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Wednesday, 05/25/2016 5:22:29 PM

Wednesday, May 25, 2016 5:22:29 PM

Post# of 3833
In previous posts (sparse) I have implied that GALT is working from a sound scientific platform. Some aspects have been covered by Dr. Traber in public presentations. Importantly, if the gene which codes for the Galectin-3 protein in mice is "knocked out" (Gal-3 -/- mice) Fibrosis is significantly attenuated. That's a credential for a smoking gun.
In additional support I'm here citing the titles of four rigorous scientific publications bearing on the importance of Gal-3 in the mechanics of Fibrosis.
(1) N.C. Henderson et al. "Galectin-3 regulates myofibroblast activation and hepatic fibrosis" (2006).
(2) L. Li et al. "Functions of Galectin-3 and its role in fibrotic diseases" (2014).
(3) H.W. Zimmermann and F. Tacke "In search of the magic bullet: can liver inflammation and fibrosis be reversed with medications?" (2015).
(4) W, Hsieh, A.C. MacKinnon et al. "Galectin-3 regulates progenitor cell expression during liver injury" (2016).
Abstracts for these articles can be accessed by searching Google for the exact titles. Full texts may be acquired via Pub Med.
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