Tibolone has tissue -selective estrogenic effects, with desirable effects in bone , the brain , and the vagina , and lack of undesirable action in the endometrium and breasts .  Its tissue selectivity is the result of metabolism , enzyme modulation (., of estrogen sulfatase and estrogen sulfotransferase ), and receptor modulation that vary in different target tissues, and differs mechanistically from that of selective estrogen receptor modulators (SERMs) such as tamoxifen , which produce their tissue-selectivity via means of modulation of the ER.   As such, to distinguish it from SERMs, tibolone has been described as a "selective tissue estrogenic activity regulator" (STEAR),  and also as a "selective estrogen enzyme modulator" (SEEM). 
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The precise mechanism of the antiinflammatory activity of topical steroids in the treatment of steroid-responsive dermatoses, in general, is uncertain. However, corticosteroids are thought to act by the induction of phospholipase A 2 inhibitory proteins, collectively called lipocortins. It is postulated that these proteins control the biosynthesis of potent mediators of inflammation such as prostaglandins and leukotrienes by inhibiting the release of their common precursor arachidonic acid. Arachidonic acid is released from membrane phospholipids by phospholipase A 2 .