farmcoffee
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Critical protein discovered, baldness in mice reversed!
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farmcoffee
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hair_tomorrow
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farmcoffee said:
That article about the Hopkins research hit my local news station this morning. Sounds very cool - but w/ "more research needed" (paraphrasing) - I guess we can't count on it being a viable commercial treatment any time soon.
Gene therapy is not trivial. This is because expression of the gene requires viral promotors, which are promiscuous. This presents a very serious risk. HOWEVER, I have to say my knowledge is limited to cystic fibrosis, and even then, I have not followed this topic with any seriousness. As it is, I doubt you will see anything for quite some time. I wish I knew more about gene therapy.
pleasegodno
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gene therapy is not restricted to viral vectors, and not all gene therapy necessitates the incorporatrion of foreign DNA into host DNA. also, viable RNAi treatments are relatively near.
Do you have access to the full journal article?
http://www.pnas.org/cgi/content/abstrac ... 09102v1?ct
http://www.pnas.org/cgi/content/abstrac ... 09102v1?ct
pleasegodno
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yep. thanks for the link! i was going to look for the full article sooner or later. it's only in pdf format, however. i'll try to upload it somewhere at some point. in the meantime, check out these abstracts. it may be relevant to you (as it is to me). stay on finasteride and try to stay calm (as for me: 5.5 months on finasteride, 1 year of extreme anxiety/panic and diffusing).
Am J Pathol. 2003 Mar;162(3):803-14. Related Articles, Links
Comment in:
Am J Pathol. 2003 Mar;162(3):709-12.
Stress inhibits hair growth in mice by induction of premature catagen development and deleterious perifollicular inflammatory events via neuropeptide substance P-dependent pathways.
Arck PC, Handjiski B, Peters EM, Peter AS, Hagen E, Fischer A, Klapp BF, Paus R.
Department of Internal Medicine, Charite School of Medicine, Humboldt University, Berlin, Germany. petra.arck@charite.de
It has been much disputed whether or not stress can cause hair loss (telogen effluvium) in a clinically relevant manner. Despite the paramount psychosocial importance of hair in human society, this central, yet enigmatic and controversial problem of clinically applied stress research has not been systematically studied in appropriate animal models. We now show that psychoemotional stress indeed alters actual hair follicle (HF) cycling in vivo, ie, prematurely terminates the normal duration of active hair growth (anagen) in mice. Further, inflammatory events deleterious to the HF are present in the HF environment of stressed mice (perifollicular macrophage cluster, excessive mast cell activation). This provides the first solid pathophysiological mechanism for how stress may actually cause telogen effluvium, ie, by hair cycle manipulation and neuroimmunological events that combine to terminate anagen. Furthermore, we show that most of these hair growth-inhibitory effects of stress can be reproduced by the proteotypic stress-related neuropeptide substance P in nonstressed mice, and can be counteracted effectively by co-administration of a specific substance P receptor antagonist in stressed mice. This offers the first convincing rationale how stress-induced hair loss in men may be pharmacologically managed effectively.
J Mol Med. 2005 May;83(5):386-96. Epub 2005 Mar 10. Related Articles, Links
Mast cell deficient and neurokinin-1 receptor knockout mice are protected from stress-induced hair growth inhibition.
Arck PC, Handjiski B, Kuhlmei A, Peters EM, Knackstedt M, Peter A, Hunt SP, Klapp BF, Paus R.
Biomedizinisches Forschungszentrum, Campus Virchow Klinikum, Charite University Medicine, Augustenburger Platz 1, 13353 Berlin, Germany. petra.arck@charite.de
Despite the lack of insight on distinct mediators in the skin orchestrating the pathophysiological response to stress, hair loss has often been reported to be caused by stress. Recently we revealed the existence of a "brain-hair follicle axis" by characterizing the neurokinin (NK) substance P (SP) as a central element in the stress-induced threat to the hair follicle, resulting in premature onset of catagen accompanied by mast cell activation in the skin. However, our understanding of possible SP-mast cell interactions in the skin in response to stress was limited since the receptor by which SP activates skin mast cells and the extent of mast cell mediated aggravation of SP remained to be elucidated. We now employed NK-1 receptor knockout mice (NK-1R(-/-)) and mast cell deficient W/W(v) mice and observed that stress-triggered premature induction of catagen and hair follicle apoptosis does not occur in NK1(-/-) and W/W(v) mice. Furthermore, the activation status of mast cells was less in stressed NK1(-/-) mice than in wild-type control. Additionally, stress-induced upregulation of SP positive nerve fibers was absent in both NK-1R and W/W(v) mice. These results indicate that the cross-talk between SP and mast cell activation via NK-1R appears to be the most important pathway in the regulation of hair follicle cycling upon stress response
Am J Pathol. 2003 Mar;162(3):803-14. Related Articles, Links
Comment in:
Am J Pathol. 2003 Mar;162(3):709-12.
Stress inhibits hair growth in mice by induction of premature catagen development and deleterious perifollicular inflammatory events via neuropeptide substance P-dependent pathways.
Arck PC, Handjiski B, Peters EM, Peter AS, Hagen E, Fischer A, Klapp BF, Paus R.
Department of Internal Medicine, Charite School of Medicine, Humboldt University, Berlin, Germany. petra.arck@charite.de
It has been much disputed whether or not stress can cause hair loss (telogen effluvium) in a clinically relevant manner. Despite the paramount psychosocial importance of hair in human society, this central, yet enigmatic and controversial problem of clinically applied stress research has not been systematically studied in appropriate animal models. We now show that psychoemotional stress indeed alters actual hair follicle (HF) cycling in vivo, ie, prematurely terminates the normal duration of active hair growth (anagen) in mice. Further, inflammatory events deleterious to the HF are present in the HF environment of stressed mice (perifollicular macrophage cluster, excessive mast cell activation). This provides the first solid pathophysiological mechanism for how stress may actually cause telogen effluvium, ie, by hair cycle manipulation and neuroimmunological events that combine to terminate anagen. Furthermore, we show that most of these hair growth-inhibitory effects of stress can be reproduced by the proteotypic stress-related neuropeptide substance P in nonstressed mice, and can be counteracted effectively by co-administration of a specific substance P receptor antagonist in stressed mice. This offers the first convincing rationale how stress-induced hair loss in men may be pharmacologically managed effectively.
J Mol Med. 2005 May;83(5):386-96. Epub 2005 Mar 10. Related Articles, Links
Mast cell deficient and neurokinin-1 receptor knockout mice are protected from stress-induced hair growth inhibition.
Arck PC, Handjiski B, Kuhlmei A, Peters EM, Knackstedt M, Peter A, Hunt SP, Klapp BF, Paus R.
Biomedizinisches Forschungszentrum, Campus Virchow Klinikum, Charite University Medicine, Augustenburger Platz 1, 13353 Berlin, Germany. petra.arck@charite.de
Despite the lack of insight on distinct mediators in the skin orchestrating the pathophysiological response to stress, hair loss has often been reported to be caused by stress. Recently we revealed the existence of a "brain-hair follicle axis" by characterizing the neurokinin (NK) substance P (SP) as a central element in the stress-induced threat to the hair follicle, resulting in premature onset of catagen accompanied by mast cell activation in the skin. However, our understanding of possible SP-mast cell interactions in the skin in response to stress was limited since the receptor by which SP activates skin mast cells and the extent of mast cell mediated aggravation of SP remained to be elucidated. We now employed NK-1 receptor knockout mice (NK-1R(-/-)) and mast cell deficient W/W(v) mice and observed that stress-triggered premature induction of catagen and hair follicle apoptosis does not occur in NK1(-/-) and W/W(v) mice. Furthermore, the activation status of mast cells was less in stressed NK1(-/-) mice than in wild-type control. Additionally, stress-induced upregulation of SP positive nerve fibers was absent in both NK-1R and W/W(v) mice. These results indicate that the cross-talk between SP and mast cell activation via NK-1R appears to be the most important pathway in the regulation of hair follicle cycling upon stress response
pleasegodno
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didn't know you could copy/paste pdfs....check your messages weepy.
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Lol mice have more solution to baldness than humans
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What do you want to achieve by digging up articles from early 2000’s? Do you really think that we are in the same square as those people were in? People keep whining endlessly, and decide to ignore the number of players going into phase lll trials and the totally different tools they intent to use. Even hair cloning (Tsuji) is approaching a clinical trial that they spent over 10 years and millions of cash preparing for. f*** even iPhones were primitive at the time compared to what we have now, and yet all what you are doing is dragging others with you into depressive mood.
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Seems by all post of 2005 that hair cloning was on full hype like it is just now.All these years we still only have minoxidil and finasteride.We haven't progressed in terms of hairloss.Only mice are getting hair regrowth since last 2 decades
People are obviously frustrated by the dearth of legit treatments to put a dent in the problem. There were big claims in the 1990s that said our ability to decode dna would lead to blockbuster drugs for a myriad of health problems. Being able to decode genetic instructions, it was said, and the faulty instructions that produce diseases would be known. It was supposed lead to easy street once a bad gene was ID'd. Researchers would then ID the protein coded by that gene. Then they’d target the protein. Next, they would run thousands of tests with compounds that drug companies had stockpiled, to find one that fit the target like a key in a lock, to make it work normally.
Target-based drug discovery hasn't worked according to grand plan because most diseases affecting large numbers of people are not caused by a handful of genes. This problem of “missing heritability" has resulted in them realizing that diseases are more genetically complex than what they knew. Often a drug that targets a protein square on the chin doesnt fix the problem. It is now thought the older strategies for studying cells in a petry dish with trial and error "hit and miss" methods might be more productive than high tech approaches. No shortcuts in science apparently. The human body is probably the most unique and mysterious organism ever studied. It's comparable to unexplored space or even the deepest oceans.
Target-based drug discovery hasn't worked according to grand plan because most diseases affecting large numbers of people are not caused by a handful of genes. This problem of “missing heritability" has resulted in them realizing that diseases are more genetically complex than what they knew. Often a drug that targets a protein square on the chin doesnt fix the problem. It is now thought the older strategies for studying cells in a petry dish with trial and error "hit and miss" methods might be more productive than high tech approaches. No shortcuts in science apparently. The human body is probably the most unique and mysterious organism ever studied. It's comparable to unexplored space or even the deepest oceans.
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Its just frustrating that even in all these years progress against hairloss treatement forget about cure has been so slow.Before a decade there was hpe around certain products and techniques that never came into market.Here this time around there is hype that treatement to be around 2-3 years
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A Korean guy posted a video on youtube abt RCH-01 I Think.He said It might be available only to japan and japnese citizens first.For it to be available to others it might take around 8-10 years
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You are beating a dead zombie horse. We.got.your.message, move one, you unoriginal goofball.
It doesn't help that you had to borrow this whole thread necrophilia thing idea from another user and are now reiterating it ad absurdum...
He is just a Korean-American youtuber with hair plugs, his goddamn opinions are as valid as me saying it will be available to everyone tomorrow.