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» This seems reasonable 007.
I hope that is the case anyways, because I would hate to see the monopolistic hair mill continue on as is for the next decade. But only time will tell.
BTW, thanks for posting all the information that you did. It is one of the better things to be posted here in a long time.
I emailed the company conducting the trials for Aderans in June. Here is the reply I got (posted it before)
Thank you for your inquiry. The trial has been underway for approximately
14 months and progressing well. Due to confidentiality, I cannot disclose
details of the trial. It will be up to the sponsor of the trial, Aderans
Research Inc., to disclose details of the trial once they have been
presented to the various regulatory agencies. If a Phase 2 trial will take
place, it is likely to be planned for sometime in 2008. You are welcome to
contact the sponsor, Aderans Research, and advise them of your potential
interest in taking part in further trials.
No problem 007. It sparked my interest. I will be going to the ISHRS meeting and plant to attend the cell multiplication meetings and listen to the speakers. I will try to relay this again… Hopefully in real-time if they have wireless connectivity.
So if you read Bernstein Medical’s blog it appears two cell refers to fibroblast (i.e., inducer) and keratinocytes (i.e., responder) cells. See his summary below…
Friday, November 10. 2006
Aderans vs. Intercytex
Q: I know that both Aderans and Intercytex are doing research with cloning hair. Is there any difference in their approaches?
A: Aderans is using the "two-cell” approach. They feel that the best way to produce viable hair follicles is to use a combination of inducer cells and responder cells. Each would be multiplied separately and then injected together into the skin. The inducer cells are follicular fibroblasts and lie at the base of the hair follicle. The responder cells are keratinocytes. They feel that the combination of cells will have the best chance of producing clinically useful hair. [Using the 3-d matrix you are talking about, JB?]
Intercytex prefers a one-cell approach. Their researchers feel that when the cultured inducer fibroblasts are injected into the skin there will be enough existing cells in the skin to produce a cosmetically viable hair. In their experimentation, Intercytex uses a new animal model, termed the “flap graft” model, that involves the implantation of cultured dermal papilla cells with keratinocytes placed under a flap on the back of hairless mice. Later the flap is exteriorized (turned over), allowing the hair to grow normally. Exactly how this will be applied to clinical use in humans is not clear.
»
» edit: The reason I have been saying that the research they presented used
» epithelial and mesencymal cells is because the hairs died before breaking
» the skin (I haven’t seen this in previous mouse research using dermal
» cells and keratinocytes), but I have seen dermal and epithelial mouse
» experiments where some hairs don’t break the skin and inflammation
» results). But it is entirely possible that I just jumped to conclusions
» and the hair didn’t break the skin in a normal epithelial reaction using
» dermal injections. I’d have to see the ppt to know for sure. From my
» reading, two cell approach means epithelial and mesenchymal. But it
» appears ARI is using the term to simply mean dermal fibroblasts and
» keratinocytes. But that seems really lame to me, because this is the exact
» same approach Jahoda outlined in his patent back in the 80’s.
»
» I should say though that their website is a lie for a different reason
» than you have stated, because both Gho and ICX have used fibroblasts and
» keratinocytes to grow hair on humans. And long before they did this,
» Jahoda patented the technique.
maybe aderans is slower than intercytex on purpose because intercyets has distribution agreement with aderans so it means intercytex can be first but aderans will still pocket the money
» So I took a few weeks out of my life this year and went underground to work
» at MHR and Bosley. I wanted to know how and why they were so popular and
» how they operated… a mole if you will.
»
Thomas - you are a passionate hair technician. I met you once in Atlanta. You were Cole’s best tech at the time.
But, as a self-professed “mole” why should anyone take the information being relayed from you as accurate when you are just the scribe? Washenik knew you were a mole that infiltrated his chain and that you were in on the “doctor’s only” webinar. I’m sure a confidentiality agreement would have been in place for other ISHRS webinars. Yet, during this webinar they let you post freely to a website, live?
Why should we believe that the information told to the SMALL group was the true status of the ARI reearch? Participants were all in the HT industy and all have a short to mid term interest in keeping demand for ht’s high. As soon as HM looks like it’s around the corner HT’s will dry up as demand stops. Washenik is responsible for Bosley - a HT chain.
Get it? Hairtech - you were expolited. You were used to feed misinformation to the HT forum that was designed to keep HT demand high with comments like “early stages of research”. It was Hairsite that moved this thread to the HM forum.
Hairtech , you are a known mole and were used by your former victims to feed misinformation to this website. The research is further along than was discussed in this “webinar”
Wag the dog.
Well that explains the information given out then. I get what you were saying. I only told about what I heard from this Webinar, and if mis-information was given to me then Washenik gave mis-information to his own group of colleagues. Only thing is that we cannot prove it.
Good theory though.
One thing though… No one knew I was posting live. I just sat down and decided to start posting out of the blue.
And one last thing. Washenik did not know I was working for Bosley.
Tbere’s a difference between misinformation and not telling information. From what I understand about HM, and based on your notes, everything that Washenik said is true. However he obviously didn’t tell you ANYTHING bout the 14+ months of human Phase I trials in London being conducted by ARI. Nor, I imagine, did he completely tell you the prepatory work for Phase I…
» Well that explains the information given out then. I get what you were
» saying. I only told about what I heard from this Webinar, and if
» mis-information was given to me then Washenik gave mis-information to his
» own group of colleagues. Only thing is that we cannot prove it.
»
» Good theory though.
»
» One thing though… No one knew I was posting live. I just sat down and
» decided to start posting out of the blue.
» Washenik said is true. However he obviously didn’t tell you ANYTHING bout
» the 14+ months of human Phase I trials in London being conducted by ARI.
» Nor, I imagine, did he completely tell you the prepatory work for Phase
Correct there was no mention of that…
Well, I thought about this a bit last night after posting, and now I have to retract my original claims about ARI not using this in humans. I believe there is a good chance they are using standard terminology when they say “two cell approach.” This catches me completely by surprise, because I hadn’t thought anybody would use this technique in humans for quite some time to come. I definitely need to find more of the particulars out.
It looks to me like ARI is using dermal fibroblasts to induce co-injected epithelial keratinocyte responder cells to grow new hair follicles. I apologize for any confusion my earlier posts may have caused. I haven’t been following ARI at all lately.
What I am most curious about is whether the dermal cells interact with the epithelial cells at the point of injection to start a new follicle or if ARI is including epithelial stromal tissue in the soup as a sort of cell signaling device that allows the dermal cells to call the skin cells already present in the host? Please note that the epithelial cells ARI most likely uses are the same cells Gho uses (ORS cells including bulge), so there could be some patent infringement here. But then again, ARI is using them in a different manner so perhaps not.
Dr. Lu Zhongfa from China performed a similar technique to what it appears ARI is doing, but he did it in animals and would only consider a human protocol using the one-cell approach (dermal cell based solution). If I recall correctly, Zhongfa stated his two-cell approach was inconsistent, resulted in a percentage of poor quality hairs, and formed numerous miniature benign tumours.
» So if you read Bernstein Medical’s blog it appears two cell refers to
» fibroblast (i.e., inducer) and keratinocytes (i.e., responder) cells. See
» his summary below…
»
» Friday, November 10. 2006
» Aderans vs. Intercytex
»
» Q: I know that both Aderans and Intercytex are doing research with cloning
» hair. Is there any difference in their approaches?
»
» A: Aderans is using the "two-cell” approach. They feel that the best way
» to produce viable hair follicles is to use a combination of inducer cells
» and responder cells. Each would be multiplied separately and then injected
» together into the skin. The inducer cells are follicular fibroblasts and
» lie at the base of the hair follicle. The responder cells are
» keratinocytes. They feel that the combination of cells will have the best
» chance of producing clinically useful hair. [Using the 3-d matrix you are
» talking about, JB?]
»
» Intercytex prefers a one-cell approach. Their researchers feel that when
» the cultured inducer fibroblasts are injected into the skin there will be
» enough existing cells in the skin to produce a cosmetically viable hair.
» In their experimentation, Intercytex uses a new animal model, termed the
» “flap graft” model, that involves the implantation of cultured dermal
» papilla cells with keratinocytes placed under a flap on the back of
» hairless mice. Later the flap is exteriorized (turned over), allowing the
» hair to grow normally. Exactly how this will be applied to clinical use in
» humans is not clear.
»
» »
» » edit: The reason I have been saying that the research they presented
» used
» » epithelial and mesencymal cells is because the hairs died before
» breaking
» » the skin (I haven’t seen this in previous mouse research using dermal
» » cells and keratinocytes), but I have seen dermal and epithelial mouse
» » experiments where some hairs don’t break the skin and inflammation
» » results). But it is entirely possible that I just jumped to conclusions
» » and the hair didn’t break the skin in a normal epithelial reaction
» using
» » dermal injections. I’d have to see the ppt to know for sure. From my
» » reading, two cell approach means epithelial and mesenchymal. But it
» » appears ARI is using the term to simply mean dermal fibroblasts and
» » keratinocytes. But that seems really lame to me, because this is the
» exact
» » same approach Jahoda outlined in his patent back in the 80’s.
» »
» » I should say though that their website is a lie for a different reason
» » than you have stated, because both Gho and ICX have used fibroblasts
» and
» » keratinocytes to grow hair on humans. And long before they did this,
» » Jahoda patented the technique.
» maybe aderans is slower than intercytex on purpose because intercyets has
» distribution agreement with aderans so it means intercytex can be first
» but aderans will still pocket the money
I think you might be right. Perhaps ARI is allowing ICX to continue with its one-cell approach, and if it works well, it will be offered first. Meanwhile, ARI is working privately on a two-cell approach that is a lot more complex and will take a longer to develop. That way they don’t waste any time and money performing duplicate research.
» Well, I thought about this a bit last night after posting, and now I have
» to retract my original claims about ARI not using this in humans. I
» believe there is a good chance they are using standard terminology when
» they say “two cell approach.” This catches me completely by surprise,
» because I hadn’t thought anybody would use this technique in humans for
» quite some time to come. I definitely need to find more of the particulars
» out.
Let me ask you this…
The mouse model rapidly responds(two cell theory with epidermal/dermal mixtures with injection sub-dermis…) and continues with it cycle at 21 days time. What are we seeing in HUMAN models?
we might be seeing a somewhat attenuated response no?
SLOWED down merely by human everythings. Hair cycles in mice are noted as being 21 days…
Hair cycles in humans are largely unknown… but are definitively longer than fucking 21 days yes?
Think about it… Is this reasonable?
Hey hairtech, so let me get this straight… in the human model the follicle should be fully developed before telogen due to the longer hair cycle, right? And accordingly normal shedding would occur with no inflammatory response, right? And thus… holy s**t we have the cure!! 
» SLOWED down merely by human everythings. Hair cycles in mice are noted as
» being 21 days…
»
» Hair cycles in humans are largely unknown… but are definitively longer
» than fucking 21 days yes?
»
» Think about it… Is this reasonable?
» Hey hairtech, so let me get this straight… in the human model the
» follicle should be fully developed before telogen due to the longer hair
» cycle, right? And accordingly normal shedding would occur with no
» inflammatory response, right? And thus… holy s**t we have the
» cure!!
»
Telogen is part of the follicle cycle period in any species. The follicle… should be fully developed before telogen… regardless. IF it is a “human” the cycles vary and occur at much longer time spans than 21 days, i.e. telogen may/may not last as long as a different species…
MICE have concerted(all hairs cycle at the same time on a mouse) follicular cycles every 21 days. This means telogen occurs AFTER a full development of the follicle but apparently is mutha f__ing shorter than a human.
I love biology!
Hmmm… not sure what you’re getting at, hairtech… regardless of the hair cycle length wouldn’t there be an inflammatory response based on the mouse model? That is, what is it about hair cycle duration that would affect the problems with inflammation? Thanks, BB
» Telogen is part of the follicle cycle period in any species. The
» follicle… should be fully developed before telogen… regardless. IF it
» is a “human” the cycles vary and occur at much longer time spans than 21
» days, i.e. telogen may/may not last as long as a different species…
»
» MICE have concerted(all hairs cycle at the same time on a mouse)
» follicular cycles every 21 days. This means telogen occurs AFTER a full
» development of the follicle but apparently is mutha f__ing shorter than a
» human.
»
» I love biology!
» Hmmm… not sure what you’re getting at, hairtech… regardless of the hair
» cycle length wouldn’t there be an inflammatory response based on the mouse
» model? That is, what is it about hair cycle duration that would affect the
» problems with inflammation? Thanks, BB
»
A faster haircycle… as in the mouse… would mean faster to initiate an inflammatory response because your getting to that part of the cycle faster where we are seeing the response.
One would think it would take longer to get to the inflammation in a human model…
But who knows for sure…BB.
I was under the impression that the inflammatory response was secondary to the shedding that was unable to happen…hairs “poking” through the skin.
A similar reaction IS seen post transplant when a patient does not wash and brush the scalp weeks after a transplant… which helps to remove the shedding hairs so the new ones come in.
If you just leave it alone… not wash or brush the scalp… which I have seen happen because patients were scared to touch it… then what you see is the same inflammatory response. IMO
Yes, I believe that is perfectly reasonable. Human hair cycles are much longer than 21 days. If it weren’t so, it would be impossible to grow your hair long.
Interestingly, I have read that it takes approximately 3 weeks for new cycling hair to reach the surface of the skin. I’m not really sure how accurate that is, but I recall Dr. Gho saying that it can take longer than this for HM hair to appear after the cells are injected.
» Let me ask you this…
»
» The mouse model rapidly responds(two cell theory with epidermal/dermal
» mixtures with injection sub-dermis…) and continues with it cycle at 21
» days time. What are we seeing in HUMAN models?
»
» we might be seeing a somewhat attenuated response no?
»
» SLOWED down merely by human everythings. Hair cycles in mice are noted as
» being 21 days…
»
» Hair cycles in humans are largely unknown… but are definitively longer
» than fucking 21 days yes?
»
» Think about it… Is this reasonable?
» One would think it would take longer to get to the inflammation in a human
» model…
»
» But who knows for sure…BB.
»
» I was under the impression that the inflammatory response was secondary to
» the shedding that was unable to happen…hairs “poking” through the skin.
»
» A similar reaction IS seen post transplant when a patient does not wash
» and brush the scalp weeks after a transplant… which helps to remove the
» shedding hairs so the new ones come in.
»
» If you just leave it alone… not wash or brush the scalp… which I have
» seen happen because patients were scared to touch it… then what you see
» is the same inflammatory response. IMO
I strongly suspect you are correct about this. Especially considering ICX’ HM saftey trial outcome and the known immune privileged properties of hair follicle cells.
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