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G-R Burmester

Publications and source records attributed to G-R Burmester.

28 records · Page 2Linked to original sources
PubMed2004

[Systemic inflammatory rheumatic diseases competence network].

The foundation of the competence network for rheumatology, which is funded by the "Bundesministerium für Bildung und Forschung" (BMBF) since 1999, succeeded to create a unique research structure in Germany: medical doctors and scientists from six university rheumatology centres (Berlin, Düsseldorf, Erlangen, Freiburg, Hannover und Lübeck/Bad Bramstedt) work closely together with scientists doing basic research at the Deutsches Rheuma-Forschungszentrum (DRFZ), with rheumatological hospitals, reha-clinics, and rheumatologists. Jointly they are searching for causes of systemic inflammatory rheumatic diseases and try to improve therapies-nationwide and with an interdisciplinary approach. The primary objective of this collaboration is to transfer new scientific insights more rapidly in order to improve methods for diagnosis and patients treatment.

Biomedical Research↗
PubMed2003

[Tissue engineering: chances and challenges for application in rheumatic diseases].

Current technologies of tissue engineering offer new strategies for the treatment of cartilage and bone defects. Beyond implantation of cell suspensions, second generation products of biomaterial enforced with in vitro preformed tissues are clinically applied. Ongoing research and development focus on differentiation factors and tissue protection. In search for sources of autologous cells which are easier to collect and which may serve for more complex tissues like osteochondral implants, mesenchymal stem cells are investigated. The design of in vitro experiments, which are required for these investigations, has produced tissue engineering technologies, which may serve for pathophysiology research in inflammatory joint diseases and for exploration of treatment strategies. These together with the advances in biological therapies of rheumatic diseases are the basis of new concepts, which promise application of tissue engineering also in inflammatory joint diseases.

Animals↗
PubMed2003

Bioenergetics of immune cells to assess rheumatic disease activity and efficacy of glucocorticoid treatment.

OBJECTIVE: To investigate whether activity and glucocorticoid treatment of rheumatic diseases are reflected by selected parameters of cellular energy metabolism of peripheral blood mononuclear cells (PBMC). METHODS: PBMC were obtained from 30 healthy volunteers, 28 patients (16 inactive; 12 active) with rheumatoid arthritis, systemic lupus erythematosus, vasculitis, or other autoimmune diseases, and five patients with infectious diseases. Patients with active rheumatic diseases were examined before and 4-5 days after starting, restarting, or increasing the dose of glucocorticoids. Cellular oxygen consumption (as a measure of ATP production), bioenergetic ability to be stimulated, and major ATP consuming processes were measured amperometrically with a Clark electrode. RESULTS: A normal value for oxygen consumption of 3.84 (SEM 0.1) (all data in nmol O(2)/min/10(7) cells) independent of sex was found. In patients with inactive disease the respiration rate was slightly higher, but was significantly increased in active patients to 4.82 (SEM 0.33) (p<0.001). PBMC from active patients showed a significantly lower bioenergetic response to a mitogenic stimulus than controls (p<0.05). In stimulated cells from active patients there was a significant reduction in cation transport and protein synthesis. All parameters above were almost normalised within 4-5 days upon optimised treatment with glucocorticoids. For comparison, PBMC from patients with active infectious diseases also showed an increased respiration rate; their response to mitogenic stimulation was even higher. CONCLUSIONS: This study shows for the first time that parameters describing the cellular function of PBMC in bioenergetic terms are suitable for (a) describing semiquantitatively the activity of a rheumatic disease and (b) assessing the therapeutic effect on the disease.

Adolescent↗
PubMed2002

Standardised nomenclature for glucocorticoid dosages and glucocorticoid treatment regimens: current questions and tentative answers in rheumatology.

In rheumatology and other medical specialties there is a discrepancy between the widespread use and the imprecise designation of glucocorticoid treatment regimens. Verbal descriptions of glucocorticoid treatment regimens used in various phases of diseases vary between countries and institutions. Given this background, a workshop under the auspices of the EULAR Standing Committee on International Clinical Studies including Therapeutic Trials was held to discuss this issue and to seek a consensus on nomenclature for glucocorticoid treatment. This report summarises the panel's discussion and recognises that answers derived from consensus conferences are not definitive. Nevertheless, recommendations on glucocorticoid treatment are presented that (1) reflect current and best knowledge available and (2) take into account current clinical practice. A question-answer rationale presentation style has been chosen to convey the messages, to summarise the meeting in a readable format, and to avoid dogmatism.

Drug Administration Schedule↗
PubMed2002

T cell reactivity against the SmD1(83-119) C terminal peptide in patients with systemic lupus erythematosus.

BACKGROUND: The SmD1(83-119) peptide is a major target of the B cell response in patients with systemic lupus erythematosus (SLE). OBJECTIVE: To investigate the T cell response directed against this peptide, its disease specificity, and possible impact on SLE pathogenesis. METHODS: Peripheral blood mononuclear cells derived from 28 patients with SLE and 29 healthy and disease controls were stimulated by the SmD1(83-119) and the recombinant (r)SmD1 protein, and [3H]thymidine incorporation was measured. Patients with SLE were simultaneously tested for autoantibodies, disease activity, clinical symptoms, and medical treatments. RESULTS: T cell reactivity against the SmD1(83-119) peptide was detected in 11/28 (39%) patients with SLE and against the rSmD1 protein in 10/28 (36%) patients. In contrast, only 2/29 (7%) controls exhibited SmD1 reactivity. An analysis of proliferation kinetics showed that SmD1 reactive T cells are activated in vivo, as additionally confirmed by cytometric analysis. Addition of mammalian dsDNA to rSmD1 enhanced the rSmD1-specific T cell response. SmD1(83-119)-specific T cell reactivity was significantly more common in patients with cardiac and pulmonary symptoms. No correlation between T and B cell responses and disease activity was seen. CONCLUSION: SmD1(83-119) is a major T cell epitope of SmD1, commonly recognised by T cells from patients with SLE and much less commonly found by healthy or disease controls. This strong T cell reactivity as well as the high frequency and specificity of anti-SmD1(83-119) antibodies in SLE suggest a possible role in SLE pathogenesis, at least in a subset of patients.

Adult↗
PubMedDate not supplied

Effects of dexamethasone and celecoxib on calcium homeostasis and expression of cyclooxygenase-2 mRNA in MG-63 human osteosarcoma cells.

OBJECTIVE: Glucocorticoids and selective COX-2 inhibitors are potent anti-inflammatory agents. They are also suggested to influence bone physiology and remodeling. Here we searched for effects of dexamethasone and celecoxib on crucial parameters of bone physiology that could be therapeutically relevant. METHODS: The human osteosarcoma cell line MG-63 was used to measure effects of these drugs on (i) intracellular calcium concentration ([Ca2+]i) using a microfluorometric technique, (ii) alkaline phosphatase and osteocalcin levels (EIA) and (iii) the expression of cox-2 mRNA (quantitative real time PCR). Measurements were performed in Vitamine D-incubated quiescent cells and in cells stimulated with TNF-alpha and IL-1beta. RESULTS: We found the cytokine-stimulation to increase [Ca2+]i which was prevented by dexamethasone already after 30 min and still after 48 h. Dexamethasone was without any effect on [Ca2+]i in quiescent cells. Celecoxib had no measurable short-term or long-term effects neither in quiescent nor in stimulated cells. Vitamin D stimulated the expression of cox-2 mRNA which was further enhanced by TNF-alpha/IL-1beta. Dexamethasone did not have any measurable effects on COX-2 expression after 30 min, but a pronounced inhibition was seen after 48 h. In contrast, celecoxib had no effect on COX-2 expression. Neither of the drugs had any effect on the secretion of alkaline phosphatase and osteocalcin. CONCLUSION: We found dexamethasone to inhibit the [Ca2+]i increase in MG-63 cells following stimulation and to reduce considerably COX-2 expression via the genomic pathway. In contrast, celecoxib did not show any measurable short-term or long-term effects on the parameters of bone physiology measured.

Alkaline Phosphatase↗