M
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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Journal ArticleDOI
Immunostimulatory DNA Sequences Necessary for Effective Intradermal Gene Immunization
Yukio Sato,Mark Roman,H Tighe,Delphine J. Lee,Maripat Corr,Minh-Duc Nguyen,Gregg J. Silverman,Martin Lotz,Dennis A. Carson,Eyal Raz +9 more
TL;DR: Although ISS are necessary for gene vaccination, they down-regulate gene expression and thus may interfere with gene replacement therapy by inducing proinflammatory cytokines.
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Effect of neuropeptides on production of inflammatory cytokines by human monocytes
TL;DR: The findings identify a potent mechanism for nervous system regulation of host defense responses in inflammation and immunity and since neuropeptides can be released from peripheral nerve endings into surrounding tissues.
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Cytokines in symptomatic asthma airways.
David H. Broide,Martin Lotz,Anthony J. Cuomo,David A. Coburn,Edward C. Federman,Stephen I. Wasserman +5 more
TL;DR: In episodes of asthma, several cytokines, including TNF, GM-CSF, IL-1 beta, IL,2, and IL-6 are detectable in BALF, suggesting activation of alveolar macrophages and T cells.
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Direct Human Cartilage Repair Using Three-Dimensional Bioprinting Technology
TL;DR: The importance of direct cartilage repair and promising anatomic cartilage engineering using 3D bioprinting technology is indicated and the need to integrate implants with surrounding native tissues is highlighted.
Journal Article
Chondrocyte apoptosis induced by nitric oxide.
TL;DR: In this paper, the role of NO and IL-1 in the induction of chondrocyte cell death was analyzed, and it was shown that NO alone is not the primary inducer of cell death.