Parents with mental illness - a qualitative study of identities and experiences with support services.

WHAT IS KNOWN ON THE SUBJECT?: According to estimates more than half of adult mental health service users are parents, but their experiences are largely lacking from research literature. Parental mental illness can often be viewed from a risk perspective. Parents with mental illness and their families have unmet support needs. WHAT THIS PAPER ADDS TO EXISTING KNOWLEDGE?: Parents with mental illness want acknowledgement that they can be able and responsible. Many parents adopt an expert by experience identity. Fathers can feel their parental role is not recognized and mothers express fears of being judged if they discuss their illness. WHAT ARE THE IMPLICATIONS FOR PRACTICE?: Adult mental health services need to recognize and support parental role of service users. Joint care planning and family oriented care should be promoted. Professionals should take advantage of the knowledge of these parents and they could be more actively engaged in service development. ABSTRACT: Introduction Parental mental illness is often viewed from a risk perspective. Despite this, being a parent can be both valuable and motivating. Research literature lacks the perspective of mothers and fathers, who have experienced mental illness. Aim This study explores how parents with mental illness construct their identities as mothers and fathers and their experiences with health and social care services. Method Three focus groups with 19 participants were conducted in Finland and Scotland. Methods of discourse analysis have been used in to analyse the interview data. Results Adult service users want their parenting role recognized and supported. Parents have knowledge and skills which can be utilized and many have adopted an expert by experience identity. Discussion Being able to see oneself as a 'good' parent can be challenging but important. Parents may require support, but want to be included in the planning of their care. Services could make more use of the knowledge and skills parents and families have, and joint working could lessen parents' anxieties. Implications for practice Mental health practitioners are in a key position in providing more family centred, resource focused care. Service user expertise should be acknowledged in clinical practice.

Treatment of experimental autoimmune encephalomyelitis with a neurotropic alphavirus vector expressing tissue inhibitor of metalloproteinase-2.

Prompted by our recent observations of increased MMP-8 and MMP-9 with simultaneous downregulation of tissue inhibitor of metalloproteinase-2 (TIMP-2) and TIMP-3 mRNA levels in the central nervous system (CNS) of mice with severe experimental autoimmune encephalomyelitis (EAE), we used Semliki Forest virus (SFV) to transfer and express recombinant murine TIMP-1-3 genes in the CNS. TIMP-1, TIMP-2 and TIMP-3 expression was confirmed in cultured cells and in the CNS of infected mice. Following intraperitoneal infection with 10(6) plaque-forming units (PFU) of SFV-TIMP, focal TIMP protein expression was achieved throughout the brain. Although already treatment with empty vector inhibited development of EAE to some extent, the expression of TIMP-2 by the virus significantly enhanced the inhibition. TIMP-3-administered mice also had lower disease grade, but the inhibition was not statistically significant. In contrast, SFV-TIMP-1 had no effect, similar to co-infection with TIMP-2 and TIMP-3. We found TIMP-2 expression also by non-infected CNS-resident cells surrounding the virus-positive areas, suggesting a bystander TIMP-2 induction. These data strengthen the view that matrix metalloproteinases are involved in the pathogenesis of EAE and provide clear evidence that virus-mediated delivery of their protein inhibitors can be effective in preventing the clinical disease. TIMPs might be candidates for novel treatment regimens in CNS autoimmune disorders, such as multiple sclerosis.

Adenovirus mediated intra-articular expression of collagenase-3 (MMP-13) induces inflammatory arthritis in mice.

OBJECTIVES: To better understand the role of collagenase-3 (MMP-13) in joint inflammation by investigating the consequences of transient overexpression of human collagenase-3 (matrix metalloproteinase-13 (MMP-13)), introduced by adenoviral gene delivery, in the mouse knee joint. METHODS: A single dose (5x10(7) pfu) of recombinant adenovirus coding either for beta-galactosidase (RAdLacZ) or human MMP-13 (RAdMMP-13) was injected intra-articularly into the knee joint of adult mice. The joints were analysed at frequent intervals up to 4 weeks by histology, immunohistochemistry, and RNA analysis. RESULTS: When RAdLacZ reporter virus was used, adenoviruses efficiently infected synovial cells, chondrocytes of articular cartilage, and hypertrophic chondrocytes of the growth plate. The infection was transient as no reporter gene activity was detected 3 weeks after the injection. After RAdMMP-13 injection into the knee joints, expression of human MMP-13 in joint tissues resulted in an arthritis characterised by recruitment of inflammatory cells and increased production of cytokines and chemokines, synovial hyperplasia, and pannus formation. After the loss of MMP-13 transgene expression at 3 weeks, these inflammatory changes began to diminish. CONCLUSIONS: MMP-13 has a role in the onset of inflammatory reaction in synovium. However, damage to articular cartilage was only rarely detected after the short term overexpression of MMP-13.

Temporospatial expression of tissue inhibitors of matrix metalloproteinases-1, -2 and -3 during development, growth and aging of the mouse skeleton.

Proteolytic degradation of collagen-rich extracellular matrices is a key feature in the development, growth and aging of skeleton. Matrix metalloproteinases (MMPs) are a family of enzymes capable of performing this function, whereas tissue inhibitors of MMPs (TIMPs) are believed to play an important role in regulating their activity. To better understand the roles of TIMP-1, -2 and -3, we have studied their mRNA levels in several different mouse tissues with special emphasis on the skeleton and the developing eye. A systematic analysis of TIMP-1, -2 and -3 mRNA levels in mouse knee joints during growth and aging demonstrated markedly different expression patterns for each TIMP. Immunohistochemical analysis revealed several time-dependent changes in the distribution of TIMP-1 and -2 in articular and growth cartilages, synovial tissue and bone. The data suggest that upon aging synovial tissue becomes the major source of synovial fluid TIMPs. In articular cartilage these inhibitors were mainly found in the deep layer and in subchondral bone. Compared with epiphyseal growth plate, the amounts of TIMP-1 and -2 in articular cartilage were quite low. These findings suggest that the capacity of articular cartilage chondrocytes to inhibit MMP activities by local production of TIMPs is limited, which may be of consequence during osteoarthritic cartilage degeneration.