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Priapus Shot Received

Originally Posted by marinera
The sole explanation is that TA is stretched. Being stretched axially gives more room for circumfenrential expansion. No in vitro studies has shown that smooth muscle hypertrophy leads to bigger penis size, whereas surgery using tunica grafting without increasing smooth muscle content leads to big gains in size.

“The smooth muscle of the tunica”? You don’t have even clear what you are speaking of.

I did not get much sleep last night, I had to work late. I meant the smooth muscle *inside* the tunica.

How can axial stretching cause circumferential expansion? Imagine attaching a lead weight to the end of a rubber tube. Would that lead to circumferential expansion? Obviously not.

I agree that the evidence for PRP is actually quite week.

I typed “PLATELET RICH PLASMA” into google scholar and asked for papers from after 2008. The studies listed on the first page (excluding the review articles) were a balance of success and failure.

Achilles tendinopathy: Failed to work
arthroscopic rotator cuff repair: Failed to work
intra-articular knee injections: Worked successfully
jumper’s knee: Worked successfully

I am not really surprised that PRP is not a particularly effective technique. The body is almost perfectly evolved to deal with muscle damage. The relative ineffectiveness of PRP as a treatment for damaged muscle does not necessarily mean that the substance is incapable of inducing new muscle growth. The individual constituent hormones have been shown to do this.

Originally Posted by london100
I did not get much sleep last night, I had to work late. I meant the smooth muscle *inside* the tunica.

How can axial stretching cause circumferential expansion? Imagine attaching a lead weight to the end of a rubber tube. Would that lead to circumferential expansion? Obviously not.

Do you stretch a balloon before you blow it up?


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Originally Posted by london100
I agree that the evidence for PRP is actually quite week.

I typed “PLATELET RICH PLASMA” into google scholar and asked for papers from after 2008. The studies listed on the first page (excluding the review articles) were a balance of success and failure.

Achilles tendinopathy: Failed to work
arthroscopic rotator cuff repair: Failed to work
intra-articular knee injections: Worked successfully
jumper’s knee: Worked successfully
…..


The ‘worked successfully cases’ you are referring to are these?
http://www.prpcure.com/pdf/prp_aric…cle_10-2009.pdf
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2989009/

Notice a few things: first, both studies were done by the same team; second, they are pretty shitty works - some of the issues of the first study are for example raised here
http://www.springerlink.com/content/e7123kt6t8275067/

Third, the second study raise some doubts about the correcteness of the inference:
“….We treated 15 patients affected by chronic jumper’s knee, who had failed previous nonsurgical or surgical treatments, with multiple PRP injections and physiotherapy. We also compared the clinical outcome with a homogeneous group of 16 patients primarily treated exclusively with the physiotherapy approach.
……….
The analysis showed comparable results with the control group, with an even higher improvement in sports activity level in the PRP group.
…”
No blind study, no correct separation of groups, comparable results, no objective measure of the outcome, etc. etc..

But the foremost thing to note, is that the fancy mechanisme of regeneration is not observed in any of the study. PRT was used as a filler, in those ‘studies’. It acts reducing the friction, that’s all. And they even failed to demonstrate a objective superiority compared to other fillers or even no fillers at all. In the first study subjects had a worsening after 12 months. I would be courious to know if a 24 and 36 months follow up was performed.

Marinera,

That is a good point. I did not have time to look into the quality of the studies, but based on what you say they sound pretty poor.

Nevertheless, the aim of injecting PRP into the dick is to enlarge healthy smooth muscle, rather than repair damaged smooth muscle.

Thunderss,

That is also a good point. But I don’t think the two things are comparable. When you stretch a balloon you alter the property of the rubber by extending it past a certain point. I don’t think a comparable thing takes place when you hang. The stretch is not enough to fundamentally alter the properties of the collagen in the same way. That is just my opinion. It would be difficult to prove or disprove.
If the collagen is being weakened by proximal stretching than the whole penis should enlarge circumferentially in a uniform way. Apparently hanging tends to result mainly in base girth gains. That phenomenon supports my theory of stress-induced SM hypertrophy, because the base would be the area stressed the most by hanging. The actual swinging of the weight would damage the base and not the midsection of the dick.

LOL. If anyone was missing Fantom, here you are a heir.

Originally Posted by marinera

LOL. If anyone was missing Fantom, here you are a heir.

:)

Another guy willing to engage. Logically. Good. ;) :)

START looking at PRFM not prp only, prp is the mere base… Its the fact that the PRP turns to PRFM that makes it all work guys… Your looking in not all the right places if you are focused on PRP alone as the basis of the Priapus shot its PRFM that is the real key…

Its activated PRP remember not just plain PRP, that realeases growth factors, if not activated or if no real source of actual injury the PRFM does not form… The fibrin matrix needs to be activated, and this can happen via various means, such as collegan in the skin, thrombrin, and or calcium chloride and most specificly site specific injury. The healing cascased otherwise does not take effect and activate. PRP must be properly activated to WORK, else its much less effective then PRFM.

By the way I thought I would report something I have found to be interesting… I recently tried another TB4 shot and wow it really really reminded me of the way I felt when I got the priapus shot, my erection responce went way up, I am more full, I have more libido, when I first take the shot I feel really strong desire and pressure to be with my wife and when I am the volume of my semen is more then ever. Anyway I say this about TB4 and it reminded me even more of PRP\PRFM… Much described here sounds just like the element involved in PRP\PRFM and plasma and wound healing, etc etc, its quite striking. And it was the effects TB4 had on me that reminded me of when I got my priapus shot that sparked me to look for this info and bam I found it on some site the gogle cached…. If you search that title you can find the site..

The nature of Tb4

Thymosin beta 4 is a small 43 amino acid protein (a peptide) that was originally identified in calf thymus, an organ that is central in the development of immunity. Tb4 was later found in all cells except red blood cells. It is highest in blood platelets that are the first to enter injured areas, in wound healing. Tb4 is also detected outside cells, in blood plasma and in wound and blister fluids.

Its unique potential as a healing substance lies in that it interacts with cellular actin and regulates its activity. Tb4 prevents actin from assembling (polymerizing) to form filaments but supplies a pool of actin monomers (unpolymerized actin) when a cell needs filaments for its activity. A cell cannot divide if actin is polymerized. Tb4 therefore serves in vivo to maintain a reservoir of unpolymerized actin that will be put to use when cells divide, move and differentiate.

Tb4 has other effects that are needed in healing and repair of damaged tissue. It is a chemo-attractant for cells, stimulates new blood vessel growth (angiogenesis), downregulates cytokines and reduces inflammation, thus protecting newly formed tissue from damaging inflammatory events. Tb4 has been shown to reduce free radical levels (with similar efficiency as superoxide dismutase), decrease lipid peroxidation, inhibit interleukin 1 and other cytokines, and decrease inflammatory thromboxane (TxB2) and prostaglandin (PGF2 alpha).

An effective healer, Tb4 can be administered topically on the surface of cells and systemically, through injection. Besides healing skin wounds, Tb4 has been shown to promote repair in the cornea of the eye, in rats, thus preventing loss of vision.

Wound healing

A critical step in wound healing is angiogenesis. New vessels are needed to supply nutrients and oxygen to the cells involved in repair, to remove toxic materials and debris of dead cells and generate optimal conditions for new tissue formation. Another important step is the directional migration of cells into the injured area, joining up to repair the wound. This requires an attractant that will direct the cells to the wound and propel them to the site. These critical steps in wound healing are regulated by beta 4, as seen in the following experiments.

Endothelial cells

Cells that line blood vessels (endothelial cells), taken from human umbilical chord veins, were grown in culture and the layer of cells subjected to a scratch wound. Cultures were then treated with Tb4 or kept in growth medium without Tb4. When examined four hours later, Tb4 treatment attracted cells to migrate into the wound and accelerated their movement, showing it is a chemoattractant. Cell migration was four to six times faster in the presence of Tb4 compared to the migration of untreated cells. Tb4 also hastened wound closure and increased the production of enzymes, called metalloproteases, that could pave the way for angiogenesis by breaking down barrier membranes and facilitating the invasion of new cells to the needy area, to form new vessels. Other experiments showed Tb4 acts in vivo. When endothelial cells were implanted under the skin in a gel supplemented with Tb4, the cells formed vessel-like structures containing red blood cells, indicating the ability to stimulate angiogenesis in the animals.

Skin repair

Thymosin beta 4 accelerated skin wound healing in a rat model of a full thickness wound where the epithelial layer was destroyed. When Tb4 was applied topically to the wound or injected into the animal, epithelial layer restoration in the wound was increased 42% by day four and 61% by day seven, after treatment, compared to untreated. Furthermore, Tb4 stimulated collagen deposition in the wound and angiogenesis. Tb4 accelerated keratinocyte migration, resulting in the wound contracting by more than 11%, compared to untreated wounds, to close the skin gap in the wound. An analysis of skin sections (histological observations) showed that the Tb4 treated wounds healed faster than the untreated. Proof of accelerated cell migration was also seen in vitro, where Tb4 increased keratinocyte migration two to three fold, within four to five hours after treatment, compared to untreated keratinocytes.

More recently than when you first started this thread? :rolleyes:

Has this actually worked for you elsewhere, or is this the first forum you’ve tried this on? (I don’t mean the treatment.)


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J Mol Cell Cardiol. 2012 Jan;52(1):43-7. Epub 2011 Aug 26.
Thymosin beta 4 treatment after myocardial infarction does not reprogram epicardial cells into cardiomyocytes.

Zhou B, Honor LB, Ma Q, Oh JH, Lin RZ, Melero-Martin JM, von Gise A, Zhou P, Hu T, He L, Wu KH, Zhang H, Zhang Y, Pu WT.
Source

Key Laboratory of Nutrition and Metabolism, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai, China. zhoubin@sibs.ac.cn
Abstract

Myocardial infarction (MI) is one of the leading causes of morbidity and mortality world-wide. Whether endogenous repair and regenerative ability could be augmented by drug administration is an important issue for generation of novel therapeutic approach. Recently it was reported that in mice pretreated with thymosin beta 4 (TB4) and subsequently subjected to experimental MI, a subset of epicardial cells differentiated into cardiomyocytes. In clinical settings, epicardial priming with TB4 prior to MI is impractical.

Here we tested if TB4 treatment after MI could reprogram epicardium into cardiomyocytes and augment the epicardium’s injury response.
…………
Our result thus indicates that TB4 treatment after MI does not alter epicardial cell fate to include the cardiomyocyte lineage, providing both cautions and insights for the full exploration of the potential benefits of TB4 in the clinical settings.

http://www.ncbi.nlm.nih.gov/pubmed/21907210

Am J Sports Med. 2012 Feb;40(2):286-93. Epub 2011 Oct 20.
Effects of platelet-rich fibrin matrix on repair integrity of at-risk rotator cuff tears.

Bergeson AG, Tashjian RZ, Greis PE, Crim J, Stoddard GJ, Burks RT.

The augmentation of at-risk rotator cuff tears with PRFM did not result in improved retear rates or functional outcome scores compared with controls.
http://www.ncbi.nlm.nih.gov/pubmed/22016459

Am J Sports Med. 2011 Feb;39(2):258-65. Epub 2010 Dec 15.
Platelet-rich plasma augmentation for arthroscopic rotator cuff repair: a randomized controlled trial.

……
Eighty-eight patients with a rotator cuff tear were randomly assigned by a computer-generated sequence to receive arthroscopic rotator cuff repair without (n = 45) or with (n = 43) augmentation with autologous platelet-rich fibrin matrix (PRFM).
………
RESULTS:

All the patients completed follow-up at 16 months. There was no statistically significant difference in total Constant score when comparing the results of arthroscopic repair of the 2 groups (95% confidence interval, -3.43 to 3.9) (P = .44). There was no statistically significant difference in magnetic resonance imaging tendon score when comparing arthroscopic repair with or without PRFM (P = .07).
……….
http://www.ncbi.nlm.nih.gov/pubmed/21160018

Guess you did not read my post, it shows how to find the site it came from…

You just keep looking at the parts that fail, and not realizing why these mainly fail… No platelets… Not everyone will have it work… Thats a fact thanks for pointing it out, 30% of people will get no results…

Keep up the good work…

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