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Does anyone have any info at all from that 400 person trial in Vietnam? I believe Dr. Xu has something to do with it?
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chill
Dr. Xu has nothing to do with this, are you for real?
he works for Penn medicine, and is not in taiwan.
it doesn't really matter what the taiwanese are doing, according to xu and gardner and everyone else, they have not achieved enough inductivity or gene expression to really make a difference as far as a "cure". will be interesting to see what kind of hairs they can grow though- probably not impressive. will have to wait til they finish their trials and publish.
also, for whoever was asking what the difference betwen gene expression and inductivity is. well, they are two completely different things. are they correlated? yes. gene expression is how much of the original genetic coding a cultured cell retains. In other words, how much of the original DNA is intact. Iductivity is the cells capacity to say "ok time to grow hair." This clearly happens more when the cell is more akin to its original version, because that is what normal DP cells do. On the other hand, say you restore 100 percent gene expression- that doesnt mean that in every situation the DP cell is going to induce hair. inducing hair also depends on its environment, signalling between other cells, etc.
However, the good news is that it seems to be the case that the more they restore the gene expression, the more likely it is that some kind of hair is induced. My guess is that the type and health of this hair is going to depend on many environmental factors that are going to take a long time to figure out and test. It's like planting a good new plant in crappy soil. you have to palnt a good plant but also fix the soil situation. hopefully things like replicel and histogen and -fingers crossed- other newer therapies will come to fruition and provide the necessary boost for our scalps so that new follicles can grow. in any case, you can see how complicated its all going to be. my bet is that by the time all that comes to pass, ill have stopped giving a shit to undergo all that expensive treatment. Hopefully by the time our children are adults, the preventative treatments will be great and they wont have to go through any of it. interesting stuff nonetheless.Comment
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Nearly all women with advanced hair loss wear a wig. Contrast that to men. Women's wigs are more convincing that men's hairpieces IMO. I saw a young woman a while ago who's hair looked perfectly natural. I later learned that she was wearing a wig because of extensive hair loss.
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Does anyone knows if Desmond has been able to upload the videos from the conference somewhere?
I believe he was having issues with the format but probably fix them by nowComment
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Hi guys,
So as promised here's the first video. Since Dr Cotsarelis has so much following, I thought I'll upload his presentation first. So here you go
Many more videos to follow in the coming days.
Dr George Cotsarelis: Advances in Understanding Androgenetic Alopecia
We originally localised hair follicle stem cells to the mouse and hair follicle bulge. Much progress has been made in our understanding of mouse bulge cells, but the relevance of this information to human hair follicle biology is not often studied. So, we evaluated the status of hair follicle stem cells in Androgenetic Alopecia. We analysed bald and non-bald scalp from men with Androgenetic Alopecia (AGA) for the presence of hair follicle stem and progenitor cells. Cells expressing cytokeratin 15 (KRT15), CD200, CD34, and alpha-6 Integrin (ITGA6) were quantified via flow cytometry. High levels of KRT15 expression correlated with stem cell properties of small size and quiescence. These KRT15hi stem cells were maintained in bald scalp samples. However, CD200hi/ITGA6hi and CD34hi cell populations - which both possessed a progenitor phenotype, in that they localised closelyto the stem cell-rich bulge area but were larger and more proliferative than the KRT15hi stem cells - were marked diminished. These findings support the notion that a defect in conversion of hair follicle stem cells to progenitor cells plays a role in the pathogenesis of AGA.
We then showed that prostaglandin D2 Synthase (PTGDS) is elevated at the mRNA and protein levels in balding scalp compared to haired scalp of men with AGA. The product of PTGDS enzyme activity, prostaglandin D2 (PGD2), is similarly elevated in bald scalp. PGD2 inhibits hair growth in explanted human hair follicles and when applied topically to mice. Hair growth inhibition requires the PGD2 receptor (GPR44). Furthermore, we find that a transgenic mouse, K14-Ptgs2, demonstrates elevated levels of PGD2 in skin and develops alopecia, follicular miniturisation, and sebaceous gland hyperplasia, which are all hallmarks of human AGA. These results define PGD2 as an inhibitor of hair growth in AGA and suggest the PGD2-GPR44 pathway as a potential target for treatment.
Last edited by Winston; 05-26-2014, 04:11 AM.Comment
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Tahnks for posting Bro.
Question: this is pretty much what they knew before the June 2013 news release. No mention at all about FGF9...
Hopefully they really are trying to recycle the Asthma clinical trials to deliver a treatment, but he made no mention at all about effectiveness of such a treatment, especially over a bald scalp (Although he did mention that the stem cells are still there, so that should be positive, correct??)Comment
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Yeah I know! Cotsarelis made the least contribution in this conference by a mile! I guess he had nothing new to talk about. I just thought you guys should see it for yourself
He does mention some stuff about developing a new PGD2 blocker in the near future though. I guess it is a good sign.
There are many amazing presentations to come. There was a few that literally blew my mind in terms of being out there. TBC
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Thanks Desmond!Hi guys,
So as promised here's the first video. Since Dr Cotsarelis has so much following, I thought I'll upload his presentation first. So here you go Many more videos to follow in the coming days.
Dr George Cotsarelis: Advances in Understanding Androgenetic Alopecia
We originally localised hair follicle stem cells to the mouse and hair follicle bulge. Much progress has been made in our understanding of mouse bulge cells, but the relevance of this information to human hair follicle biology is not often studied. So, we evaluated the status of hair follicle stem cells in Androgenetic Alopecia. We analysed bald and non-bald scalp from men with Androgenetic Alopecia (AGA) for the presence of hair follicle stem and progenitor cells. Cells expressing cytokeratin 15 (KRT15), CD200, CD34, and alpha-6 Integrin (ITGA6) were quantified via flow cytometry. High levels of KRT15 expression correlated with stem cell properties of small size and quiescence. These KRT15hi stem cells were maintained in bald scalp samples. However, CD200hi/ITGA6hi and CD34hi cell populations - which both possessed a progenitor phenotype, in that they localised closelyto the stem cell-rich bulge area but were larger and more proliferative than the KRT15hi stem cells - were marked diminished. These findings support the notion that a defect in conversion of hair follicle stem cells to progenitor cells plays a role in the pathogenesis of AGA.
We then showed that prostaglandin D2 Synthase (PTGDS) is elevated at the mRNA and protein levels in balding scalp compared to haired scalp of men with AGA. The product of PTGDS enzyme activity, prostaglandin D2 (PGD2), is similarly elevated in bald scalp. PGD2 inhibits hair growth in explanted human hair follicles and when applied topically to mice. Hair growth inhibition requires the PGD2 receptor (GPR44). Furthermore, we find that a transgenic mouse, K14-Ptgs2, demonstrates elevated levels of PGD2 in skin and develops alopecia, follicular miniturisation, and sebaceous gland hyperplasia, which are all hallmarks of human AGA. These results define PGD2 as an inhibitor of hair growth in AGA and suggest the PGD2-GPR44 pathway as a potential target for treatment.
Interesting stuff starts at 22:55
Cotsarelis says that there are at least 7 drug companies that have developed inhibitors of PGD2.
Now... which ones are they?Comment
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I think this information is public on clinical trials . GovComment
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