Bryan said:
S Foote. said:
OK Bryan, you have shown us you can't comprehend the significance of that study to the point in hand. I am not going to waste any more of my time trying to teach you scientific deduction.
People reading this can see that i have answered your question, even if you don't understand the answer.
Oh, my goodness...ending our little discussion with a whimper, Stephen?
Let the record show, for posterity, that no matter how hard he's looked (and there's no doubt at all in my mind that he's searched REALLY hard), Mr. Stephen Foote has never been able to find a single example in biology where contact inhibition causes a "flip" in the way that a given tissue reacts to androgens. He has utterly FAILED at that task. That's a pity, because if he could find such an example, it might lend a tiny bit of credibility to his unusual theory. But alas, it looks like it simply is not to be...
Bryan
Pretty pathetic response, even by your standards Bryan :roll:
If you had any true scientific aptitude, you would easily see the validity of my argument in the context of the in-vitro issue.
I have also referenced a study that showed prior contact inhibition and the activity of TGF Beta-1, the growth factor active in the in-vitro follicle studies, are linked. This is the abstract:
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Cell cycle arrest in G0/G1 phase by contact inhibition and TGF-beta 1 in mink Mv1Lu lung epithelial cells.
Wu F, Buckley S, Bui KC, Yee A, Wu HY, Liu J, Warburton D.
Department of Surgery, Children's Hospital of Los Angeles, California, USA.
We postulated that contact inhibition and transforming growth factor (TGF)-beta 1 may target the same molecules to negatively regulate the Mv1Lu cell cycle in G0/G1. Both contact inhibition and TGF-beta 1 suppressed the expression of a 45-kDa protein (p45); cyclins D2 and B1; cyclin-dependent protein kinase (Cdk)-4, Cdc-2, and Cdc-2-associated activity; and the phosphorylation of retinoblastoma tumor-suppressor protein (pRb) but did not affect the expression of cyclins D1, E, and A or the expression of Cdk-2 and Cdk-5. Expression of p45 reappeared 12 h after release from contact inhibition and 6-8 h after release from TGF-beta 1, while TGF-beta 1 prevented release from contact inhibition and maintained suppression of both p45 and cyclin D2. Additionally, cyclin D2 phosphorylation and its associated kinase activity were strongly inhibited by contact inhibition and TGF-beta 1. Thus suppression of p45, cyclin D2/Cdk-4, and cyclin B1/Cdc-2 expression and/or activities is targeted both by contact inhibition and by TGF-beta 1 and may define common mechanisms through which these negative growth signals are integrated.
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But again you just can't comprehend the significance of this can you Bryan :wink:
People will again note that you don't even attempt to give us any references for "your" explaination Bryan 8) So i will borrow your phrasing from above!
Let the record show, for posterity, that no matter how hard he's looked (and there's no doubt at all in my mind that he's searched REALLY hard), Mr. Bryan Shelton has never been able to find a single example in biology where contact with androgens over time, causes a "flip" in the way that a given tissue reacts to androgens. He has utterly FAILED at that task.
S Foote.