett tänk där klienten får anpassa sig efter organisationen och inte tvärt om. Det som möjliggör evidensbaserad praktik är ett gemensamt arbetssätt för socialarbetarna. En slutsats är att det finns en ambition om ett evidensbaserat arbetssätt men att det finns många hinder på vägen mot en evidensbaserad socialtjänst

Mentally disordered offenders in Sweden : differentiating recidivists fromnon-recidivists in a 10-year follow-up study

Background: Forensic psychiatric patients present a challenge as they manifest severe mental disorders together with criminal behaviour. There are well-known risk factors for criminal behaviour in the general population, yet knowledge of what predicts reconviction in the Swedish forensic population in the long-term perspective is still insufficient. Aims: The study aims to (1) describe background and clinical characteristics of forensic psychiatric patients in a 10-year follow-up, (2) analyse risk factors associated with recidivism, and (3) test the predictive validity of risk factors for general and violent criminality. Methods: Detailed information on all offenders from the Malmö University Hospital catchment area sentenced to forensic psychiatric in-patient treatment from 1999–2005 (n = 125) was collected. Court decisions were collected up until the end of 2008 (median follow-up time = 6.2 years, range = 0.6–9.7 years). Results: Relapse in general crime (n = 30) was predicted by low educational attainment, mental disorder in a first degree relative, and low age at first sentenced crime. Relapse in violent crime (n = 16) was predicted by low educational attainment and low GAF scores. Patients with a restriction order were less likely to relapse in both crime categories. Conclusions: Signs of childhood adversities together with early debut in criminality appeared as important risk factors for general and violent recidivism. Forensic psychiatric treatment combined with a restriction order was demonstrated as a protective factor against recidivism, suggesting that the risk of recidivism is strongly related to the level of supervision. Although the low number of recidivism cases is highly desirable, it unfortunately reduces the power of the analyses in this paper

Introduction of <it>in vitro </it>transcribed <it>ENO1 </it>mRNA into neuroblastoma cells induces cell death

Abstract Background Neuroblastoma is a solid tumour of childhood often with an unfavourable outcome. One common genetic feature in aggressive tumours is 1p-deletion. The α-enolase (ENO1) gene is located in chromosome region 1p36.2, within the common region of deletion in neuroblastoma. One alternative translated product of the ENO1 gene, known as MBP-1, acts as a negative regulator of the c-myc oncogene, making the ENO1 gene a candidate as a tumour suppressor gene. Methods Methods used in this study are transfection of cDNA-vectors and in vitro transcribed mRNA, cell growth assay, TUNEL-assay, real-time RT-PCR (TaqMan) for expression studies, genomic sequencing and DHPLC for mutation detection. Results Here we demonstrate that transfection of ENO1 cDNA into 1p-deleted neuroblastoma cell lines causes' reduced number of viable cells over time compared to a negative control and that it induces apoptosis. Interestingly, a similar but much stronger dose-dependent reduction of cell growth was observed by transfection of in vitro transcribed ENO1 mRNA into neuroblastoma cells. These effects could also be shown in non-neuroblastoma cells (293-cells), indicating ENO1 to have general tumour suppressor activity. Expression of ENO1 is detectable in primary neuroblastomas of all different stages and no difference in the level of expression can be detected between 1p-deleted and 1p-intact tumour samples. Although small numbers (11 primary neuroblastomas), there is some evidence that Stage 4 tumours has a lower level of ENO1-mRNA than Stage 2 tumours (p = 0.01). However, mutation screening of 44 primary neuroblastomas of all different stages, failed to detect any mutations. Conclusion Our studies indicate that ENO1 has tumour suppressor activity and that high level of ENO1 expression has growth inhibitory effects.</p

Self-Assembly of Recombinant Silk as a Strategy for Chemical-Free Formation of Bioactive Coatings: A Real-Time Study

Functionalization of biomaterials with biologically active peptides can improve their performance after implantation. By genetic fusion to self-assembling proteins, the functional peptides can easily be presented on different physical formats. Herein, a chemical-free coating method based on self-assembly of the recombinant spider silk protein 4RepCT is described and used to prepare functional coatings on various biomaterial surfaces. The silk assembly was studied in real-time, revealing the occurrence of continuous assembly of silk proteins onto surfaces and the formation of nanofibrillar structures. The adsorbed amounts and viscoelastic properties were evaluated, and the coatings were shown to be stable against wash with hydrogen chloride, sodium hydroxide, and ethanol. Titanium, stainless steel, and hydroxyapatite were coated with silk fused to an antimicrobial peptide or a motif from fibronectin. Human primary cells cultured on the functional silk coatings show good cell viability and proliferation, implying the potential to improve implant performance and acceptance by the body

-mut and -constructs with translation starts (ATG) and mutated (ATG→ATC) sites in -mut at positions 374 and 383 indicated

<p><b>Copyright information:</b></p><p>Taken from "Introduction of transcribed mRNA into neuroblastoma cells induces cell death"</p><p>BMC Cancer 2005;5():161-161.</p><p>Published online 16 Dec 2005</p><p>PMCID:PMC1327688.</p><p>Copyright © 2005 Ejeskär et al; licensee BioMed Central Ltd.</p> The mutations introduce I and I restriction enzyme sites respectively. Size determination of cDNA-constructs in pIRES-EGFP-vector by I/I-digest. Confirmation of mutations in -mut DNA by I and I digests

Aberrant immunostaining pattern of the CD24 glycoprotein in clinical samples and experimental models of pediatric medulloblastomas.

The CD24 glycoprotein is a mediator of neuronal proliferation, differentiation and immune suppression in the normal CNS, and a proposed cancer biomarker in multiple peripheral tumor types. We performed a comparative analysis of CD24 gene expression in a large cohort of pediatric and adult brain tumors (n = 813), and further characterized protein expression in tissue sections (n = 39), primary brain tumor cultures (n = 12) and a novel orthotopic group 3 medulloblastoma xenograft model. Increased CD24 gene expression was demonstrated in ependymomas, medulloblastomas, anaplastic astrocytomas and glioblastomas, although medulloblastomas displayed higher expression than all other tumor entities. Preferential expression of CD24 in medulloblastomas was confirmed at protein level by immunostaining and computerized image analysis of cryosections. Morphologies and immunophenotyping of CD24(+) cells in tissue sections tentatively suggested disparate functions in different tumor subsets. Notably, protein staining of medulloblastoma cells was associated with prominent cytoplasmic and membranous granules, enabling rapid and robust identification of medulloblastoma cells in clinical tissue samples, as well as in experimental model systems. In conclusion, our results implicate CD24 as a clinically and experimentally useful medulloblastoma immunomarker. Although our results encourage further functional studies of CD24 as a potential molecular target in subsets of brain tumors, the promiscuous expression of CD24 in vivo highlights the importance of specificity in the future design of such targeted treatment