Pillows, Pillows, Pillows..??..

[Bryan]

BTW, I apologize if I appear to be pressing everybody on this specific issue! It's just that except for Stephen and me in multiple past posts, nobody else has really addressed it until now...

 

[michael barry]

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?




Here is the article that came out about it a couple of months back:

First Demonstration of New Hair Follicle Generation in an Animal Model



Implications for Treating Hair Loss, Skin Disorders, According to Penn Study

PHILADELPHIA, May 16 /PRNewswire-USNewswire/ --

Researchers at the University of Pennsylvania School of Medicine have found that hair follicles in adult mice regenerate by re-awakening genes once active only in developing embryos. These findings provide unequivocal evidence for the first time that, like other animals such as newts and salamanders, mammals have the power to regenerate. These findings are published in the May 17 issue of Nature.

A better understanding of this process could lead to novel treatments for hair loss, other skin and hair disorders, and wounds.
"We showed that wound healing triggered an embryonic state in the skin which made it receptive to receiving instructions from wnt proteins," says senior author George Cotsarelis, MD, Associate Professor of Dermatology.

"The wnts are a network of proteins implicated in hair-follicle development."

Researchers previously believed that adult mammal skin could not regenerate hair follicles. In fact, investigators generally believe that
mammals had essentially no true regenerative qualities. (The liver can regenerate large portions, but it is not de novo regeneration; some of the original liver has to remain so that it can regenerate.)

In this study, researchers found that wound healing in a mouse model created an "embryonic window" of opportunity. Dormant embryonic molecular pathways were awakened, sending stem cells to the area of injury. Unexpectedly, the regenerated hair follicles originated from
non-hair-follicle stem cells.

"We've found that we can influence wound healing with wnts or other proteins that allow the skin to heal in a way that has less scarring and
includes all the normal structures of the skin, such as hair follicles and oil glands, rather than just a scar," explains Cotsarelis.
By introducing more wnt proteins to the wound, the researchers found that they could take advantage of the embryonic genes to promote
hair-follicle growth, thus making skin regenerate instead of just repair.

Conversely by blocking wnt proteins, they also found that they could stop the production of hair follicles in healed skin.
Increased wnt signaling doubled the number of new hair follicles. This suggests that the embryonic window created by the wound-healing process can be used to manipulate hair-follicle regeneration, leading to novel ways to treat hair loss and hair overgrowth.

These findings go beyond just a possible treatment for male-pattern baldness. If researchers can effectively control hair growth, then they
could potentially find cures for people with hair and scalp disorders, such as scarring alopecia where the skin scars, and hair overgrowth.

This research was funded in part by the National Institute of Arthritis, Musculoskelatal and Skin Disease and the Pennsylvania Department
of Health. Other co-authors in addition to Cotsarelis are Mayumi Ito, Zaixin Yang, Thomas Andl, Chunhua Cui, Noori Kim, and Sarah E. Millar, all from Penn.

Cotsarelis and Ito are listed as inventors on a patent application related to hair-follicle neogenesis and owned by the University of
Pennsylvania. Cotsarelis also serves on the scientific advisory board and has equity in Follica, a start-up company that has licensed the patent from the University of Pennsylvania. Cotsarelis was also a co-founder of Follica.

This release and a related image can be viewed at http://www.pennhealth.com/news.

PENN Medicine is a $2.9 billion enterprise dedicated to the related missions of medical education, biomedical research, and high-quality
patient care. PENN Medicine consists of the University of Pennsylvania School of Medicine (founded in 1765 as the nation's first medical school) and the University of Pennsylvania Health System.

Penn's School of Medicine is ranked #2 in the nation for receipt of NIH research funds; and ranked #3 in the nation in U.S. News & World Report's most recent ranking of top research-oriented medical schools. Supporting 1,400 fulltime faculty and 700 students, the School of Medicine is recognized worldwide for its superior education and training of the next generation of physician-scientists and leaders of academic medicine.

The University of Pennsylvania Health System includes three hospitals, all of which have received numerous national patient-care honors [Hospital of the University of Pennsylvania; Pennsylvania Hospital, the nation's first hospital; and Penn Presbyterian Medical Center]; a faculty practice; a primary-care provider network; two multispecialty satellite facilities; and home care and hospice.



SOURCE University of Pennsylvania School of Medicine






....................Me again, when I first saw this I thought, "so what, you'll just have more male pattern baldness hair", but now when I think about it..........it seems like it could aid a conventional FUE transplant into being a real cure for baldness.




By the way, have any of you noted the hair-regrowth in animals with the ACELL (it comes from pig cells) product in testing? Look at these pictures and pay attention to how the hair as well as skin regrows in dogs.:
http://acell.com/vetcases/chadwick.html

http://acell.com/vetcases/fancy.html

http://acell.com/vetcases/lucille.html

http://acell.com/vetcases/twinkie.html (the most impressive one)


I think this could be used much the same way as the Wnt-protiens, with a FUE transplant back in the FUE-'wounds' in the back of the head, regerating new donor area hair.





Have you two followed any of this stuff? Its very exciting.

BTW----for Stephen, ICX has shown their first cloning photo over at hairsite. There is definetely new hair growth from dermal papilla cell injects. It was one cm2 from phase 1, phase 2 test results should be in from England later this year. Im hoping they will release more pics.............



Didn't mean to hijack the thread with the "newish" therapies, but thought everyone would enjoy a look.




Bryan,

I guess Im stumped on how hair "becomes" male pattern baldness. I was thinking that once androgen receptor expression and alpha five activity reaches a certain point, that it would be too much for given hairs located in particular parts of the scalp------------------while other hairs would be fine and dandy still. I was assuming this was the reason that having numerous androgen receptors and elevated alpha five levels in balding scalp even mattered. If its just a case of "sensitive or not sensitive", then I suppose men with alot of DHT transcription (think Jose Canseco) would still not be affected at all. I freely admit Im nowhere near smart enough to really intelligently postulate on prescision genetic matters at sub-cellular levels. Its fun to guess though....................

 

[wookster]

Stephen Foote's contact inhibition idea explains much :hairy:

The David Hatch engineering theory might not be 100% correct but it is interesting. Pressure from mechanical stress provides the required contact inhibition :hairy:

http://www.malepatternbaldness.net/

Wook,


Its Wnt signalling that Costarialis and Stenn were working with. Minxoidil supposeldy ups Wnt signalling...

:hairy:

http://www.pubmedcentral.nih.gov/botren ... tid=110627

Wnt proteins can induce cell growth and loss of contact inhibition.

http://www.kitp.ucsb.edu/~shraiman/BIS_mech_PNAS.pdf

large mechanical stress suppresses growth and triggers apoptosis

http://www.gourmetstylewellness.com/newsletter/article203.htm

I want Wnt! Or do I...

That’s really “WOW!â€￾ 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.

 

[S Foote.]

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?

The problem as Fuchs found out, was that you have to be very careful with Wnt's or you will get tumours. Wnts is involved in the contact inhibition process as i have referenced before, and messing with contact inhibition can cause tumours. The main problem would be approval of such a treatment in humans.

Personaly, i don't think the "cure" lies in generating "new" follicles like this, even if this was possible in the male pattern baldness area. Remember i don't think follicles are any "different", and will respond to male pattern baldness in the same way without a external matrix as i argued before.

Remember that immune mouse study where human male pattern baldness follicles enlarged? I think male pattern baldness follicles can recover given the right "external" conditions.

That mouse study is yet another reason why i don't read too much into the relevance of the in-vitro studies.

This is from the EHRS, poster presentation 6:

Study of Cell Senescence in Cultured
Primary Balding and Non-Balding
Dermal Papilla Cells
A.W. Bahta
Dermatology (QMUL), London, UK
The dermal papilla (DP) expresses androgen receptors and is
known to control normal hair growth. The paradox of androgen action
in human hair growth is well established but the molecular mechanisms
are poorly understood. DP cells derived from frontal (balding)
human scalp hair follicles (BDPC) are used to study androgenetic
alopecia. Cultured BDPC are known to have a much slower rate of
growth in vitro than DP from non-balding sites (NBDPC), however,
the cause of this has not been reported. In this study we have investigated
the growth of human BDPC and NBDPC in vitro. We observed
that BDPC have a limited life span of 2–6 passages. We observed that
from passage 2 onwards BDPC but not NBDPC showed a large flattened
morphology characteristic of senescent fibroblasts and that
once they had assumed this morphology they could no longer be
passaged. We showed that these BDPC but not NBDPC of the same
passage expressed senescence-associated -galactosidase activity at
pH-6. Moreover, stress-induced premature senescence was induced
with more prominent characteristic behaviour in BDPC than NBDPC
after exposure to sub-cytotoxic levels of H2O2 a known inducer of
oxidative stress. Finally BDPC also expressed a wide range of oxidative
stress markers including HSP27, Super Oxide Dismutase and
Catalase. These data suggest that the well documented, slower in vitro
proliferative rate of BDPC is due in part to premature senescence.
Moreover, our observation that cultured BDPC express markers of
oxidative stress and their response to H2O2 suggest that oxidative
stress may play a major role in male pattern hair loss. Others and we
have observed that DHT is able to induce TGF-1 in BDPC. TGF-1
is known to induce oxidative stress and this may therefore, link androgens
with oxidative stress and help explain the paradox of androgen
action on hair growth.

This shows a basic difference in the culturing response "before" androgens are introduced in the experiment.

During the culturing there are "NO" androgens involved at all. So why don't these bald cells then recover and grow like the other samples?

According to this, even if we remove every last androgen molecule from male pattern baldness follicles, they are still "screwed" growth wise!

Do you think that is so in-vivo?

That mouse study using whole human male pattern baldness follicles in an in-vivo model tells a different story, even in the presence of "some" androgens!

I have said before that variations on that immune mouse study should be done, and are vital to further understanding of male pattern baldness.

S Foote.

 

[michael barry]

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.

 

[docj077]

Michael Barry,

Just a little food for thought. Did you know that if you take normal scalp cells and put them with human scalp dermal papillae or rat whisker dermal papillae you will see that normal scalp actually potentiates the growth of these cells? However, if you put balding scalp cells with those same two cells types there will be inhibition of growth with the follicle still potentiating some growth, but the release of inhibitory factors eventually overcomes any growth signals.

By the way, cultured hair follicles do appear to maintain their genetic (and in-vivo) response to androgens in-vitro.

 

[michael barry]

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?


But transplatns grow.............................so where are we, right?





Doctor,

Did you get to look at the ACELL pictures I posted a few posts up and see the hair growth with the wound healing? It would seem to me that a FUE transplant could move hair "up front" and ACELL could be placed on the FUE-wounds in the back to regenerate hair back in the wreath.

I was thinking the same thing with the Stenn/Cosarialis Wnt-signalling pathway protiens that generated brand new hairs on genetically nude mice who were purposely wounded. It would seem that one could make new hair back in the donor hair with donor area genetics and move the extracted hairs up front.


Along with ICX-Aderans cloning research, this would seem to be three ways that will possibly give balding men hair in the future. Surely one of the three will work out. Im optomistic anyway.

 

[S Foote.]

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.

Yes i did see that Michael, and it is impressive.

But i think any protocol that would modify Wnt's in humans, will be classed as to dangerous by the FDA etc.

S Foote.

 

[docj077]

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?

It demonstrates that the inhibition is molecular and not physical. Once the follicles become "balding follicles" (as some people refer to them), all that is required for progression is surrounding follicles producing inhibiting signals.

Fortunately for us, such a phenomenon explains the progression of male pattern baldness in individuals with typical male pattern hairloss.

 

[michael barry]

Doctor,

Perhaps its the TGF-beta and the dermal fibroblasts in the cells that are the suppressive signal???



Stephen,......................Costarialis was extremely optomistic about the Wnt being available in "2 or 3 years" if research results were good. I have a hard time believing that applying Wnt protiens for just a month or so will be tumor city personally. I could be wrong. ACELL, which you seen regenerated a bunch of dog, cat hair and skin..............hasn't produced tumors so far. I think we have reason to be cautiously optomistic about these possibilities. I am.




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]

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.

I am in about the same condition as you with receded temples and Norwood 3. You are still in better shape than me though with your "thick vertex" I just have a medium vertex :wink:

I have been religiously doing the scalp exercise every day since October of 2005 and my scalp skin is in very good shape so I am not a good test subject either.

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...


How many times has that particular experiment been rigorously tested and repeated? I know it cannot be based on JUST the Nordstom study???


:hairy: :hairy: :hairy:

 

[Bryan]

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!!

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:

 

[wookster]

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!!

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:

Then again, balding follicles transplanted on immune deficient mice regrew. There appears to be a strong immune component associated with the balding process.

Mr. Foote gives an interesting explanation:

http://www.gourmetstylewellness.com/discussions ... 18&start=0

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.

 

[michael barry]

Wook,

In my opinion, the immuno-deficient mice considerations also has to take into account the RU58841 study in which only 2% of balding hairs regenerated for a second phase on THOSE MICE, vs. 28% of the balding hairs treated five days a week (instead of 7) with RU58841.

If fibrose scaffolds were formed for these hairs, and mice dont have edema.................then all of them should have enlarged.


When nordstrom moved balding follicles to people's arms-------------there should have been no edema present there.



We have seen that balding follicles can apparently regenerate because of the one immuno deficient mice study though.............so it stands to reason that they can indeed do it, and have the cellular machinery to make it possible-----sans an immune system and most hormonal stimulis.




Im guessing that an overprodcution in a particular growth factor downstream of androgen uptake causes some microinflammation in the upper portion of the follicle, and that is what gets the immune system to attack in MOST cases-------------------but we have to remember, that some balding men simply bald and dont have inflammation and hence probably no immuno attack. Hormones just shut their hairs down----like the apes. These guys would probably do very well on finasteride alone. This is my opinion on this.




To me, Stephen needs to get with a Doctor who can measure such things and find the tissue pressure in the telogen or catagen LEVEL of the dermis----where the scene of the crime is in balding scalp vs. wreath area scalp and see if there is a difference. All this speculation on this forum, HLR, HS, isn't going to get him anywhere unless he can show that there is indeed more pressure where he proposes it to be in the first place. THEN he would have a good starting point to argue his theory. Right now we have someone merely SPECULATING that there is higher pressure in the balding areas.




Guys, Im pretty excited about ICX, Aderans, Follica (Stenn and Costarialis Wnt/wounding company that they have formed to defeat alopecia), or ACELL ending baldness for all intents and purposes in the next 5-7 years anyway. I honestly think one of these four companies is going to end this for all of us and give us donor-area hair for our entire heads. Some of the smartest people on this planet are working on it now, and they are funded. I really think its almost over.

 

[Old Baldy]

Michael: This is nit picking but where did you read, or hear, that some men don't have an immune system attack at all?

Didn't Dr. Uno conclude that the immune system component of our "mammalian" type of Androgenetic Alopecia is unique to humans? And THAT is what makes it so da** difficult to reverse?

I balded late in life and it isn't very agressive. So maybe my immune system attack and/or sensitivity to androgens is less than some men but I always assumed there was an immune system component in all of us suffering with male pattern baldness?

Also, even though my male pattern baldness is not very agressive, it still marches on. I know old age balding is a component for me but I always figured the immune system affects us badly in all cases?

In fact, I assumed my immune system reaction was the major problem for a guy like me who balded late in life and not agressively? I assumed I could handle androgens fairly well but the LONG TIME my follicles were exposed to androgens eventually caused the dreaded immune system attack.

Am I out in leftfield on this one? :?

 

[Bryan]

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:

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?

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.

Yeah. I guess they maintained the extra "pressure" inside those graphs for the full TWO YEARS or so that Nordstrom observed them. I wish the tires on my car could maintain their pressure for that long! :wink:

This is how my theory explains Norstroms observations with these large grafts over the test period.

About as ad hoc an explanation as you can get. Stephen should be embarrassed.

 

[S Foote.]

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:

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?

No lack of consistency at all Bryan, just a lack of basic inteligence on your part. :roll:

Do we have any details of the exact size of the hair growth classed as "balding" in that study, and the density of the balding follicles in these large grafts? How many of these fading follicles in an already thinning piece of tissue were right next to the scar, allowing a fibrotic scaffold to form ?

There is no reference at all in Nordstroms study of transplanting "balding" follicles, regarding the issues concerning my explaination, so you are just guessing as you usually do!

What is clear from Nordstroms and other old studies using large grafts is this. The now recognised major long term hair loss throughout large grafts to the male pattern baldness area, cannot be for the reason (excuse) given by the transplantation industry.

In the long term alledged DHT resistent hair transplanted to the bald area in these large grafts, thins and "balds" untill all that is left is that around the edges. If Nordstrom etc had run their original studies for more than two years, they would have seen for themselves what is common knowledge in the industry today.

A whole transplant repair industry exist today, and a major part of their work is repairing the hair loss in these "DHT resistent" grafts known as "doughnutting".

Just one link, there are more if people Google "graft doughnutting":

http://www.hairtransplantadviser.org/re ... argegrafts

Quote:

"hair loss caused by a phenomenon called "doughnutting." In doughnutting, the centers of grafts get insufficient oxygen following transplantation and therefore, the follicles in the central portion of the grafts fail to survive. This results in hair growing only in the periphery of the grafts. This was a common phenomenon in 4- and 5-mm plugs, but can also be noted in grafts 3-mm in size."

The size of grafts used in the early studies was even bigger!

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:

I have now explained the scientific time line to you about three times Bryan. If you dont get it now, you must be just plain stupid! :roll:

S Foote.

 

[michael barry]

old baldy,

some of Doctor's posts about balding mentioned the lack of inflammation in some men who balded......................thats where I got that from. You'd have to dig back in his posts though, and there are alot of them. Ask him about it and he can probably detail where he found that info.



Rick, Im thinking were close on the ICX, Aderans, ACELL, or Follicla (Wnt) fronts anyway man. I honestly think we are going to have headfulls of donor-area quality hair in the next decade. Im getting very confident about this as the big names in hair are all researching in this area now and all seem so confident about it.

On inflammation, I'd read an article a while back that discussed the first feature of inflammation in Androgenetic Alopecia was around the infidulum or the hole in the dermis where the follicle emerges. It starts there.................very interesting that. An overproduction by the dermal fibroblasts of some growth inhibitor? What could it be? I wish I knew man.

 

[Bryan]

No lack of consistency at all Bryan, just a lack of basic inteligence on your part. :roll:

Why didn't you address the specific issues I raised, instead of just repeating your usual theories about "doughnutting"?

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:

Really? How does it do that? BE SPECIFIC.

 

[Bryan]

BTW, I'm extending an open invitation to Michael Barry, docj, and any others who follow transplant procedures and theory a lot more closely than I do: what can you tell us about "doughnutting"?