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The authors regret that 2 investigators were not included in the 311 Study Group. Members of the 311 Study Group are listed in the Appendix. The authors would like to apologize for any inconvenience caused.

The publisher regrets that the members of the 311 Study Group were not included as collaborative authors. Members of the 311 Study Group are listed in the Appendix. The publisher would like to apologize for any inconvenience caused.

Concepts of health management and improved quality of health care are of growing importance. In this context, the concept of empowerment is widely accepted in health-related disciplines. The aim of the present study was to investigate whether theory-based empowerment, using motivational interviewing, can be facilitated within clinical research in patients with severe chronic diseases.We here present a qualitative in-depth interview study using grounded theory methodology. Participants were twenty-seven patients undergoing chronic haemodialysis who were taking part in a research programme investigating cardiovascular function in chronic renal failure (CRF) by ultrasound measurements and blood samples.With the exception of one patient, all interviewed patients emphasized the benefit of the detailed and structured information given. All patients pointed out a deepened understanding of cardiovascular health and its relation to CRF. Improved health knowledge was associated with a strengthened sense of control in our participants. This process resulted in high levels of patient satisfaction. Fifty percent of the interviewed patients were more likely to attend further education sessions with cardiologists and primary care practitioners to improve health management.Facilitating empowerment in a clinical research project is ethically essential and can positively enhance self-care-oriented, disease-specific skills in patients with severe chronic diseases. Clinical research may open up new avenues to additionally strengthen patient sovereignty in interdisciplinary health sciences.

Effect of flosulide, a selective cyclooxygenase 2 inhibitor, on passive Heymann nephritis in the rat.BackgroundNonsteroidal anti-inflammatory drugs (NSAIDs) induce an inhibition of cyclooxygenase (COX), an enzyme that makes prostaglandins. Two isoforms of COX exist: COX-1 represents the constitutively expressed enzyme, whereas COX-2 is the inducible isoform. This study investigated the role of COX-2 in the inflammatory processes of the kidneys of rats with passive Heymann nephritis (PHN), and focused of the effect of a selective COX-2 inhibitor, flosulide. COX-2–selective inhibitors are thought to represent potent anti-inflammatory agents without major renal side effects.MethodsPHN was induced by injecting heterologous Fx1A antiserum into female Wistar rats. Two treatment groups, each consisting of 12 rats with PHN, received either 3 or 9 mg of flosulide/kg body wt/day and were compared with untreated controls. After four weeks, the generation of thromboxane B2 (TxB2) and 6-keto-PGF1α were determined in renal tissue and in urine. COX-2 protein expression was investigated by Western blotting using a selective antibody.ResultsRats with PHN exhibited a marked proteinuria of 71 ± 8 mg/24 hr as compared with 2.0 ± 0.3 mg/24 hr in healthy controls (P < 0.01). Treatment with flosulide reduced the proteinuria to 26.1 ± 9 mg/24 hr at 3 mg flosulide/kg body wt/day and 35.5 ± 6 mg/24 hr at 9 mg/kg body wt/day, which was equivalent to a reduction of proteinuria by a maximum of 65% (P < 0.05). This was accompanied by an increase in glomerular TxB2 from 3073 ± 355 to 5255 ± 1041 pg/mg glomerular protein and 6-keto-PGF1α from 1702 ± 161 to 2724 ± 770 pg/mg glomerular protein in rats with PHN. COX-2 protein expression was also highly elevated in comparison to healthy controls. Low-dose flosulide treatment had no effect on COX protein expression and renal prostaglandin formation. High-dose flosulide treatment reduced renal prostaglandin production and caused a marked decline in COX-1 and COX-2 protein expression. Urine prostanoid excretion remained unchanged in all therapeutic groups. There was a small though significant reduction in renal creatinine clearance from 0.86 ml ± 0.2/min in untreated controls to 0.6 ml ± 0.1/min in flosulide-treated rats with PHN (P < 0.01) after four weeks.ConclusionsUnder the influence of flosulide, a highly COX-2–selective inhibitor, we observed an antiproteinuric drug effect. The inflammation in PHN induced COX-2 protein expression that was not affected by low-dose flosulide. COX-1 and COX-2 protein expression was affected by high-dose flosulide, which therefore might lose its selectivity. High-dose flosulide induced a decrease in glomerular prostanoid production possibly because of COX-1 inhibition. Our results suggest that the therapeutic use of flosulide in proteinuria seems advantageous and deserves further studies because the basal prostaglandin levels remain unchanged in the low-dose–treated group, indicating that the compensatory capacity of prostaglandin production, which is essential for the regulation of renal hemodynamics, is maintained.