A5090127748- Diabetes and associated disorders
- Pancreatic function and diabetes
- Diabetes Management and Research
- Adipokines, Inflammation, and Metabolic Diseases
- Immune Cell Function and Interaction
- Diet, Metabolism, and Disease
- T-cell and B-cell Immunology
- Nitric Oxide and Endothelin Effects
- Diabetes Treatment and Management
- Glycosylation and Glycoproteins Research
- Immune Response and Inflammation
- Metabolism, Diabetes, and Cancer
- Adipose Tissue and Metabolism
- Heat shock proteins research
- Atherosclerosis and Cardiovascular Diseases
- Diabetes Management and Education
- Diet and metabolism studies
- Monoclonal and Polyclonal Antibodies Research
- Diabetes, Cardiovascular Risks, and Lipoproteins
- Hyperglycemia and glycemic control in critically ill and hospitalized patients
- Cell Adhesion Molecules Research
- Erythrocyte Function and Pathophysiology
- Dietary Effects on Health
- Endoplasmic Reticulum Stress and Disease
- Pancreatitis Pathology and Treatment
Heinrich Heine University Düsseldorf
2012-2023
Deutsches Diabetes-Zentrum e.V.
2008-2023
Verbund Katholischer Kliniken Düsseldorf
2013-2019
German Center for Diabetes Research
1973-2013
Düsseldorf University Hospital
2012
Dorn Research Institute
2009
Universität Ulm
2003-2006
University of North Carolina at Chapel Hill
2005-2006
Heidelberg University
2005
Hochschule Düsseldorf University of Applied Sciences
2004
Abstract Human heat shock protein 60 (hsp60) elicits a potent proinflammatory response in cells of the innate immune system and therefore has been proposed as danger signal stressed or damaged cells. We report here that macrophages C3H/HeJ mice, carrying mutant Toll-like-receptor (Tlr) 4 are nonresponsive to hsp60. Both induction TNF-α NO formation were found dependent on functional Tlr4 whereas stimulation by CpG DNA was independent. conclude mediates hsp60 signaling. This is first putative...
Abstract Mammalian 60-kDa heat-shock protein (hsp60) is a key target of T cell and Ab responses in chronic inflammation or atherosclerosis. We show this study that human hsp60 also an Ag recognized by cells the innate immune system, such as macrophages. Both mouse macrophages respond to contact with exogenous rapid release TNF-α; addition produce nitric oxide. The proinflammatory macrophage response dose dependent similar kinetics extent LPS stimulation. Human was found synergize IFN-γ its...
The underlying cause of type 1 diabetes, loss beta-cell function, has become the therapeutic target for a number interventions in patients with diabetes. Even though insulin therapies continue to improve, it remains difficult achieve normal glycemic control especially long term. associated risks hypoglycemia and end-organ diabetic complications remain. Retention function diabetes is known result improved reduced hypoglycemia, retinopathy, nephropathy. To facilitate development aimed at...
Specific autoantibodies characterize type 1 diabetes in childhood but are also found adult-onset diabetes, even when initially non-insulin requiring, e.g., with latent autoimmune (LADA). We aimed to diabetes.
OBJECTIVE Ingestion of probiotics can modify gut microbiota and alter insulin resistance diabetes development in rodents. We hypothesized that daily intake Lactobacillus reuteri increases sensitivity by changing cytokine release secretion via modulation the glucagon-like peptides (GLP)-1 -2. RESEARCH DESIGN AND METHODS A prospective, double-blind, randomized trial was performed 21 glucose-tolerant humans (11 lean: age 49 ± 7 years, BMI 23.6 1.7 kg/m2; 10 obese: 51 35.5 4.9 kg/m2)....
Background: Previous studies have suggested that lowgrade systemic inflammation is involved in the pathogenesis of type 2 diabetes mellitus.Objective: To investigate association between Creactive protein (CRP), classic acute-phase protein, and incident mellitus among middle-aged men.Methods: A total 2052 initially nondiabetic men aged 45 to 74 years who participated 1 3 MONICA (Monitoring Trends Determinants Cardiovascular Disease) Augsburg surveys 1984 1995 were followed up for an average...
Activation of the nuclear enzyme poly(ADP-ribose) polymerase (PARP) is an early response cells exposed to DNA-damaging compounds such as nitric oxide (NO) or reactive oxygen intermediates (ROI). Excessive poly-(ADP-ribose) formation by PARP has been assumed deplete cellular NAD+ pools and induce death several cell types, including loss insulin-producing islet in type I diabetes. In present study we used from mice with a disrupted thus inactivated gene provide direct evidence for causal...
Beta-cell function in type 1 diabetes clinical trials is commonly measured by C-peptide response to a secretagogue either mixed-meal tolerance test (MMTT) or glucagon stimulation (GST). The Type Diabetes TrialNet Research Group and the European Trial (ECPT) Study conducted parallel randomized studies compare sensitivity, reproducibility, tolerability of these procedures.In sequences, 148 subjects completed 549 tests with up 2 MMTT GST on separate days, 118 ECPT 348 (up 3 each) two MMTTs...
Type 1 diabetes results from an immune-mediated destruction of pancreatic beta cells. The disease can be transmitted by bone marrow transplantation in humans1 and animals.2,3 Furthermore, T cells that are reactive to several islet autoantigens have been identified both mice humans.4,5 Although it is generally accepted a role during the process, possible B autoantibodies type humans has not fully resolved. When they activated, produce beta-cell antigens — such as glutamic acid decarboxylase...