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Jeanette A.M. Maier

Researcher at University of Milan

Publications -  194
Citations -  8100

Jeanette A.M. Maier is an academic researcher from University of Milan. The author has contributed to research in topics: Endothelial stem cell & Endothelium. The author has an hindex of 42, co-authored 178 publications receiving 7071 citations. Previous affiliations of Jeanette A.M. Maier include W. Alton Jones Cell Science Center & University of Brescia.

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Cyclooxygenase is an immediate-early gene induced by interleukin-1 in human endothelial cells.

TL;DR: The data suggest that Cox is an immediate-early gene induced by IL-1 in HUVEC and may contribute to the regulation of the endothelial cell differentiation pathway in vitro.
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Extension of the life-span of human endothelial cells by an interleukin-1 alpha antisense oligomer

TL;DR: Treatment of human endothelial cell populations with an antisense oligodeoxynucleotide to the human IL-1 alpha transcript prevented cell senescence and extended the proliferative life-span of the cells in vitro, suggesting that human endothelium cellsenescence in vitro is a dynamic process regulated by the potential intracellular activity of IL- 1 alpha.
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Recovery of mitogenic activity of a growth factor mutant with a nuclear translocation sequence.

TL;DR: Attachment of the nuclear translocation sequence from yeast histone 2B at the amino terminus of HBGF-1U yields a chimeric polypeptide (HBGF- 1U2) with mitogenic activity in vitro and indicates that nuclear translocated is important for this biological response.
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Magnesium and the inflammatory response: Potential physiopathological implications

TL;DR: Experimental findings showing that magnesium modulates cellular events involved in inflammation suggest that inflammation is the missing link to explain the role of magnesium in many pathological conditions.
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In vivo cyclooxygenase expression in synovial tissues of patients with rheumatoid arthritis and osteoarthritis and rats with adjuvant and streptococcal cell wall arthritis.

TL;DR: Observations suggest that, in vivo, COX expression is upregulated in inflammatory joint diseases, the level of expression is genetically controlled and is a biochemical correlate of disease severity, sustained high level up-regulation is T cell dependent, and expression is down-regulated by antiinflammatory glucocorticoids.