I don't even know who posted that. The amount of bull**** and snake oil that have been posted in this forum in comparison is probably 10-1. You're contradicting yourself by even using a dermaroller cause many would say it's a home made hippie solution...Sqeegee, you shouldn't laugh cause 80% of your posts about immunity gut, vitamin D, etc. I have seen the same thing on that forum with the corresponding studies so laughing at them would be the same as laughing at yourself. I personally keep an open mind and look for intelligent arguements with some supportive evidence and anecdotal on top of it. Whoever contributes to that cause at whatever forum, I don't care, but I don't jump to ignorant conclusions and join the hate bandwagon. I'll leave you guys be, it's not worth my time arguing common sense.
This is called learning process.. But I never said that Amalgam filings causes hairloss and laser helmets are the cure hahaha
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@benjt, when I started I wanted to replaced minoxidil with something else, and topical capsaicin was ideal, this burns like a mofo, but I attributed most of the initial growth spurt to that plus use of topical calcipotriol (VDR is critical for hair cycling and calcitriol strongly increases wnt/b catenin in the hair follicle for up to 48 hours), I noted way back in the beginning of my treatment (in my calcipotriol thread) that I was going to try dermarolling everytime before applying calcipotriol, for absorption as I had ordered many batches of the cream instead of the scalp ointment (dummy me) this I did up to starting the aggressive dermarolling in august, this wasn't wounding theory based, it was very light rolling 3-4 times a week with a 0.5mm roller and apply calcipotriol.
I have used other topical including topical EGCG, resveratrol, and something else that I will no longer mention here
. I think my internals were the most aggressive one, I basically wanted to blunt dht and fibrosis without using finasteride. There are a lot of things that will work but absorption is necessary and critical. I will have an unrelated post about those internals backed by publications. The reason I don't like mentioning stuff is some people will show up, and say x y z doesn't work for $hit because they have done it 2000 bc.
There are some french publications that show that even saw palmetto, when absorbed properly can inhibit 5AR 3 times more than 5mg finasteride. Again this is something I don't like mentioning but since you asked..., but soon, some random dude will start yelling at me... *waiting for random dude to mingle*.
Now let's go back to the wounding and PGD2 talk
PGd2 is induced by inflammation.
PGD[SUB]2[/SUB] and Inflammation
PGD[SUB]2[/SUB] is a major eicosanoid that is synthesized in both the central nervous system and peripheral tissues and appears to function in both an inflammatory and homeostatic capacity.[SUP]
101[/SUP] In the brain, PGD[SUB]2[/SUB] is involved in the regulation of sleep and other central nervous system activities, including pain perception.[SUP]
102,
103[/SUP] In peripheral tissues, PGD[SUB]2[/SUB] is produced mainly by mast cells but also by other leukocytes, such as DCs and Th[SUB]2[/SUB] cells.[SUP]
104–106[/SUP] Two genetically distinct PGD[SUB]2[/SUB]-synthesizing enzymes have been identified, including hematopoietic- and lipocalin-type PGD synthases (H-PGDS and L-PGDS, respectively). H-PGDS is generally localized to the cytosol of immune and inflammatory cells, whereas L-PGDS is more restrained to tissue-based expression.[SUP]
107[/SUP]
PGD[SUB]2[/SUB] can be further metabolized to PGF[SUB]2α[/SUB], 9α,11β-PGF[SUB]2[/SUB] (the stereoisomer of PGF[SUB]2α[/SUB]) and the J series of cyclopentanone PGs, including PGJ[SUB]2[/SUB], Δ[SUP]12[/SUP]-PGJ[SUB]2[/SUB], and 15d-PGJ[SUB]2[/SUB].[SUP]
108[/SUP] Synthesis of J series PGs involves PGD[SUB]2[/SUB] undergoing an initial dehydration reaction to produce PGJ[SUB]2[/SUB] and 15d-PGJ[SUB]2[/SUB], after which PGJ[SUB]2[/SUB] is converted to 15d-PGJ[SUB]2[/SUB] and Δ[SUP]12[/SUP]-PGJ[SUB]2[/SUB] via albumin-dependent and albumin-independent reactions, respectively.[SUP]
109[/SUP]
PGD[SUB]2[/SUB] activity is principally mediated through DP or DP1 and CRTH2 or DP2, as described previously (Table). Also, 15d-PGJ[SUB]2[/SUB] binds with low affinity the nuclear PPARγ.[SUP]
110[/SUP]
PGD[SUB]2[/SUB] has long been associated with inflammatory and atopic conditions, although it might exert an array of immunologically relevant antiinflammatory functions as well.
PGD[SUB]2[/SUB] is the predominant prostanoid produced by activated mast cells, which initiate IgE-mediated type I acute allergic responses.[SUP]
104,
111[/SUP] It is well established that the presence of an allergen triggers the production of PGD[SUB]2[/SUB] in sensitized individuals. In asthmatics, PGD[SUB]2[/SUB], which can be detected in the bronchoalveolar lavage fluid within minutes, reaches biologically active levels at least 150-fold higher than preallergen levels.[SUP]
112[/SUP] PGD[SUB]2[/SUB] is produced also by other immune cells, such as antigen-presenting DCs and Th[SUB]2[/SUB] cells, suggesting a modulatory role for PGD[SUB]2[/SUB] in the development of antigen-specific immune system responses.[SUP]
104,
105[/SUP] PGD[SUB]2[/SUB] challenge elicits several hallmarks of allergic asthma, such as bronchoconstriction and airway eosinophil infiltration,[SUP]
113,
114[/SUP] and mice that overexpress L-PGDS have elevated PGD[SUB]2[/SUB] levels and an increased allergic response in the OVA-induced model of airway hyperreactivity.[SUP]
115[/SUP]
The proinflammatory effects of PGD[SUB]2[/SUB] appear to be mediated by both DP1 and DP2/CRTH2 receptors. Because both receptors bind PGD[SUB]2[/SUB] with similar high affinity, PGD[SUB]2[/SUB] produced by activated mast cells or T cells would be capable of activating multiple signaling pathways leading to different effects, depending on whether the DP1 or DP2/CRTH2 receptors or both are locally expressed.
The DP1 receptor is expressed on bronchial epithelium and has been proposed to mediate production of chemokines and cytokines that recruit inflammatory lymphocytes and eosinophils, leading to airway inflammation and hyperreactivity seen in asthma.[SUP]
116[/SUP] Mice deficient in DP1 exhibit reduced airway hypersensitivity and Th2-mediated lung inflammation in the OVA-induced asthma model, suggesting that the DP1 plays a key role in mediating the effects of PGD[SUB]2[/SUB] released by mast cells during an asthmatic response.[SUP]
62[/SUP] Furthermore, PGD[SUB]2[/SUB] may inhibit eosinophil apoptosis via the DP1 receptor.[SUP]
117[/SUP]
DP1 antagonists exert antiinflammatory properties in several experimental models, including inhibition of antigen-induced conjunctival microvascular permeability in guinea pigs and OVA-induced airway hyperreactivity in mice.[SUP]
118,
119[/SUP]
DP2/CRTH2 receptors contribute largely to pathogenic responses by mediating inflammatory cell trafficking and by modulating effector functions. PGD[SUB]2[/SUB] released from mast cells may mediate recruitment of Th2 lymphocytes and eosinophils directly via the DP2/CRTH2 receptor. In humans, the DP2/CRTH2 receptor is expressed on Th2 lymphocytes, eosinophils, and basophils,[SUP]
8,
120,
121[/SUP] and an increase in DP2/CRTH2[SUP]+[/SUP] T cells has been positively associated with certain forms of atopic dermatitis.[SUP]
122[/SUP] The DP2/CRTH2 receptor has been demonstrated to mediate PGD[SUB]2[/SUB]-stimulated chemotaxis of these cells in vitro and leukocyte mobilization in vivo.[SUP]
123[/SUP]
In contrast to the proinflammatory role of PGD[SUB]2[/SUB] in allergic inflammation, PGD[SUB]2[/SUB] may act to inhibit inflammation in other contexts. The DP1 receptor is expressed on DCs that play a key role in initiating an adaptive immune response to foreign antigens. PGD[SUB]2[/SUB] activation of the DP1 receptor inhibits DC migration from lung to lymph nodes following OVA challenge, leading to reduced proliferation and cytokine production by antigen specific T cells.[SUP]
124[/SUP] DP1 activation also reduces eosinophilia in allergic inflammation in mice and mediates inhibition of antigen-presenting Langerhans cell function by PGD[SUB]2[/SUB].[SUP]
125,
126[/SUP] As mentioned, PGD[SUB]2[/SUB] and its degradation product 15d-PGJ[SUB]2[/SUB] have been suggested as the COX-2 products involved in the resolution of inflammation.[SUP]
28,
127[/SUP] Administration of a COX-2 inhibitor during the resolution phase exacerbated inflammation in a carrageenan-induced pleurisy model [SUP]
28[/SUP]. In a zymosan-induced peritonitis model, deletion of H-PGDS induced a more aggressive inflammatory response and compromised resolution, findings that were moderated by addition of a DP1 agonist or 15d-PGJ[SUB]2[/SUB].[SUP]
123[/SUP] Although these data appear to implicate PGD[SUB]2[/SUB] and 15d-PGJ[SUB]2[/SUB] in resolution, there is a large disparity between the nanomolar to picomolar amounts of 15d-PGJ[SUB]2[/SUB] detected by physicochemical methodology in in vivo settings and the amount needed to have a biological effect in vitro on PPARγ or nuclear factor-κB (micromolar amounts).[SUP]
32,
128,
129[/SUP] This discrepancy is supported by recent data reported in zymosan-induced peritonitis, where we observed evoked biosynthesis of PGD[SUB]2[/SUB] only during the proinflammatory phase and not during resolution. Consistent with this observation, DP2/CRTH2 deletion reduced the severity of acute inflammation, but neither DP1 or DP2/CRTH2 deletion affected resolution. Although 15d-PGJ[SUB]2[/SUB] is readily detected when synthetic PGD[SUB]2[/SUB] is infused into rodents,[SUP]
130[/SUP] endogenous biosynthesis of 15d-PGJ[SUB]2[/SUB] was not detected during promotion or resolution of inflammation (J. Mehta et al, unpublished data, 2010).
PGD[SUB]2[/SUB] may play a role in the evolution of atherosclerosis. In the context of inflamed intima, PGD[SUB]2[/SUB] in part derives from H-PGDS-producing inflammatory cells that are chemotactically compelled to permeate the vasculature.[SUP]
131,
132[/SUP] Additionally, L-PGDS expression is induced by laminar sheer stress in vascular endothelial cells and is actively expressed in synthetic smooth muscle cells of atherosclerotic intima and coronary plaques of arteries with severe stenosis.[SUP]
133–135[/SUP] PGD[SUB]2[/SUB] has been shown to inhibit expression of proinflammatory genes, such as inducible nitric oxide synthase and plasminogen activator inhibitor.[SUP]
136,
137[/SUP] Indeed, L-PGDS deficiency accelerates atherogenesis.[SUP]
138[/SUP]
In summary, studies with COX-2 inhibitors suggest that products of this enzyme may play a role in resolution in several models of inflammation. However, the identity of such products, whether formed directly by COX-2 or because of substrate diversion consequent to COX-2 inhibition, remains, in many cases, to be established.
http://atvb.ahajournals.org/content/31/5/986.full
Introduction to the Eicosanoids
http://themedicalbiochemistrypage.org/eicosanoids.php
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Prostaglandin D2 inhibits wound-induced hair follicle neogenesis through the receptor, Gpr44.
Nelson AM,
Loy DE,
Lawson JA,
Katseff AS,
Fitzgerald GA,
Garza LA.
Source
Department of Dermatology, Johns Hopkins University School of Medicine, Baltimore, MD, USA.
Abstract
Prostaglandins (PGs) are key inflammatory mediators involved in wound healing and regulating hair growth; however, their role in skin regeneration after injury is unknown. Using wound-induced hair follicle neogenesis (WIHN) as a marker of skin regeneration, we hypothesized that PGD2 decreases follicle neogenesis. PGE2 and PGD2 were elevated early and late, respectively, during wound healing. The levels of WIHN, lipocalin-type prostaglandin D2 synthase (Ptgds), and its product PGD2 each varied significantly among background strains of mice after wounding, and all correlated such that the highest Ptgds and PGD2 levels were associated with the lowest amount of regeneration. In addition, an alternatively spliced transcript variant of Ptgds missing exon 3 correlated with high regeneration in mice. Exogenous application of PGD2 decreased WIHN in wild-type mice, and PGD2 receptor Gpr44-null mice showed increased WIHN compared with strain-matched control mice. Furthermore, Gpr44-null mice were resistant to PGD2-induced inhibition of follicle neogenesis.
In all, these findings demonstrate that PGD2 inhibits hair follicle regeneration through the Gpr44 receptor and imply that inhibition of PGD2 production or Gpr44 signaling will promote skin regeneration.
