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Martin Lotz

Researcher at Scripps Research Institute

Publications -  382
Citations -  33862

Martin Lotz is an academic researcher from Scripps Research Institute. The author has contributed to research in topics: Cartilage & Chondrocyte. The author has an hindex of 97, co-authored 343 publications receiving 30942 citations. Previous affiliations of Martin Lotz include Japan Agency for Medical Research and Development & University of California, San Diego.

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Induction of cytokine expression by leukemia inhibitory factor.

TL;DR: The results suggest that through the induction of cytokines, LIF can modulate inflammation, immune responses, and connective tissue metabolism, and act as a pathogenetic mediator in different disease states.
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Biomechanics of cartilage articulation: effects of lubrication and degeneration on shear deformation.

TL;DR: During articulation, peak cartilage shear is highest near the articular surface and decreases markedly with depth, and with degeneration and diminished lubrication, the markedly increased cartilageShear strain near theArticular surface may contribute to progressive cartilage deterioration and osteoarthritis.
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Biomechanical, structural, and biochemical indices of degenerative and osteoarthritic deterioration of adult human articular cartilage of the femoral condyle

TL;DR: Even in the cartilage of knees exhibiting overt fibrillation but not extensive erosions characteristic of clinical osteoarthritis, most features of advanced cartilage degeneration were present, providing evidence of coordinated mechanical dysfunction, collagen network remodeling, and surfacefibrillation.
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Regulation of Epstein-Barr virus infection by recombinant interferons: selected sensitivity to interferon-γ

TL;DR: Of the three recombinant IFN, only IFN‐γ reduced EBV‐induced proliferation and Ig secretion when added 3–4 days after virus infection;IFN‐α/β were only effective up to 24 h; and B lymphoblastoid lines already transformed by EBV are insensitive to the anti‐proliferative actions of all three types of IFN.