michael barry said:Wook,
Its Wnt signalling that Costarialis and Stenn were working with. Minxoidil supposeldy ups Wnt signalling...
Wnt proteins can induce cell growth and loss of contact inhibition.
large mechanical stress suppresses growth and triggers apoptosis
I want Wnt! Or do I...
That’s really “WOW!†So, why don’t we rub our scalps with Wnt? As these furry mice aged, they grew benign lumps in their skin that resembled a common human scalp tumor called pilotricoma. But, if we learn to deliver Wnt in a pattern that mimics nature or if we can manipulate other steps in the Wnt signaling cascade, we may have a way to correct disorders of the hair, including male pattern baldness.
michael barry said:Bryan (and Stephen), let me run something by you both.
Kurt Stenn and George Costarialis have been fooling around with Wnt-pathways and wound healing regenerating brand new hairs in mice. If they can make pure skin re-organize itself into brand new follicles in humans, then I see no reason that they cant "wound" donor area skin by an FUE transplant, move the donor hair up front, and put Wnt protiens in the new "wounds" created in the former donor area, ............thus creating brand new hair back there with DONOR area genetics. Guys see any problems with this?
michael barry said:Stephen,
my idea with the WNT was not what you think it was.
It was to use it in the context of a FUE transplant. Get a FUE-job done..................and in the donor area where the FUE-hairs have been taken out, cover the wound with Wnt protiens for a few weeks (thats all they were doing with the mice, not months or years), and have new follicles regenerate in the donor area. The hair that was moved up front would be like a tradtional transplant.
Did you look at the ACELL pictures of new hair growing on the dogs where there were deep skin wounds (all the way to the bone on a couple of the animals). Thast done with some pig cells or whatnot. Joetronic, a transplant salesguy with Hasson and Wong in Vancouver, is in communication with these folks for the same type strategy as I mentioned above with the Wnt protocol.
michael barry said:Doctor,
I did not know that balding scalp cells would inhibit normal scalp cells or rat cells in vitro.
Thats kinda depressing to be honest. Makes you wonder about " the very close surround" doesn't it?
michael barry said:Wook.............................can you provide any proof that there is increased "scalp tension" in an X-shape pattern over the top of the skull? THE SIDES of my scalp are tighter than my recessed temples or thick vertex. I can move the temples with less effort than it takes to move the sides or back or vertex. I have never heard of experiments being done to assess that....................maybe doing the scalp excercise for the past few years has made my scalp very malleable though, so perhaps Im not a good test subject.
wookster said:Which theory is most correct? the molecular interaction theory or the Foote contact inhibition idea?
You mentioned something about transplanting balding follicles anywhere on the human body, not just the scalp, and those follicles will continue to miniaturize. If that is true then ther molecular theory appears to be the most correct one...
wookster said:How many times has that particular experiment been rigorously tested and repeated? I know it cannot be based on JUST the Nordstom study???
Bryan said:wookster said:Which theory is most correct? the molecular interaction theory or the Foote contact inhibition idea?
You mentioned something about transplanting balding follicles anywhere on the human body, not just the scalp, and those follicles will continue to miniaturize. If that is true then ther molecular theory appears to be the most correct one...
BINGO!!![]()
wookster said:How many times has that particular experiment been rigorously tested and repeated? I know it cannot be based on JUST the Nordstom study???
Hmmm... Well, Orentrich did something similar to that in his original late 1950's study on hair transplantation, but I'm sure he didn't do it with anywhere nearly the same rigor and precision that Nordstrom did. Orentreich simply rotated hair follicles of both classes to both kinds of scalp areas to cover all the possible permutations (balding follicles to balding areas of scalp, balding follicles to non-balding areas of scalp, non-balding follicles to non-balding areas of scalp, and non-balding follicles to balding areas of scalp), and found donor dominance in all four cases (balding follicles to non-balding areas of scalp stayed bald). But it was Nordstrom who really demonstrated that effect with precision and great generality by even transplanting balding follicles to someone's ARM, with the same presentation of donor dominance, much to Stephen Foote's consternation! :wink:
S Foote. said:According to my theory, it is the `pressure' conditions in the tissue around the follicles, that effects their growth in anagen through normal contact inhibition. Any such `change' in tissue pressure will `NOT' effect existing scalp follicles already in anagen. Such a pressure change will only effect these follicles when they go through another normal cycle and re-enter anagen.
The balding tissue transplanted to the body in Norstrom's experiment, is `swollen' tissue. The edema that started the balding process, has `already' condemed the remaining follicles in these `large' grafts. As soon as they enter anagen again, the tissue `re-modeling' and micro- fibrosis caused by the prior edema, is `still' going to cause further balding as subsequent follicles try to re-enlarge in anagen again.
The now better drainage conditions in the surrounding body tissue, may over time allow some growth improvement, `BUT' because of the large size of the grafts used in Norstrom's study, this would likely take a lot longer than the duration of Norstrom's observations, and also depend on the pre-existing fibrotic conditions. Fibrosis was not a recognised factor in male pattern baldness at the time of this study!!!!!!
In contrast, the `healthy' follicle grafts transplanted to the body, are devoid of any pre-existing adverse tissue conditions like follicle fibrosis, and would likely benefit from the reduced fluid pressure `feed' into these grafts created by the transplantation process itself.
This seemed to be the case as these grafts improved growth slightly.
This is how my theory explains Norstroms observations with these large grafts over the test period.
wookster said:Mr. Foote gives an interesting explanation:
http://www.gourmetstylewellness.com/discussions ... 18&start=0
S Foote. said:According to my theory, it is the `pressure' conditions in the tissue around the follicles, that effects their growth in anagen through normal contact inhibition. Any such `change' in tissue pressure will `NOT' effect existing scalp follicles already in anagen. Such a pressure change will only effect these follicles when they go through another normal cycle and re-enter anagen.
The balding tissue transplanted to the body in Norstrom's experiment, is `swollen' tissue. The edema that started the balding process, has `already' condemed the remaining follicles in these `large' grafts. As soon as they enter anagen again, the tissue `re-modeling' and micro- fibrosis caused by the prior edema, is `still' going to cause further balding as subsequent follicles try to re-enlarge in anagen again.
S Foote. said:The now better drainage conditions in the surrounding body tissue, may over time allow some growth improvement, `BUT' because of the large size of the grafts used in Norstrom's study, this would likely take a lot longer than the duration of Norstrom's observations, and also depend on the pre-existing fibrotic conditions.
S Foote. said:This is how my theory explains Norstroms observations with these large grafts over the test period.
Bryan said:wookster said:Mr. Foote gives an interesting explanation:
http://www.gourmetstylewellness.com/discussions ... 18&start=0
It's pure Foote-ian ad hoc bullshit. Let's take a look at his claims:
S Foote. said:According to my theory, it is the `pressure' conditions in the tissue around the follicles, that effects their growth in anagen through normal contact inhibition. Any such `change' in tissue pressure will `NOT' effect existing scalp follicles already in anagen. Such a pressure change will only effect these follicles when they go through another normal cycle and re-enter anagen.
The balding tissue transplanted to the body in Norstrom's experiment, is `swollen' tissue. The edema that started the balding process, has `already' condemed the remaining follicles in these `large' grafts. As soon as they enter anagen again, the tissue `re-modeling' and micro- fibrosis caused by the prior edema, is `still' going to cause further balding as subsequent follicles try to re-enlarge in anagen again.
Notice his lack of consistency here. The alleged fibrosis around the follicles should at least maintain their current size, but for some reason they continued to miniaturize, in lock-step with the other balding follicles still on the patient's scalp. Coincidence? I think not! :wink:
BTW, how come there wasn't any of that "scaffolding" in those transplants, also protecting the current size of the follicles, which he has used as an excuse to explain the success of transplanted non-balding hair follicles into areas of alleged "edema"? Do you see his lack of consistency, and how he'll use any ad hoc excuses he can think of, just to try to keep his theory afloat?
S Foote. said:No lack of consistency at all Bryan, just a lack of basic inteligence on your part. :roll:
S Foote. said:The excuse of lack of oxygen, is the industries way of trying to cover up contined balding over time in alledged "resistent" grafts. The importance of Nordstroms early study is it proves this excuse wrong! :wink: