The Chemical PE Thread

Altered Sonic hedgehog signaling is associated with morphological abnormalities in the penis of the BB/WOR diabetic rat.

Altered Sonic hedgehog signaling is associated with morphological abnormalities in the penis of the BB/WOR diabetic rat - PubMed <<Basically without SSH you get ED is the spirit of these implications… So with it would you build smooth muscle yet break down collagen?

Unique functions of Sonic hedgehog signaling during external genitalia development.

Unique functions of Sonic hedgehog signaling during external genitalia development - PubMed <<< Further reveals the role of SHH in penile development along with the other indicated factors such as BMP-4, and Fgf, ie if you take SHH away bad things happen for the penis or good things never will at least, which is bad.

Molecular analysis of external genitalia formation: the role of fibroblast growth factor (Fgf) genes during genital tubercle formation. http://en.wikip … enital_tubercle

Molecular analysis of external genitalia formation: the role of fibroblast growth factor (Fgf) genes during genital tubercle formation - PubMed <<< However, the abnormal external genitalia development of Fgf10(-/-) perinatal mice suggested the importance of Fgf10 in the development of the glans penis and the glans clitoridis. These results suggest that the FGF system is a key element in orchestrating GT development.

SHH inhibition in the penis induces apoptosis and ED, and SHH treatment at the time of CN injury suppresses smooth muscle apoptosis and promotes regeneration of erectile function.

The genital tubercle is sensitive to dihydrotestosterone and rich in 5-alpha-reductase, so that the amount of fetal testosterone present after the second month is a major determinant of phallus size at birth.

hydrogen sulfide (H(2)S) on neovascularization and wound healing in vitro and in vivo. Incubation of endothelial cells (ECs) with H(2)S enhanced their angiogenic potential, evidenced by accelerated cell growth, migration, and capillary morphogenesis on Matrigel. Treatment of chicken chorioallantoic membranes (CAMS) with H(2)S increased vascular length.

Hydrogen sulfide is an endogenous stimulator of angiogenesis - PubMed

SMC-derived MMPs may be an additional source of proteases to digest vascular basement membrane, which is a crucial step in the initial stage of angiogenesis. The MMPs may also contribute to SMC migration in angiogenesis and atherogenesis.

Vascular endothelial growth factor upregulates the expression of matrix metalloproteinases in vascular smooth muscle cells: role of flt-1 - PubMed

Matrix metalloproteinases and angiogenesis.

Matrix metalloproteinases and angiogenesis - PubMed

Matrix metalloproteinases (MMPs) are a family of enzymes that proteolytically degrade various components of the extracellular matrix (ECM). Angiogenesis is the process of forming new blood vessels from existing ones and requires degradation of the vascular basement membrane and remodeling of the ECM in order to allow endothelial cells to migrate and invade into the surrounding tissue. MMPs participate in this remodeling of basement membranes and ECM

Hydrogen sulfide and nitric oxide are mutually dependent in the regulation of angiogenesis and endothelium-dependent vasorelaxation - PubMed

the results of the current study show that H(2)S and NO are mutually required to elicit angiogenesis and vasodilatation.

Hydrogen sulphide increases cell growth, migration and the formation of tube-like structures in cultured endothelial cells. ++

Mechanisms of angiogenesis: role of hydrogen sulphide - PubMed

The effect of finasteride on the expression of vascular endothelial growth factor and microvessel density: a possible mechanism for decreased prostatic bleeding in treated patients.

CONCLUSIONS Decreased expression of VEGF by finasteride inhibits angiogenesis and significantly decreases microvessel density

http://www.ncbi .nlm.nih.gov/pu … is+penile+penis

Dr Pezzi???

Effects of finasteride on vascular endothelial growth factor.

Effects of finasteride on vascular endothelial growth factor - PubMed

both IGF-I and VEGF and their receptors, which may be important in the control of vascularity in human penile architecture

Ex vivo expression of angiogenic growth factors and their receptors in human penile cavernosal cells - PubMed

[Pathologic change of elastic fibers with difference of microvessel density and expression of angiogenesis-related proteins in internal hemorrhoid tissues].

CONCLUSION:
Angiogenesis is evident in hemorrhoid tissue, suggesting the possible mechanism in the pathogenesis of hemorrhoids. The direct degeneration effect of MMP9 on supporting structure elastic fibers in anal cushion is another important mechanism. The high expression of iNOS suggests the inflammatory factors involve in the pathogenesis of hemorrhoids, and NO may be involve in pathological effect on hemorrhoids

[Pathologic change of elastic fibers with difference of microvessel density and expression of angiogenesis-related proteins in internal hemorrhoid tissues] - PubMed

Yes yes, I know this may be strange, but if you keep looking you will see a connection to whats going on when penis grows and when well yep you guessed it hemorrhoids grow. There are commonalities, but what I believe is what we are doing with mechanical forces with various forms of PE, hemorrhoids are simulating via basal pressure in the anus, more stress more clinch, and if you clinch a vein that weaves up into the external anal tissue and weaves back internally and you clinch you trap blood. That pressure extends into a hemorrhoid, and the growth factors involved are analogus to what goes on in say clamping for instance. I think clamping is like whats going on with hemorrhoids and the processes are similar and so are the involved growth factors.

Inuic

…

I would bet that the rate of growth of hemorrhoids can be compared to what gains are achieved with clamping. I am saying that at the micro-scale what’s going on with hemorrhoids, something like it is going on under the tunica, and MMP-9 may be whats needed to break it down properly like it does with other elastic fibers made of collagen. Then throw in the Relaxin-2 and stretch boom bang.. Along with timing the healing cascade, and knowing what growth factors are released and what to inject into the penis to compliment this healing cascade over it course.

Like take a PRP shot, know when what is going to be released and inject to compliment each phase of the healing process. But you have to injure first via PE forces of all sorts and kinds. Like braces it starts to work,but with complimenting growth factors you synergize the healing cascade. PRP Growth factors are activated via injury or chemically. Like via Thrombrin or Calcium Chloride. I understand that MMP-9 to can be activate via Thrombrin, makes me think calcium chloride would to the same as it does with PRP. Something has to inflame it and break down the base bed tissue to sprout to blood vessicles. Forces and biochemicals can both do this, this forum is dedicated to discovering out which ones from the outside in and the inside out.

That’t my hypothesis.

Inuic

Hey all, I know there’s been a ton of interesting things linked to in this thread so far, but I just stumbled upon this tonight and was curious to perhaps get an opinion.

http://en.wikip edia.org/wiki/S … eptor_modulator

"SARMs provide the opportunity to design molecules that can be delivered orally, but that selectively target the androgen receptors in different tissues differently. The goal of research in this area is to allow a customized response: Tissues that are the target of the therapy will respond as they would to testosterone; other tissues where undesirable side-effects are produced will not."

The quote is in reference to T, but there’s been studies with DHT that produce the same result. Unless I’m reading this wrong, wouldn’t a compound of this nature prioritize DHT and it’s expression on penile tissues? Not sure how easy it would be to acquire such a thing, but it’s certainly interesting to think about.

Unfortunately when puberty is over the penis doesn’t get larger with testosterone.

http://yakushi. pharm.or.jp/FUL … 0_2/pdf/211.pdf

http://www.ncbi .nlm.nih.gov/pm … 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!

Thats my Patent! LOL a mini vacuum delivery system for nutrients and growth factors or what have you.