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The Chemical PE Thread

http://www.google.com/patents/CA2762355A1?cl=en

Publication number CA2762355 A1
Publication type Application
Application number CA 2762355
Publication date Jun 16, 2013 <<< A fairly recent publication… for the 2011 update to the patent.

Originally Posted by inuic
http://yakushi.pharm.or.jp/FULL_TEXT/130_2/pdf/211.pdf

http://www.ncbi.nlm.nih.gov/pmc/art…s00455-0166.pdf

Someone posted these links the other day, and if this is correct it does compliment the implications in the patent as well as other evidence as seen on the NCBI.

Basically PGF2a (Prostaglandin F2a) is complimented by either PGE-1 or PGE-2. From what I understand PGE-2 burns quite bad when injected.

Not sure about the PGF2a (Prostaglandin F2a), but my gut tells me it burns, I think PGCL is a synthetic that is stronger then PGF2a (Prostaglandin F2a). I have read this stuff gives you the runs and irritates hemerrhoids and leaves you on the toilet so take imodium ad a few hours before hand.

Any way the idea in the links:

PGF2a (Prostaglandin F2a) causes hyperplasia in smooth muscle tissue, and is syngergized by adding either PGE-2 or PGE-1 to the mix. So mixing say PGF2a (Prostaglandin F2a) and PGE-1 should induce hyperplasia synergistically. DMSO can mix these two also perhaps for a good topical.

Imagine a mini bath mate filled with DMSO and all the growth factors you need, you create a vacuum seal and leach all the goodies into the skin under vacuum! Or what ever!

Hey Inuic! PGF2A was a big realization for me too, hence my original post in this thread. Seeing it mentioned as the preferred prostaglandin in the patent, but never tried by anyone around these parts, really piqued my curiosity. I, as of right now, am under the impression that a tri-mix of prostglandins, injected, would be of great benefit. I’ve heard about both the pain of PGF2A and it’s sides, but I’d personally be willing to see if I could tolerate it, if it seems like a valuable addition to one’s protocol.

I’m somewhat familiar with PGCL. Like you mentioned, PGCL is a synthetic analogue of PGF2A that’s much stronger and has less side effects. I believe this is the “topical prostaglandin F analogue” mentioned in the original listing of the patent. As that statement would imply, I believe both PGF2A and PGCL are small enough to be used transdermally with DMSO. I’ve heard people throw around the idea of “chemical pumping” before, but I think a glass or similar device would be needed due to DMSO’s ability to eat through and carry so many different materials into the skin.

Also, thanks for linking to the new version of the patent. I hadn’t seen it, and it looks like there’s some interesting, updated info in the new version. Definitely going to go over it and see what it’s about as soon as possible.

Edit: I see that’s actually a separate patent, also by the same doctor, rather than an update to the old one. Seems this one just consists of some documents and newer ideas. Still, a good find and I’m excited to read it!


Last edited by Atmospheric : 12-24-2013 at .

I have access to all the Prostaglandins except to PGE-2. I am thinking of the same thing you are? I wonder if I can tolerate it? I know it should work. Right now I am on the hunt for a new PRP Kit supplier, my last supplier can no longer ship to me from his area. I am excited about my Relaxin-2 trial coming up after the first of the year. I dont’ know if it burns, but I get the feeling that anything that does remodel the Tunica or break down the collagen will be felt as inflammation. Thats my theory. But my supplier also has benzocaine and lidocaine powder that I am ordering along with my Hospital Grade PGE-1. I have tried some local PGE-1 from a supplier that claims 97% purity, but there is a big difference between this stuff and my Hospital grade stuff, my stuff feels so clean the other stuff makes me feel funny and take longer and takes more. Its weird. Anyway. HO HO HO…. Merry XMAS! But mixing two of the prostags seems like it will synergize…

Inuic…

Also I think injury is needed for starts to bud into new vessicles. I think growth factors will syngergize if there exist injured tissue from work outs, injuries at the micro level seeded with growth factors I think is what causes growth. I think activated PRP is simulating injury. I know that when injured stuff like calcium chloride and thrombrin activate the platelets. But I have seen new methods in PRP technology recently that show physical ways to activate the PRP by sucking it into one tube into another over and over fast and hard about 20 or 30 times activates the platelets. Also collagen activates platelets also, and releases even more VEGF then either Thrombin or Calcium Chloride, but now via PRP kits like the Genesis PRP kit you dont need additives like either of the 3 I mention. You just need the special mixer to activate the PRP then inject. My theory about PRP since I have done 2 priapus shots and administered and produced my own PRP via my own centrifuge successfully as well. But I didn’t get to inject myself, only my wife. We think stuff she was doing kicked up her androgens and shrank her boob, and she was like near double D. She went to a C cup and had flat nipples, when I gave her the PRP her nipples formed more fully, the got more bottle tip like. Its like the PRP optimized her genetic potential. Like a fruit that you pick early or let get ripe on the vine, I think adding PRP simulates leaving the fruit on the vine, it takes it to what the fullness of what it can or could ever be but not more. Thats what i think PRP is doing taking you to that fullness but not past. To go past you have to injure and grow new veins and cells, like with hemorrhoids, you have to balloon out the veins and micro burst to grow new bud sites for new veins. And its during the healing cascade which PRP compliments various growth factors are released during during during different phases of the reconstruction of tissues. Its not just random. My theory is understand the healing cascade and learn how to optimally injure tissue to maximize the potential of various peptides and growth factors to do their healing regrowth and repair, via angiogenesis and hyperplasia.

One thing that keeps sticking in my craw about all this is PGE-1, it is said to impede platelet aggragation. Well to maximize the amount of PRP you get you need high level platelet aggragation to maximize the growth factors released from the granules. This is why I think that EPO may help PE as well because adding oxyegen is required and EPO causes angiogenesis also, but more importantly maximizes red blood cell count, which means more granules and hence more PRP charged with way more of a high volume of growth factors… These get released according to the healing cascade. Now my theory is inject with substances that compliment the healing cascade during that phase of its process. Like on day 1 growth factors bFGF and PDGF say get released naturally during the healing cascade, this is when you inject more of these, but not stuff not occuring during that phase like IGF-1 or whats not released at that time. Say on day 2 it VEGF and fGF, then on these days of the 30 day cycle I think it is you do those or complimentary functional wise peptides or growth factors or what have you. Say when you know the cascade will naturally release IGF-1 thats the day you inject it as well as put DMSO with that stuff in it. You do this process in cycles according to the healing cascade principle.

These are my private theories backed my all my research. Anyway Im serious about this, I feel like a pioneer or like a RPG player looking for rare items so I can learn to craft special items in the quest. LOL…

Hey all, as I mentioned, I was previously unaware of that short 2011 addendum to the patent. I went through it and picked out the relevant, important info. It’s below for anyone interested.

It basically speculates on what the “plateau” period is, confirms the importance of Relaxin and PGF2A, explains that Verapamil and similar compounds only work in higher than commonly recommended dosages, there’s mentions of collagen IGF1 and other prostaglandins, and I pasted the 3 PE-relevant examples (there are more related to PD & ED at the link). Link is, again: http://www.google.com/patents/CA2762355A1?cl=en
————————
*”The invention relates to methods and compositions for increasing growth of the penis comprising an erectile function-enhancing amount of: a calcium channel blocker, a calmodulin blocker, a pharmaceutically acceptable diluent or carrier.”

*”Males stimulating growth in their penis by any form of biomechanical stimulation will also stimulate a build up of collagen in the penis.

*”Certain doses of: Calcium Channel Blockers, Calmodulin Blockers, Prostaglandins, IGF1 receptor agonists can increase the rate of penis growth and increase the effectiveness of penis enlargement.”

*”The inventor hypothesizes that an important reason why penis growth slows and stops after several months in all patients he has observed who have enlarged their penises is because the rate of new collagen formed is faster than the rate that it is being removed and that this hypertrophy of the structural collagen fibers which the inventor has observed in all patients whose growth has slowed, must reduce the effectiveness of any further biomechanical stimulation.”

*”The inventor treated several patients’ Peyronies’s Disease and penis enlargement patients with the recommended dosing and frequency for direct Verapamil injections into the penis and into plaque with no observable effect.”

*”However, the inventor discovered that certain doses of Calcium Channel Blockers and Calmodulin Blockers, when applied topically, infused continuously, or applied intermittently at a higher frequency than was recommended in the medical literature improved their clinical efficacy.”

*”There seems to be an overall synergist effect of Calcium Channel Blockers and Calmodulin Blockers on all observable and measurable parameters of penile growth and enlargement. This effect is not limited to the connective tissue growth and structural collagen elongation within the penis, but could potentiate collagen elongation and remodeling outside of the penis. The inventor has observed that Calcium Channel Blockers and Calmodulin Blockers will potentate biomechanical growth in other tissues when they are combined with any of the multitude of methods that produce biomechanical stimulation.”

*”The inventor has found that local application of small doses of: IGF1 receptor agonists, relaxin receptor agonists, certain prostinoid receptor agonists, when combined with biomechanical stimulation can also potentiate, accelerate and generally increase the rate of penis growth. In summary, the inventor has found that penis enlargement can be accelerated and potentiated by Calcium Channel Blockers and Calmodulin Blockers.”

*”The inventor had previously discovered that penis growth with vasodilators alone was potentiated by Relaxin receptor agonists. The inventor has also discovered the Relaxin receptor agonists will accelerate and potentiate the penile growth experienced by men using effective traction devices.”

*”The inventor discovered that prostinoid receptor agonists: PGF2alpha, Dinoprost, Bitamoprost, PGE2, and Dinoprostone when applied in very low doses locally to the penis, would accelerate penis growth rates from biomechanical stimulation, such as a man using a traction device. And even men whose growth had stopped in some cases could be induced to start growing again with the prostinoid receptor agonists, PGF2alpha and PGE2, listed above.”

*”-The inventor has also discovered that penis enlargement can be accelerated and potentiated with IGF1 receptor agonists such as IGF1 and LR3 IGF1.”

*”To summarize, the presence of: Calcium Channel Blockers, Calmodulin Blockers, specific Prostaglandins, and IGF1 receptor agonists at therapeutic levels, for sufficient duration of time, can cause penis growth if combined with penile traction devices or other forms of biomechanical stimulation to enlarge the penis.”

*”Preferably, the calcium channel blocker is: verapamil, diltiazem, felodipine. And the calmodulin blocker is: trifluoperazine.”

* [Example] “55 year old male on penis enlargement using traction combined with intracavernosal injections for 7 months. After 1 inch of growth in length of erect penis, growth rate had slowed and stopped and had been static for over 4 months. After 3 months without any new additional growth, the patient was started on topical Verapamil 200mg/m1, resulting in new penile growth of 1-1.5/16th of an inch in the 1st month on Verapamil, and a total of 6/16 inches of new growth over the first 3 months on topical Verapamil.”

* [Example] “46 year old male on penis enlargement using IC injections; initial growth rate without topical Verapamil was: 1-2/16” per month for the first 4 months. Patient started: Verapamil 0.1 ml, 5-6 times/day. In the fifth month of treatment, growth rate increased to 3-4/16” per month. The active growth rate of the patient did not decelerate at 4-6 months.”

* [Example] “39 year old male on penis enlargement using traction combined with intracavernosal injections stopped growing. For three months there was no further increase in his penis length measurements despite adequate biomechanical stimulation. The patient added on drop of a 0.01 percent by weight PGF2alpha aqueous solution, applied topically to the skin of the penis at mid shaft, 2-6 times per day. When the patient returned in four weeks he experienced 1.5-2/16ths of an inch growth. After three months there had been 6.5-7/16th of an inch of new growth in erect length.”

* [Claim] “3. A composition for penis enlargement, comprising a blocker selected from a calcium channel blocker, a calmodulin blocker, relaxin receptor agonist, and a pharmaceutical acceptable diluent or carrier.”

Atmospheric,

Nice summary,

I will chunk up some of my analysis as well. I found this before I saw your notes:

“Human Fibroblasts-New

The main function of fibroblasts is to maintain the structural integrity of connective tissues by continuously secreting precursors of the extracellular matrix. Like other cells of connective tissue, fibroblasts are derived from primitive mesenchyme. Thus they express the intermediate filament protein vimentin, a feature used as a marker to distinguish their mesodermal origin.

In addition forming and maintaining extracellular matrices, they also regulate interstitial fluid volume and pressure, and wound healing. Many diseases are associated with dysregulation of the injury repair response and fibroblast function, leading to increased or decreased deposition of extracellular matrix proteins, altered tissue architecture, impaired function and in some cases significant morbidity and mortality. This includes association with cancer cells at all stages of cancer progression (cancer associated fibroblasts).”

So it looks like ” calcium channel blockers” have the job of keeping the calcium\fibroblasts out. In so doing the calcium blockers keep the formation of collagen down.

And as for “calmodulin blockers” there only seem be one mentioned ” trifluoperazine”, it seems to have the job of disallowing platelet aggregation. Which would contribute to disallowing the formation of growth factors including bFGF and FGF.

But perhaps other good growth factors responsible for Angiogenesis, such as VEGF

http://www.pdlabs.net/peyronies/wha…lverapamil.html

One interesting thing to note is PGE-1 also tries to impede the aggregation of platelets.

I think this all contributes to the idea that the real limiting factor is not the growth of additional blood vessels but to break down the cross linkages in the collagen of the tunica. Seems when the main treatment reached a near halt after months of no more results
the Doctor turned to these two substances.

http://www.ncbi.nlm.nih.gov/pubmed/3161211

From the looks of this link ” trifluoperazine” seems to inhibit things that activate platelets. Like thrombin, and even collagen, and other agents that activate platelets.

So it looks like his approach is to combine these two effects along with his other older methods to kick start regrowth when his old method starts failing. Seem as if he also notices with these agents in play growth takes place at a faster rate.

What is counter intuitive is ” trifluoperazine” would impede the effects of say a Priapus Shot and impact the delivery of growth factors. So it seems like knowing what growth factors to foster and which to inhibit are key. The Priapus or PRP Shot releases various growth factors, but some of these do what we want and some do what we dont want. Like we want the effects of angiogenesis from growth factors like VEGF, but it would seen we dont want the growth factors in play that build the Tunica or Collagen up. Seem the doctor has realized that various agents such as fibroblasts build up the Collagen which ultimately impedes further penis growth.

So if you injure your tissue you only want certain agents involved in the healing cascade to be in play. So its not a matter of just syngergizing each step of the cascades process, but knowing which to compliment and synergize and which to impede.

I often theorize did I get gains from my Priapus shot because I used PGE-1 during the process, hence impeding platelet aggrigation. This is the mystery, but the doctor seems to have solved a key piece, the fibroblast and calcium blockers and platelet inhibition to foster this. This is the piece that lets the tunica expand.

The other piece are the veins, and the angiogenisis. We want lots of new, long and wide vessicles growing under the Tunica TOO!, So we need both to loosen the Tunica so we can ballon past that limit, yet we need the internal force and growth of new veins to push past the Tunicas limits,

So the trick is how to induce both processes. So again its knowing the healing cascade and which aspects of it to impede and which to foster. Which growth factors and when. The odd thing is certain fribroblasts create the “collagenase”, so knowing which are the bad ones that grow collagen and knowing the good ones that create the “collagenase” is also key. Perhaps bFGF does one and FGF does another?

What a mystery but were getting closer!

Inuic

Very interesting. Does anyone know whether or not Dr Adams has been doing penis enlargement recently? It sure would be interesting to hear from someone who has talked with him and/or had his penis enlarged by treatment from him.

http://www.ncbi.nlm.nih.gov/pubmed/17367443

Topical verapamil HCl, topical trifluoperazine, and topical magnesium sulfate for the treatment of Peyronie’s disease—a placebo-controlled pilot study.

CONCLUSIONS:
Topical verapamil gel proved effective in eliminating pain on erection, decreasing the size of plaque, decreasing curvature, and improving erection quality in patients with Peyronie’s Disease. Treatment results improved significantly after 9 months’ treatment as compared with 3 months’ treatment.

We have investigated the long term effects of excess IGF-2 on mammals…

… indicating a local action of the excess IGF-2 on cell multiplication!

… indicate distinct local and systemic actions for IGF-2

This stuff was seen to multiple uterus cells to enlarge it, which of course is made of smooth muscle.

http://www.pnas.org/content/91/22/10365.full.pdf

As an ASIDE… This stuff looks crazy good for your BRAIN!!!! Check out its radical effects on memory! http://www.naturalheightgrowth.com/…nd-galantamine/

But wait there is more: Grow Taller with IGF-2 injections?! : http://www.naturalheightgrowth.com/…s-breakthrough/

if you make a localized injection of IGF-2 in the distal epiphysis femur region you would get about an increase of 1.6-1.7% in length - WOA!!!!

Overall the IGf-2 has been shown to be a really good supplement for muscle mass building, increased energy, and sexual enhancement and drive. -

Looks like there is a connection between IGF-2 and MMP-9! …. This may help breakdown the collagen.

Collectively these results suggest that IGF-2 increases MATRIX DEGRADATION and invasion of endothelial progentor cells EPC’s through the IGF-2R dependent generation of MMP-9.
http://bloodjournal.hematologylibra…/1/233.full.pdf

IGF-2 is one of those rare blends that can deliver superior benefits on multiple fronts. Endurance. Strength. Lean Mass. Hypertrophy. cAMP-and-cGMP-boosting. Testosterone Modulation. Glucocorticoid Antagonism/Cortisol Regulation. Prolactin Inhibition. Glycogen Regulation. Phospho-Creatine Boosting. Insulin Modulation. Growth-Hormone Synthesis. Adaptogenic Protection…

http://www.ncbi.nlm.nih.gov/pubmed/2991611

The use of collagenase in the treatment of Peyronie’s disease.

Guys, what about http://en.wikipedia.org/wiki/Pentoxifylline ? I’ve noticed many guys on the peyronies forums are raving about this as being superior to other substances like verapimil


Starting stats: 6.4" / 5.6" Current Stats: 7.4" / 5.8" Short term goal: 7" / 6" Long term goal: 8" / 6.5"

Originally Posted by inuic
Atmospheric,

Nice summary,

I will chunk up some of my analysis as well. I found this before I saw your notes:

“Human Fibroblasts-New

The main function of fibroblasts is to maintain the structural integrity of connective tissues by continuously secreting precursors of the extracellular matrix. Like other cells of connective tissue, fibroblasts are derived from primitive mesenchyme. Thus they express the intermediate filament protein vimentin, a feature used as a marker to distinguish their mesodermal origin.

In addition forming and maintaining extracellular matrices, they also regulate interstitial fluid volume and pressure, and wound healing. Many diseases are associated with dysregulation of the injury repair response and fibroblast function, leading to increased or decreased deposition of extracellular matrix proteins, altered tissue architecture, impaired function and in some cases significant morbidity and mortality. This includes association with cancer cells at all stages of cancer progression (cancer associated fibroblasts).”

So it looks like ” calcium channel blockers” have the job of keeping the calcium\fibroblasts out. In so doing the calcium blockers keep the formation of collagen down.

And as for “calmodulin blockers” there only seem be one mentioned ” trifluoperazine”, it seems to have the job of disallowing platelet aggregation. Which would contribute to disallowing the formation of growth factors including bFGF and FGF.

But perhaps other good growth factors responsible for Angiogenesis, such as VEGF

http://www.pdlabs.net/peyronies/wha…lverapamil.html

One interesting thing to note is PGE-1 also tries to impede the aggregation of platelets.

I think this all contributes to the idea that the real limiting factor is not the growth of additional blood vessels but to break down the cross linkages in the collagen of the tunica. Seems when the main treatment reached a near halt after months of no more results
The Doctor turned to these two substances.

http://www.ncbi.nlm.nih.gov/pubmed/3161211

From the looks of this link ” trifluoperazine” seems to inhibit things that activate platelets. Like thrombin, and even collagen, and other agents that activate platelets.

So it looks like his approach is to combine these two effects along with his other older methods to kick start regrowth when his old method starts failing. Seem as if he also notices with these agents in play growth takes place at a faster rate.

What is counter intuitive is ” trifluoperazine” would impede the effects of say a Priapus Shot and impact the delivery of growth factors. So it seems like knowing what growth factors to foster and which to inhibit are key. The Priapus or PRP Shot releases various growth factors, but some of these do what we want and some do what we don’t want. Like we want the effects of angiogenesis from growth factors like VEGF, but it would seen we don’t want the growth factors in play that build the Tunica or Collagen up. Seem the doctor has realized that various agents such as fibroblasts build up the Collagen which ultimately impedes further penis growth.

So if you injure your tissue you only want certain agents involved in the healing cascade to be in play. So its not a matter of just syngergizing each step of the cascades process, but knowing which to compliment and synergize and which to impede.

I often theorize did I get gains from my Priapus shot because I used PGE-1 during the process, hence impeding platelet aggrigation. This is the mystery, but the doctor seems to have solved a key piece, the fibroblast and calcium blockers and platelet inhibition to foster this. This is the piece that lets the tunica expand.

The other piece are the veins, and the angiogenisis. We want lots of new, long and wide vessicles growing under the Tunica TOO!, So we need both to loosen the Tunica so we can ballon past that limit, yet we need the internal force and growth of new veins to push past the Tunicas limits,

So the trick is how to induce both processes. So again its knowing the healing cascade and which aspects of it to impede and which to foster. Which growth factors and when. The odd thing is certain fribroblasts create the “collagenase”, so knowing which are the bad ones that grow collagen and knowing the good ones that create the “collagenase” is also key. Perhaps bFGF does one and FGF does another?

What a mystery but were getting closer!

Inuic

Hey, this is a good post for sure. You brought up pretty much all the same questions I had whilst reading it.

That’s definitely an interesting and thought-provoking theory you’ve got. If I understand it correctly, you’re suggesting that things like the calcium and calmodulin blockers be used at a particular time in a chain of events to enhance certain effects - rather than just be relied on as a way to re-start growth when it slows? That does makes sense. I get how it would be tricky to figure out what are both good and bad growth factors and when they appear though

Although, my understanding of that recent reading made it seem way more simple. By being able to inject compounds of our choosing at any time, you could somewhat customize the chain of events for certain effects, no? (The simplest example I can think of would be cycling things like the verapamil/triflouperazine and things of that nature.)

The doctor seems to think this is the way to do it, and simply. From my understanding, the growth injection of prostaglandins and growth factors would give mechanical stress, angiogenesis, smooth muscle growth, etc. Then once that starts to give gains, you can use the 2 discussed compounds to maintain that the tunica allows for aforementioned expansion. I think that the blockers are meant to be used before/after, on their own, and not in combination with anything else, so as not to cancel out any “good” growth factors, while still keeping the bad ones at bay. Your theory makes sense too and I don’t doubt that it’s more complex than it seems. I just found it to be an interesting contrast in regard to how simply the doctor alleges this part of the process to be.

I very much appreciate you looking into it in as detailed of a manner as possible. This is really the only place I’ve found where people are discussing new ChemPE ideas and I’m glad to see all these interesting ideas thrown around.

Originally Posted by alin
Guys, what about http://en.wikipedia.org/wiki/Pentoxifylline ? I’ve noticed many guys on the peyronies forums are raving about this as being superior to other substances like verapimil

Hey,

I mentioned it a few pages ago along with some other topicals of interest, but I agree for sure. It’s listed briefly in the patent and seems to have the ability to decrease the production of collagen, fibronectin and glycosaminoglycan. I’ve never seen anyone use it solely for PE purposes and I was unaware that people with PD were using it as part of their treatment, but it makes sense that they would. It’s great to hear that people are reporting successes in that realm. I plan to look into it’s effects in greater detail to see how much of a benefit it would have for PE, but I’d like to think it’s a worthwhile compound to add.

Originally Posted by Atmospheric
Hey,

I mentioned it a few pages ago along with some other topicals of interest, but I agree for sure. It’s listed briefly in the patent and seems to have the ability to decrease the production of collagen, fibronectin and glycosaminoglycan. I’ve never seen anyone use it solely for PE purposes and I was unaware that people with PD were using it as part of their treatment, but it makes sense that they would. It’s great to hear that people are reporting successes in that realm. I plan to look into it’s effects in greater detail to see how much of a benefit it would have for PE, but I’d like to think it’s a worthwhile compound to add.

http://peyroniesforum.net/index.php?topic=1136.0

I think it’s helpful to check on PD guys’s experiments with these compounds.


Starting stats: 6.4" / 5.6" Current Stats: 7.4" / 5.8" Short term goal: 7" / 6" Long term goal: 8" / 6.5"

Relaxin Modulates Synthesis and Secretion of Procollagenase and
Collagen by Human Dermal Fibroblasts*

http://www.jbc.org/content/265/18/10681.full.pdf

Together, these
results indicate that relaxin can mediate significant turnover
of collagen matrices by human dermal fibroblasts.

We have shown that a synthetic human relaxin can induce

major changes in the extracellular collagenous matrix phe-

notype expressed by human dermal fibroblasts in culture,

demonstrating that relaxin can significantly affect cells out-

side those classically accepted as relaxin targets. I

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