[Trends in treatment of rheumatic diseases].
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to Gerd-Rüdiger Burmester.
Explore the source record for details and available documents.
Human bone marrow-derived mesenchymal stem cells (MSCs) have been shown to differentiate into distinct mesenchymal tissues including bone and cartilage. The capacity of MSCs to replicate undifferentiated and to mature into cartilaginous tissues suggests these cells as an attractive cell source for cartilage tissue engineering. Here we show that the stimulation of human bone marrow-derived MSCs with recombinant bone morphogenetic protein-2 (BMP2) results in chondrogenic lineage development under serum-free conditions. Histological staining of proteoglycan with Alcian blue and immunohistochemical staining of cartilage-specific type II collagen revealed the deposition of typical cartilage extracellular matrix components. Semi-quantitative real-time gene expression analysis of characteristic chondrocytic matrix genes, such as cartilage link protein, cartilage oligomeric matrix protein, aggrecan, and types I, II, and IX collagen, confirmed the induction of the chondrocytic phenotype in high-density culture upon stimulation with BMP2 and transforming growth factor-beta3 (TGFbeta3). Histologic staining of mineralized extracellular matrix with von Kossa, immunostaining of type X collagen (typical for hypertrophic chondrocytes), and gene expression analysis of osteocalcin and adipocyte-specific fatty acid binding protein (aP2) further documented that BMP2 induced chondrogenic lineage development and not osteogenesis and/or adipogenesis in human MSCs. These results suggest BMP2 as a promising candidate for tissue engineering approaches regenerating articular cartilage on the basis of mesenchymal progenitors from bone marrow.
BACKGROUND/AIMS: Malnutrition is common among hospitalized patients. We investigated whether certain diseases predispose more frequently for malnutrition than others. METHODS: Nutritional state was assessed by clinical scores, anthropometry and bioimpedance analysis in 502 consecutively admitted patients in the departments of internal medicine in two hospitals in Berlin (n = 300, university hospital; n = 202, district hospital). The prevalence of malnutrition was compared in patient groups with a different diagnosis. RESULTS: Malnutrition was present in 24.2% of all patients. A clear association between diagnoses and malnutrition was found: the prevalence of malnutrition was significantly higher in malignant than in non-malignant diseases (50.9 vs. 21.0%, p < 0.0001). High prevalence rates >30% were observed in subgroups of patients with inflammatory bowel diseases, chronic heart failure and benign lung diseases. Patients with gastrointestinal diseases, however, were not more frequently malnourished than other medical patients (28.8 vs. 22.0%). Malnourished patients were significantly older (70.0 +/- 13.6 vs. 58.3 +/- 15.6 years, p < 0.0001) and had a 40% longer hospital stay (13.1 +/- 8.1 vs. 9.3 +/- 6.8 days, p < 0.0001) than well-nourished patients. CONCLUSIONS: Patients with malignancies, inflammatory bowel disease, chronic heart failure and benign lung diseases need special attention due to the high prevalence of malnutrition.
Autoimmune phenomena may precede or accompany lymphoid malignancies, especially B-chronic lymphocytic leukemia (B-CLL). We report a patient with a 7-year history of primary (idiopathic) cold agglutinin (CA) disease in whom B-CLL subsequently developed. Immunophenotyping and single-cell reverse transcription-polymerase chain reaction (RT-PCR) were applied to investigate the origin and diversification of leukemic B cells. The obtained data indicate a memory cell-type origin of the B-CLL cells. Remarkably, the IgV(kappa) genes of the B-CLL cells showed intraclonal diversity, whereas the mutational pattern of their paired IgV(H) genes were invariant. Thus, the light-chain-restricted intraclonal diversity in individual leukemic B cells in this patient strongly indicates a differential regulation or selection of the ongoing mutational process. Of note, our findings suggest that this B-CLL had developed from the patient's CA-producing B-cell population.
The adult bone marrow stroma contains a subset of nonhematopoietic cells referred to as mesenchymal stem or mesenchymal progenitor cells (MSC). These cells have the capacity to undergo extensive replication in an undifferentiated state ex vivo. In addition, MSC have the potential to develop either in vitro or in vivo into distinct mesenchymal tissues, including bone, cartilage, fat, tendon, muscle, and marrow stroma, which suggest these cells as an attractive cell source for tissue engineering approaches. The interest in modern biological technologies such as tissue engineering has dramatically increased since it is feasible to isolate living, healthy cells from the body, expand them under cell culture conditions, combine them with biocompatible carrier materials and retransplant them into patients. Therefore, tissue engineering gives the opportunity to generate living substitutes for tissues and organs, which may overcome the drawbacks of classical tissue reconstruction: lacking quality and quantity of autologous grafts, immunogenicity of allogenic grafts and loosening of alloplastic implants. Due to the prerequisite for tissue engineering to ensure a sufficient number of tissue specific cells without donor site morbidity, much attention has been drawn to multipotential progenitor cells such as embryonic stem cells, periosteal cells and mesenchymal stem cells. In this report we review the state of the art in tissue engineering with mesenchymal stem and mesenchymal progenitor cells with emphasis on bone and cartilage reconstruction. Furthermore, several issues of importance, especially with regard to the clinical application of mesenchymal stem cells, are discussed.
We describe a patient with primary biliary cirrhosis (PBC) and secondary Sjogren's syndrome (SS) with pulmonary involvement who developed a cutaneous T cell lymphoma. The clinical course of secondary SS in PBC is thought to be less complicated than in progressive systemic scleroderma and SS. In contrast to secondary SS, the risk for developing non-Hodgkin's lymphoma is highly increased in patients with primary SS. Moreover, these lymphomas are usually of B cell origin. There are few reports of T cell lymphoma in primary SS. The occurrence of a T cell lymphoma in a patient with PBC and secondary SS indicates the necessity to investigate lymphoma in patients with secondary SS.
CONTEXT: Glucocorticoids are frequently and successfully used drugs that mediate important immunosuppressive and anti-inflammatory effects. These drugs are also relatively inexpensive, but it is their broad range of adverse reactions that continuously stimulate efforts to optimise glucocorticoid treatment. STARTING POINT: Last year, Mary Leonard and colleagues studied 60 children and adolescents with nephrotic syndrome intermittently treated with high-dose glucocorticoids (N Engl J Med 2004; 351: 868-75). The patients received an average of 23 g glucocorticoids and were significantly shorter, had a significantly greater body-mass index, and the prevalence of obesity was significantly higher than in controls. The expected deficits in the bone-mineral content of the spine or whole body were not seen, although this finding could be attributed to the highly increased body-mass index of many of the patients. WHERE NEXT: Glucocorticoids are urgently needed to treat a wide range of diseases in children and adults. Therefore strategies such as preferred local application or fine-tuned dose regimens have been developed over the past five decades to improve the benefit-risk ratio. However, these efforts with conventional glucocorticoid drugs seem to have almost reached their limits. A further improvement needs qualitatively new drugs, which are currently in the development pipeline, with the most promising being the nitrosoglucocorticoids (nitrosteroids) and selective glucocorticoid-receptor agonists.