Publications (5)28.59 Total impact
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Article: Clinical research for patient empowerment--a qualitative approach on the improvement of heart health promotion in chronic illness.
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ABSTRACT: 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.Medical science monitor: international medical journal of experimental and clinical research 07/2008; 14(7):CR358-65. · 1.70 Impact Factor -
Article: Association of SGK1 gene polymorphisms with type 2 diabetes.
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ABSTRACT: The serum and glucocorticoid inducible kinase SGK1 is genomically upregulated by glucocorticoids and in turn stimulates a variety of carriers and channels including the renal epithelial Na(+) channel ENaC and the intestinal Na(+) glucose transporter SGLT1. Twin studies disclosed an association of a specific SGK1 haplotype with moderately enhanced blood pressure in individuals who are carrying simultaneously a homozygous genotype for a variant in intron 6 [I6CC] and a homozygous or heterozygous genotype for the C allele of a polymorphism in exon 8 [E8CC/CT] of the SGK1 gene. A subsequent study confirmed the impact of this risk haplotype on blood pressure. SGK1 knockout mice are resistant to the insulin and high salt induced increase of blood pressure, glucocorticoid induced increase of electrogenic glucose transport, and glucocorticoid induced suppression of insulin release. The present study explored whether the I6CC/E8CC/CT haplotype impacts on the prevalence of type 2 diabetes. The prevalence of the I6CC genotype was 3.1% in a healthy German, 2.4 % in a healthy Romanian and 11.6 % in a healthy African population from Ghana (p=0.0006 versus prevalence in Caucasians). Comparison of genotype frequencies between type 2 diabetic patients and the respective control groups revealed significant differences for the intron 6 T>C variant. Carriers of at least one T allele were protected against type 2 diabetes (Romanians: p=0.023; OR 0.29; 95% CI 0.09-0.89; Germans: p=0.01; OR 0.37; 95% CI 0.17-0.81). The SGK1 risk haplotype (I6CC/E8CC/CT) was significantly (p=0.032; OR 4.31, 95% CI 1.19-15.58) more frequent in diabetic patients (7.2 %) than in healthy volunteers from Romania (1.8%). The observations support the view that SGK-1 may participate in the pathogenesis of metabolic syndrome.Cellular Physiology and Biochemistry 02/2008; 21(1-3):151-60. · 2.86 Impact Factor -
Article: Podocyte damage resulting in podocyturia: a potential diagnostic marker to assess glomerular disease activity.
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ABSTRACT: A decrease in podocyte number contributes to the development of glomerulosclerosis in most forms of glomerular disease [1, 2, 3, 4, 5]. Traditionally, it has been argued that this decrease may be caused by the inability of podocytes to proliferate and replace those lost following immune, metabolic, toxic or hemodynamic injury. These data contrast with recent studies showing that podocytes are able to enter the cell cycle after injury, to progress through the different phases of the cell cycle and even enter mitosis. However, experimental and human data suggest that entry of podocytes into the cell cycle may result in reduced adhesion to the glomerular basement membrane with subsequent loss of podocytes into the urine and excretion of both viable and apoptotic podocytes. Viable urinary podocytes can be cultivated ex vivo for up to 2-3 weeks and in experimental models precede the onset of proteinuria. More importantly, podocyturia can decrease despite persistent proteinuria. The latter observation suggests that podocyturia may serve as the first non-invasive marker of 'active' glomerular damage and might thus drive therapeutic interventions in the future. However, at present technical issues still prevent a broad clinical application of podocyturia detection in clinical practice.Nephron Clinical Practice 02/2007; 106(2):c61-6. · 2.04 Impact Factor -
Article: Mesangial cell expression of proto-oncogene Ets-1 during progression of mesangioproliferative glomerulonephritis.
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ABSTRACT: Ets-1 is a transactivator of matrix-associated genes and key factor in neoangiogenesis. The expression of Ets-1 mRNA and protein was analyzed in healthy rat kidney and in a model for mesangioproliferative disease without and with inhibition of platelet-derived growth factor-B (PDGF-B) activity. Immunohistochemistry was performed using a specific noncrossreacting anti-Ets-1 antibody and included a counterstain with alpha-smooth muscle actin (alpha-SMA). Nuclear proteins from isolated glomeruli were analyzed by Western blotting. Changes in Ets-1 mRNA levels were detected by in situ hybridization and Northern blotting. PDGF-B antagonism was performed in nephritic rats by specific aptamers. The distribution of Ets-1-positive cells in healthy rats was heterogenous with exclusively nuclear staining of glomerular, tubular, and vascular cells. Profound changes were detected in the anti-Thy 1.1 glomerulonephritis. Nuclear Ets-1 staining was intense in mesangial cells, whereas podocyte and endothelial cell staining was unchanged. The strongest signal was seen on days 2 to 7. By Western blotting of glomerular proteins a single 52 kD band was detected in healthy rats, which was increased 4.5-fold after disease induction. At the same time a 54 kD band appeared that most likely represents phosphorylated Ets-1. Ets-1 transcripts were detected in mesangial cells that include exon IV but lack exon VII. A concordant 6.4-fold up-regulation of mRNA was detected in glomeruli. Specific PDGF-B antagonism by aptamer treatment from days 3 to 7 after disease induction led to reduced Ets-1 expression on day 7, correlating with decreased mesangial cell numbers. A temporal increase of mesangial cell Ets-1 expression correlates with mesangial cell activation in mesangioproliferative glomerulonephritis. PDGF-B may partially contribute to the increased expression.Kidney International 09/2004; 66(2):622-32. · 6.61 Impact Factor -
Article: The serum protein alpha 2-Heremans-Schmid glycoprotein/fetuin-A is a systemically acting inhibitor of ectopic calcification.
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ABSTRACT: Ectopic calcification is a frequent complication of many degenerative diseases. Here we identify the serum protein alpha2-Heremans-Schmid glycoprotein (Ahsg, also known as fetuin-A) as an important inhibitor of ectopic calcification acting on the systemic level. Ahsg-deficient mice are phenotypically normal, but develop severe calcification of various organs on a mineral and vitamin D-rich diet and on a normal diet when the deficiency is combined with a DBA/2 genetic background. This phenotype is not associated with apparent changes in calcium and phosphate homeostasis, but with a decreased inhibitory activity of the Ahsg-deficient extracellular fluid on mineral formation. The same underlying principle may contribute to many calcifying disorders including calciphylaxis, a syndrome of severe systemic calcification in patients with chronic renal failure. Taken together, our data demonstrate a critical role of Ahsg as an inhibitor of unwanted mineralization and provide a novel therapeutic concept to prevent ectopic calcification accompanying various diseases.Journal of Clinical Investigation 09/2003; 112(3):357-66. · 15.39 Impact Factor
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Institutions
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2007
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University Hospital RWTH Aachen
Aachen, North Rhine-Westphalia, Germany
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