Promoting physical health in severe mental illness: patient and staff perspective.

OBJECTIVE: To explore physical health problems and their causes in patients with severe mental illness, as well as possibilities for prevention and treatment from the patients' and staff's perspectives. METHOD: We conducted six focus groups with patients and staff separately, from three out-patient clinics treating patients with schizophrenia or substance-use disorder comorbid to another psychiatric disorder. Focus groups were audio-recorded, transcribed verbatim and analysed using a template approach. RESULTS: Paramount physical health problems are weight issues, cardiovascular diseases and poor physical shape. Main causes are lifestyle, the mental disorder and organisational issues. Patients and staff expressed similar opinions regarding physical health problems and their causes. Possibilities for prevention and treatment includes a case manager and binding communities with like-minded, as well as management support and implementation of physical health into daily psychiatric practice. Although patients and staff suggested different possibilities for prevention and treatment, they support one strategy: less fragmentation of the treatment system and cooperation between psychiatric and somatic healthcare. CONCLUSION: To prevent and treat physical health problems in patients with severe mental illness, support in daily structure and lifestyle changes is needed. Management support is needed to change daily practice and implement routines regarding physical health.

The gap between available knowledge and its use in clinical psychiatry.

OBJECTIVE: The time span between knowledge becoming available and its integration into daily clinical routine is lengthy. This phenomenon is explored in this study. METHOD: We used the outcomes of our activities for investigating and strengthening the research-based activities to improve physical health in the routines of clinical psychiatric wards as examples for our analyses. RESULTS: The time span between new knowledge becoming available and its implementation into general clinical treatment is very long. However, a shortening of this time span is seen through active leadership backup and clinical research experience among psychiatrists and staff in the wards. In particular, the involvement of medical students interested in clinical research activities seems to have a positive impact. CONCLUSION: Academia needs to be re-implemented into clinical psychiatry. Staff with research experience is needed in all professions to increase evidence-based practice. Leaders must take responsibility for implementing new knowledge into the routines of the department and must support staff in these activities on a daily basis.

A systematic review of controlled interventions to reduce overweight and obesity in people with schizophrenia.

OBJECTIVE: Overweight and obesity are generally found among patients with schizophrenia. This may lead to serious implications for health and wellbeing. The aim was to review controlled intervention studies on reducing overweight/obesity and/or reducing physical illness in patients with schizophrenia. METHOD: A systematic literature search was carried out in the bibliographic databases PubMed (MEDLINE), Embase (Ovid), PsycInfo (Ovid) and Cinahl (Ebsco). We included all randomised and non-randomised clinically controlled studies that compared a non-pharmacological intervention, aimed at weight reduction and/or reducing physical illness, with standard care for patients with schizophrenia. RESULTS: All 1713 references were evaluated for inclusion in the review. Twenty-three met the inclusion criteria and were categorised into four subgroups according to tested interventions: diet, exercise and cognitive behavioural therapy, or mixed combinations of the three. In this review, interventions showed efficacy in reducing weight and improving physical health parameters confirming that physical health improvement was possible in patients with schizophrenia. CONCLUSION: The included studies indicate that the interventions reduced weight and improved physical health parameters in patients with schizophrenia.

Construction of the simplest model to explain complex receptor activation kinetics.

We study the mathematical solutions to the kinetic equations arising from various simple ligand-receptor [corrected] models. Focusing on the prediction of the various models for the activity vs. concentration curve, we find that solutions to the kinetic equations arising from the so-called dimer model exhibit features observed in some experiments, most noticeably a distinct maximum in the activity curve.

Under control of the Ren-1c promoter, locally produced transforming growth factor-beta1 induces accumulation of glomerular extracellular matrix in transgenic mice.

Our purpose was to elucidate the hypothesis that paracrine-produced transforming growth factor (TGF)-beta1 regulates the accumulation of extracellular matrix (ECM) in renal glomeruli, a hallmark of diabetic nephropathy. To produce TGF-beta1 from the juxtaglomerular apparatus in mouse kidneys, we cloned a mouse Ren-1c promoter fragment (-4.100 to +6 base pairs) upstream of porcine TGF-beta1 (pTGF-beta1) cDNA, mutated to ensure secretion of biologically active TGF-beta beta1. The resulting transgenic mice had significantly more TGF-beta1 in their kidneys than was in those of nontransgenic controls, as confirmed by immunohistochemistry, and the production of TGF-beta1 was enhanced in vivo by captopril-induced stimulation of the Ren-1c promoter. Overproduction of pTGF-beta1 close to the glomerulus resulted in a local accumulation of ECM, composed partly of collagen type IV and laminin, and thickening of the basement membrane, characteristic features of diabetic nephropathy. Interstitial accumulation of ECM and signs of tubular atrophy were present only in older mice (>5 months of age). Results from in situ hybridization and immunohistochemistry suggest that pTGF-beta1 stimulated the production of endogenous TGF-beta1 along collecting ducts and connecting tubules. The increased amount of biologically active TGF-beta1, transgenic as well as endogenous, was corroborated by heightened proteoglycan synthesis from incubated kidney slices. This transgenic model demonstrates that sustained local expression of TGF-beta1 leads to glomerulopathy. We conclude that autocrine- or paracrine-produced TGF-beta1 may play a role in the development of glomerular diseases, such as diabetic nephropathy.