moxsom
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TCI's are topical calcineurins inhibitors. Bascially the NFAT-1 - calceineurin pathway is responsible for keeping hair in quiescenence and not divinding and proliferating into more hair cells. Calcerineurins inhibitors will inhibit this pathway and activate growth of new hair cells potentially. Heres some quotes from some papers I have been reading. Also keep in mind this is a major activity of the immunosupressent cyclosporin A and why some completly balding men can grow their hair back on CSA.
Now what I purpose is using TCI's which are normal used in the Treatment of Atopic Dermatitis to induce new hair proliferation. It may work, and it may not, but I can't imagine they would be too damn expensive.
Also this not a pathway you want going throughout your body which is why im adding an journal artice about absorption of TCI's
http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=18243104
http://ajpcell.physiology.org/cgi/content/full/284/6/C1593
http://www.ncbi.nlm.nih.gov/pubmed/...nel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum
One of the most common side effects of treatment with cyclosporin A (CsA) is hypertrichosis. This study shows that calcineurin activity is associated with hair keratinocyte differentiation in vivo, affecting nuclear factor of activated T cells (NFAT1) activity in these cells.
CsA inhibited the expression of keratinocyte terminal differentiation markers associated with catagen, along with the inhibition of calcineurin and NFAT1 nuclear translocation. This was associated with induction of hair growth in nude mice and retardation of spontaneous catagen induction in depilated normal mice.
These data provide the first evidence that calcineurin is functionally active in follicular keratinocytes and that inhibition of the calcineurin-NFAT1 pathway in these cells in vivo by CsA enhances hair growth.
As stem cells become activated during hair growth, NFATc1 is downregulated, relieving CDK4 repression and activating proliferation. When calcineurin/NFATc1 signaling is suppressed, pharmacologically or via complete or conditional NFATc1 gene ablation, stem cells are activated prematurely, resulting in precocious follicular growth. Our findings may explain why patients receiving cyclosporine A for immunosuppressive therapy display excessive hair growth
Now what I purpose is using TCI's which are normal used in the Treatment of Atopic Dermatitis to induce new hair proliferation. It may work, and it may not, but I can't imagine they would be too damn expensive.
Also this not a pathway you want going throughout your body which is why im adding an journal artice about absorption of TCI's
http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=18243104
http://ajpcell.physiology.org/cgi/content/full/284/6/C1593
http://www.ncbi.nlm.nih.gov/pubmed/...nel.Pubmed_DefaultReportPanel.Pubmed_RVDocSum