glaub er hat sich im thread vertan.

was zum lumigan, vll kann man die wirkung
mit retinol verbessern wie beim minox aber vorerst würd ich es so durchziehn,
zeit für experimente ist danach noch.

Habs mal makiert:

Edit///

hoffe auf ein gutes Zeichen.

Das werden wir demnächst erfahren, ich starte morgen mit dem Versuch und habe noch deutlich mehr Haare. Bei mir dünnt aber der gesammte Oberkopf aus, habe aber keine kahlen Stellen, bin daher vllt. ne ganz gute Testperson. Nehme dann auch nichts weiter als Progy und Lumigan.

Würden bei jemandem mit noch fast vollem Haar (aber schon leicht erkennbarem HA) die Haare an den jeweiligen Stellen verhältnissmäßig schneller zurückkommen als bei jemanden mit (fast Glatze)? Und warum?

Mir fallen aber sehr viele Haare aus.

Okay guys,
Its very hard for me to sit down layed back, and wait for the first results of blocking the crth2..
I'm still finding more and more evidence every day, about the "current theory".


http://books.google.nl/books?i...ippet&q=pgf2a&f=false
PGF2Alpha = also an CRTh2 AGONIST!! Guys please top using PGf2a (bima, latana etccccc)!

http://books.google.nl/books?i...pgf2a%20crth2&f=false
conclusion:
pgs such as pgf2a stimulate the proliferation of immature osteoblasts as well as NAPiT activity through activation of PKC ..
see this: http://www.hairloss-research.org/february1.html
PKC induces apoptosis(Cell death). Its well known that tnf-a is induced in hairloss, en thereby pkc.
Blocking the CRTH2, would affect this pathway!.

Source
PGD2 is rapidly metabolized (half-life in blood is about 6 seconds) to 13,14-dihydro-15-keto PGD2 or 11?-PGF2?. A novel metabolite, tetranor-PGDM, has also been identified. More abundant than other PGD2 metabolites, tetranor PGDM is detectable in human and murine urine2 and can be quantified using Cayman's tetranor-PGDM EIA Kit. Alternatively, through non-enzymatic means PGD2 is converted to PGJ2, ?12-PGJ2, ?12-PGD2, 15-deoxy-?12,14-PGJ2, or 15-deoxy-?12,14-PGD2. Given this instability, PGD2 or its metabolites must act discretely in close proximity to the location of their synthesis. As many general anti-inflammatory drugs target COX, which diminishes production of essentially all PG types, greater selectivity and fewer side effects could be achieved by targeting downstream synthases and specific receptors. This is particularly relevant with PGE2 for example, which has protective effects including inhibiting mast cell activation and promoting bronchodilation (see related story on page 32).


Conclusion, summed with the first posts I made in this topic, Its very stupid to use any of the PGF2a products, while you suffer from hairloss! (and yes these studies Support the PGD2 story!) the pgd2 story gets stronger and stonger.. What I post here , is just a part of te total studdies I/ we(vinman) read..

Nemesis schrieb am Mon, 26 November 2012 16:32

Mir fallen aber sehr viele Haare aus.

Am selben Tag? es wirkt...

ich störe die euphorie hier ja nur ungern aber was sagt ihr dazu:

ich störe die euphorie hier ja nur ungern aber was sagt ihr dazu:

Zitat

Okay guys,
Its very hard for me to sit down layed back, and wait for the first results of blocking the crth2..
I'm still finding more and more evidence every day, about the "current theory".


http://books.google.nl/books?i...ippet&q=pgf2a&f=false
PGF2Alpha = also an CRTh2 AGONIST!! Guys please top using PGf2a (bima, latana etccccc)!

http://books.google.nl/books?i...pgf2a%20crth2&f=false
conclusion:
pgs such as pgf2a stimulate the proliferation of immature osteoblasts as well as NAPiT activity through activation of PKC ..
see this: http://www.hairloss-research.org/february1.html
PKC induces apoptosis(Cell death). Its well known that tnf-a is induced in hairloss, en thereby pkc.
Blocking the CRTH2, would affect this pathway!.

Source
PGD2 is rapidly metabolized (half-life in blood is about 6 seconds) to 13,14-dihydro-15-keto PGD2 or 11?-PGF2?. A novel metabolite, tetranor-PGDM, has also been identified. More abundant than other PGD2 metabolites, tetranor PGDM is detectable in human and murine urine2 and can be quantified using Cayman's tetranor-PGDM EIA Kit. Alternatively, through non-enzymatic means PGD2 is converted to PGJ2, ?12-PGJ2, ?12-PGD2, 15-deoxy-?12,14-PGJ2, or 15-deoxy-?12,14-PGD2. Given this instability, PGD2 or its metabolites must act discretely in close proximity to the location of their synthesis. As many general anti-inflammatory drugs target COX, which diminishes production of essentially all PG types, greater selectivity and fewer side effects could be achieved by targeting downstream synthases and specific receptors. This is particularly relevant with PGE2 for example, which has protective effects including inhibiting mast cell activation and promoting bronchodilation (see related story on page 32).


Conclusion, summed with the first posts I made in this topic, Its very stupid to use any of the PGF2a products, while you suffer from hairloss! (and yes these studies Support the PGD2 story!) the pgd2 story gets stronger and stonger.. What I post here , is just a part of te total studdies I/ we(vinman) read..

link:
http://www.hairlosshelp.com/forums/messageview.cfm?catid=7&threadid=100447&enterthread=y

Well I will not stop you, Try it out, and report back over 6 months.. even if it only stayed local, it still activates the crth2, which we dont want, since the total pgf2a level in aga scalp is already increased + the 3x pgd2 levels.. If you manage to use an crth2 antagonist like OC, it will be an another story.. But still...

for me it *****ed my hairline 1 year ago, and it never grew back, and now I know what pgf2a does, I understand why...