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Ulf Müller-Ladner

Researcher at University of Giessen

Publications -  644
Citations -  32784

Ulf Müller-Ladner is an academic researcher from University of Giessen. The author has contributed to research in topics: Medicine & Arthritis. The author has an hindex of 77, co-authored 590 publications receiving 27658 citations. Previous affiliations of Ulf Müller-Ladner include University of Regensburg & University of Genoa.

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Actual status of antiinterleukin-1 therapies in rheumatic diseases.

TL;DR: Owing to the observation that IL-1 is not only involved in signaling processes resulting in autoimmune and crystal-induced joint destruction but also in several hereditary autoinflammatory syndromes, its value has significantly improved in the past years leading to an enrichment of the current therapeutic armamentarium for the affected patients.
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Identification of differentially expressed genes in rheumatoid arthritis by a combination of complementary DNA array and RNA arbitrarily primed-polymerase chain reaction

TL;DR: The results show that RAP-PCR combined with cDNA arrays is a suitable method for identifying differentially expressed genes in rheumatoid synovial fibroblasts, using very small amounts of RNA.
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Targeting cathepsin L (CL) by specific ribozymes decreases CL protein synthesis and cartilage destruction in rheumatoid arthritis.

TL;DR: Rozymes targeting CL could be a novel and efficient tool to inhibit joint destruction in RA and reduce cartilage destruction in in vitro and in vivo models.
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High frequency of corticosteroid and immunosuppressive therapy in patients with systemic sclerosis despite limited evidence for efficacy.

TL;DR: Despite limited evidence for the effectiveness of corticosteroids and immunosuppressive agents in SSc, these potentially harmful drugs are frequently prescribed to patients with all forms of S sc, indicating the need to develop and communicate adequate treatment recommendations.
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Activation of the IL-4 STAT pathway in rheumatoid synovium.

TL;DR: Examination of rheumatoid arthritis synovial frozen sections of patients with short-term and long-term disease and in situ hybridization and immunohistochemistry indicates that IL-4 STAT is involved in key pathomechanisms in RA synovium and that IL -4 STAT-dependent pathways operate in early and late stages of the disease.