Developing a theory of change model for a learning and innovation network: A qualitative study.

AIM: The aim of this study is to further develop a preliminary framework into a model that can translate mechanisms into output and impact, based on the views of those working in practice and the relations between the mechanisms: a model that can inform practitioners and organizations on what has to be in place to shape a learning and innovating environment in nursing. BACKGROUND: A Learning and Innovation Network (LIN) is a network of healthcare professionals, students and education representatives who come together to be part of a nursing community to integrate education, research and practice to contribute to quality of care. In a previous study a preliminary framework was developed through a concept analysis based on publications. The preliminary framework describes input, throughput and output factors in a linear model that does not explain what the components entail in practice and how the components work together. DESIGN: Focus groups. METHODS: We designed a Theory of Change (ToC) in four phases. This was based on a focus group interview with lecturer practitioners (Phase 1); a first concept ToC based on thematic analysis of the focus group interview (Phase 2); three paired interviews where the ToC was presented to other lecturer practitioners to complement and verify the ToC model (Phase 3); and adjustment of the model based on the feedback of phase 3 (Phase 4). RESULTS: The developed ToC model describes important preconditions that have to be in place to start a LIN: a shared vision, a facilitating support system and a diversity of participants who are open to change. It describes the mechanisms by which a wide range of activities can lead to an improvement of the quality of care through collaboration between practice, education and research by working, learning, performing practice based research and implementing new methods together. CONCLUSION: This study gives a comprehensive overview of the concept of the 'Learning and Innovation Network' (LIN); how the activities in the LIN can lead to impact; and under what conditions. Previously published findings supported elements of the ToC model. The overarching ToC model and the detailed appendix offer a theoretical and practice-based model for practitioners, managers and policy makers.

[Neonatal lupus erythematosus as an example of passively acquired autoimmunity]. / Neonataler Lupus erythematodes als Beispiel für passiv übertragene Autoimmunität.

Neonatal lupus erythematosus is a typical example of passively acquired autoimmune disease. Congenital heart block is the main complication caused by transplacentally transferred maternal IgG antibodies directed against SS-A- or SS-B-antigen. While the transient lupus dermatitis occurs post partum and is often triggered by UV-light exposition, the irreversible cardial damage takes place between the 18. and 24, week of pregnancy. During this period 52-kD-SS-A- and 48-kD-SS-B-antigen are expressed in the fetal cardial tissue. The autoimmune reaction leads to an irreversible fibrotic destruction of the atrioventricular node. The resulting AV block and an antibody-induced perimyocarditis support the development of fetal bradyarrhythmia and hydrops. The very early diagnosis of a fetal heart block in bradycardiac fetus by echocardiography is essential for a consecutive therapy with steroids. By a reduction of the maternal antibodies an improvement of cardial symptoms in the fetus may be achieved in cases with fetal hydrops. Pregnant women at high risk with known connective tissue disease, previous children with congenital heart block, high titers of SS-A-/SS-B-antibodies and immunogenetic predisposition (HLA-DR3) have to be monitored intensively because of the possibility of a prophylaxis with dexamethasone and, in some selected cases, plasmapheresis.

[Chronic recurrent polychondritis]. / Die chronisch rezidivierende Polychondritis.

Relapsing polychondritis (RP) is a recurrent, chronic und rare disease of unknown etiology, characterized by inflammation of cartilaginous structures of the ears, nose, respiratory tract and joints. The association with HLA-DR4 and the occurrence of antibodies to type-II collagen and other autoantibodies suggest that an immunologic mechanism is involved in its pathogenesis. In about 30% of occurrences RP is associated with other rheumatic or autoimmune diseases. Ocular inflammation, involvement of the cardiovascular system, skin, central nervous system and audiovestibular organ are most probably caused by vasculitis. The course of RP is variable. Severity and outcome primarily depend on the occurrence of associated autoimmune diseases and vasculitis. According to the activity and systemic manifestations, medical treatment includes nonsteroidal antiinflammatory drugs, corticosteroids and cytotoxic agents.

Current therapy of systemic sclerosis (scleroderma).

Treatment of systemic sclerosis (scleroderma) presents a challenge to both the patient and the physician. Established approaches include long-term physiotherapy, disease-modifying agents such as D-penicillamine, and treatment of organ involvement. These efforts are often unsatisfactory since the results are poor. However, recent advances include treatment of Raynaud's phenomenon (plasmapheresis, stanozolol, and prostacyclin analogues), scleroderma renal crisis (angiotensin-converting enzyme inhibitors), and gastric hypomotility (cisapride). This article covers the current approaches to the disease-modifying therapy including those related to the function of collagen-producing fibroblasts, vascular alterations, and the cellular and humoral immune system, as well as treatment of involved organs.