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Stretching effects at microscope. 2

A NEW METHOD TO ALIGN AND ORIENT HUMAN PATELLAR TENDON FIBROBLASTS DURING CYCLIC

MECHANICAL STRETCHING

*Wang, J H-C.; *Stone, D; +*Woo, S L-Y.

+*Musculoskeletal Research Center, Department of Orthopaedic Surgery, University of Pittsburgh

INTRODUCTION

In vitro model systems have been developed to study the effects (e.g.,

cell proliferation [1,4]) of repetitive mechanical stretching on tendon

fibroblasts without controlling the cell alignment and shape. Therefore, the

cellular responses may not be similar to those in vivo, as the tendon

fibroblasts align with collagen fibers and are subjected to tension along the

tendon stretching direction. We have developed an improved model, in which

cells are grown on microgrooved surfaces, instead of commonly used smooth

surfaces. The purpose of this study was to examine the effects of

microgrooved surfaces on alignment and shape of tendon fibroblasts, and cell

proliferation in response to cyclic mechanical stretching.

MATERIALS AND METHODS

Six-well silicone dishes were custom-made. Each well (about 3 cm2) of

the dish contained microgrooved surfaces………..

Thegrooves in the dishes were oriented either parallel or perpendicular to the dish

long axis, along which cyclic stretching was applied.

Human patellar tendon (PT) fibroblasts were isolated from surgical

tendon samples using explant tissue culture techniques. The cells, passaged

between 6 and 9 times, were transferred to silicone microgrooves and smooth

surfaces, both having been coated with 10 μg/ml of ProNectin-F (BioSystem,

CA) to promote cell adhesion to silicone surfaces. ………..

the cell shape was quantified using shape index(SI),

which is defined to be SI = 4π·A/P2, where A is a cell area and P is its

perimeter. …….

Note that the smaller the SI, the more elongated the cell. A total of 12

fibroblasts from grooves and smooth surfaces, respectively, were used in

determining cell SI. In separate experiments, cyclic stretches of 0 (i.e., without

stretching) and 8%, at 0.5 Hz, were applied to the dishes, using the stretching

apparatus previously described [3]. To determine cell proliferation, cells were

stretched for 2h, incubated in the stretching-conditioned medium for an

additional 24h, and directly counted with a hemocytometer.

….

RESULTS

Before being stretched, human PT fibroblasts aligned in silicone

microgrooves. After cyclic stretching, the cells remained aligned in the

grooves. This was true for cells in silicone microgrooves oriented both along

the stretching direction and perpendicular to the stretching direction. In

contrast, the same cells on smooth surfaces oriented away from the stretching

direction. Moreover, the cells in grooves had an elongated shape, whereas the

same cells on smooth surfaces had a well-spread shape (Fig 1).

The SI forcells in the grooves was 0.33 ± 0.10 (mean ± SD), whereas the SI for cells on

smooth surfaces was 0.60 ± 0.15. The two indexes were significantly

different (p < 0.0001).

Furthermore, cell numbers among the three conditions, that is, (a)

stretching cells in grooves oriented in the stretching direction, (b) stretching

cells in grooves oriented perpendicular to the stretching direction, and (c) no

stretching, were significantly different (p < 0.005). Specifically, cell number

under condition (a) was significantly higher than that under either conditions

(b) or (c) (p < 0.05), but cell number between (b) and (c) was not significantly

different (p > 0.05) (Fig 2).

DISCUSSION

The study showed that human PT fibroblasts can align in silicone

microgrooves with or without stretching. Further, the shape of cells in the

grooves became significantly elongated, compared with that of cells on

smooth surfaces. This elongated cell shape is similar to that of tendon

fibroblasts in vivo. Thus, these elongated cells in microgrooves may have a

metabolic state closer to that in vivo, since cell shape determines cell

functions [2].

Moreover, this study showed that human PT fibroblasts can proliferate

in silicone microgrooves, which was confirmed by assaying DNA synthesis

with BrdU incorporation. Furthermore, in response to cyclic mechanical

stretching, proliferation of the tendon fibroblasts was different when the cells

were stretched along their long axes or transverse axes, although stretching

magnitude in both cases appeared to be similar. This result suggests that other

cellular responses, for instance, stretching-induced inflammatory mediators

[1], may also depend on cells’ long axes with respect to stretching direction.

……

Link

Stretching: more is more?

DETERMINING AN EFFECTIVE STRETCHING TIME FOR ACHILLES TENDON
EXTENSION

Hiroshi Kanazawa1,2, Yukio Urabe2, Hisao Iwamoto1,2, and Taizan Shirakawa1
1 Matterhorn Rehabilitation Hospital, Rehabilitation Center, Hiroshima, Japan
2 Graduate School of Health Sciences, Hiroshima University, Hiroshima, Japan
Stretching exercises are commonly undertaken for sports and rehabilitation. However, it
is unknown how an in vivo muscle-tendon unit responds to added stretching stimulation.
The purpose of this study was to determine an effective stretching time for Achilles
tendon extension. The human medial head of the gastrocnemius muscle was stretched
and ultrasonography was used to determine and then compare the length of the Achilles
tendon between before and after stretching. Achilles tendon extension for one minute of
stretching was 3.4±2.5mm, two 6.8±2.1mm, three 6.9±1.0mm, five 7.2±0.7mm, and ten
7.4±0.8mm. Achilles tendon length was significantly increased for up to two minutes of
stretching (p<0.01). However, there were no significant differences for stretching for
three or more minutes. From these results, we conclude that two minutes of static
stretching is effective for Achilles tendon extension.

Link

Stretching: static agains cyclic. A study

Comparison of Cyclic and Sustained Passive Stretching Using a Mechanical Device to Increase
Resting Length of Hamstring Muscles

DEBORAH TURNER STARRING,
MARILYN R. GOSSMAN,
GARVICE G. NICHOLSON, JR,
and JACK LEMONS

The purpose of this study was to compare the effects of cyclic versus sustained
passive stretching with a mechanical device on resting hamstring muscles’
length. Group 1 subjects (5 men, 17 women) underwent cyclic stretching of their
right hamstring musculature, and Group 2 subjects (5 men, 16 women) underwent
sustained stretching of their right hamstring musculature. The stretching procedures
were performed for 15 minutes on 5 consecutive days.
A follow-up examination
of the subjects’ relative knee flexion range of motion was made one week
posttreatment. The Group 1 subjects had a mean ROM increase of 15.4 ± 5.0
degrees after the five stretching treatments and maintained a mean ROM increase
of 10.4 ± 5.5 degrees on the follow-up examination (p < .001). In Group 2, the
five stretching treatments resulted in a mean ROM increase of 13.4 ± 4.4 degrees,
and a mean increase of 7.9 ± 4.0 degrees was maintained on the follow-up
examination (p < .001). Linear regression analysis revealed that initial ROM, sex,
and treatment method significantly contributed to increases in ROM from Day 1
of treatment to the follow-up examination (F = 6.04; df = 4,36; p < .0008). The
cyclic stretching method resulted in a greater gain in ROM when the other
variables were considered.

Originally Posted by marinera
You are splitting hair.

To “base” a conclusion upon something is similar to declaring it as the “basis” (or foundation) for your conclusion.
To offer “supporting evidence” is to point to other circumstances/occurences that either support or do not negate your conjecture.

As you have posted so many various extracts here, I am astounded that you don’t see the difference - or do you not want to see the difference?

(1) Absolutely nothing you’ve posted “contradicts” whats in my PDF (no matter how much you might want to believe that).

(2) Pointing out that the glans did not enlarge from the priapism because priapism did not effect the glans is simply circuitous reasoning. That’s like answering the question, “How does PE enlarge the penis?” by saying “PE enlarges the penis.”

If you, again, see that they indicate that his massive engorgement resulted from a loss of elasticity of the tunica - and since that engorgement applied great pressure to the entire penis - you would conclude that the glans did not lose elasticity (or if it did, it didn’t lose enough to cause deformation).

Why? Because the glans is far more elastic than the other tissues in the penis.

One more point: am I the only one who sees the irony in all this? marinera ignores a study DIRECTLY involving *massive penis enlargement* to post extracts about patellar tendons & achilles tendons.

That’s beautiful. I think I recall seeing an extract in the forum about a rat tail tendon.

But a guy whose cock balloons 40-50% (to 7.67” of girth), draws only contempt, dismissal. Furthermore, those who’d conducted the indepth study - including thermal imaging (read: they even looked inside his penis!), their conclusions are dismissed as “opinion” (could it be because they validate my theory?).

I’m sorry. Let’s get back to the discussion about the achilles tendon. Rat tails, anyone?

No I agree that they are nothing in common or alike.

What exactly caused this guys dick to get so big and ugly?

Originally Posted by wadzilla

To “base” a conclusion upon something is similar to declaring it as the “basis” (or foundation) for your conclusion.

……..

Why? Because the glans is far more elastic than the other tissues in the penis.

If a reasoning is supported solely by a premise, that premise is the basis of that reasoning. In this case, the basis of that reasoning is that the glans wasn’t enlarged because it is more elastic: that’s false, the glans wasn’t enlarged because priapism doesn’t affect the glans.

If loss of elasticity was the cause of enlargement in that case, the enlargement had to be seen after a short time from the episodes of priapism. If you stretch a rubber band beyond its elastic limit, it remains stretched right after the application of force, not after months or years. It’s clear that the overstretching caused an augment of the tissue of the penis in the subject affected by priapism.


Last edited by marinera : 07-25-2009 at .

Originally Posted by wadzilla

One more point: am I the only one who sees the irony in all this? marinera ignores a study DIRECTLY involving *massive penis enlargement* to post extracts about patellar tendons & achilles tendons.

……

I don’t ignore. I comment, then I move along. I posted more than one study about those “massive penis enlargement”; no one supports your hypothesis that penis can grows only by ‘elastic deformation’.

All studies posted here are supporting the idea that CT is metabolically active, AKA it is similar to muscle: it is subject to changes, injuries, repairing, growth.

The Etp hypothesis is, basically, seeing the penile tissue like not-living tissues, that can be only stretched. So, according to this hypothesis, TA of the penis, despite having the same characteristcs of ligaments and tendons, is not subjected to hypertrophy, mitosis, etc.. This view is supported by nothing.


Last edited by marinera : 07-25-2009 at .

Originally Posted by wadzilla
………. Furthermore, those who’d conducted the indepth study - including thermal imaging (read: they even looked inside his penis!), their conclusions are dismissed as “opinion” …….
In that abstract (the sole you are quoting as supporting your hypothesis) :
Blood oxygen level-dependent magnetic resonance imaging revealed enlarged, hypoxic corpora cavernosa.

So, what they are saying is that….. the penis was enlarged. The exam didn’t explains anything, nor supports your opinion.

Anyway, let me ask: if megalophallus is just as simple as loss of elasticity of TA, why it is not frequently observed in all cases of priapism? Why is it rarely observed only in priapism associated with sickle cells anemia?

Reduction Phalloplasty and Penile Prosthesis Implantation in a Case of Megalophallus as a Consequence of Neglected Priapism

Authors: S Kattan1; RM Seyam1; D Al-Ghamdi1

Source: The Journal of Sexual Medicine, Volume 1, Supplement 1, November 2004 , pp. 142-142(1)

Megalophallus is a rare complication of priapism and sickle cell disease. More commonly, priapism in those patients is recurrent, difficult to prevent and ends up in erectile dysfunction as a result of cavernous tissue fibrosis

Link

No sudden loss of elasticity, Wad. And there are changes in tissue structure. Fibrosis is a consequence of impaired healing process, you may know.


Loss of elasticity is a cause, not the whole phenomenon: a cause of cellular changes in the tissue.

What we hope to achieve, through PE, is an optimal healing of micro-damages, that, with time, will enlarge our penis. That’s why most of gains are permanent.







Last edited by marinera : 07-25-2009 at .

Last but not least: is something that lasts for 9 years permanent enough in your book, Wad? Because, you see, your axiom “Gains last only three years because they are just elastic loss” doesn’t quite accords with the abstract you are citing:
“…The patient had had an intense episode of priapism 9 years previously and his penis remained enlarged….”
Link

What caused the enlarged TA to fix at that enlarged size, if not structural changes in the penile tissue? This means production of new tissue, IMO - the amount of tissue after the enlargement was bigger than before.

Also:
”..A 33 year old man presented to us with a history of neglected priapism for 12 days 2 years previously. He developed a permanent unusual enlargement of the penis..”
Link

How could an elastic enlargement achieved in 12 days last for 2 years? Elastic gains should last the same amount of time that is needed to achieved them or less - here we have exactly the opposite.

See, reading articles about rat tail tendons can be more useful than misunderstanding abstracts about priapism. ;)

Last but not least: is something that lasts for 9 years permanent enough in your book, Wad? Because, you see, your axiom “Gains last only three years because they are just elastic loss” doesn’t quite accords with the abstract you are citing:
“…The patient had had an intense episode of priapism 9 years previously and his penis remained enlarged….”

marinera, I never said “gains last only 3 years.” Never. You are now clearly just being argumentative. I said - if you even care to know - that I kept my enlargement for 3+ years without any losses - then the losses came. Some like lil12big1 kept a percentage of their gains for even longer.

What caused the enlarged TA to fix at that enlarged size, if not structural changes in the penile tissue? This means production of new tissue, IMO - the amount of tissue after the enlargement was bigger than before.

So why doesn’t this apply to weight training? Why not more tissue keeping those larger muscles for years after your last gym workout.

Also:
”..A 33 year old man presented to us with a history of neglected priapism for 12 days 2 years previously. He developed a permanent unusual enlargement of the penis..”

How could an elastic enlargement achieved in 12 days last for 2 years? Elastic gains should last the same amount of time that is needed to achieved them or less - here we have exactly the opposite.

(1) Who could “build unusual (tissue) enlargement” in 12 days? So why not just PE for 12 days then quit? Or the same with going to the gym? NO TISSUE GAINS can occur in 12 days - certainly not “unusual enlargement” unless there was deformation.

(2) Who said that elastic gains should last the same amount of time that is need to achieve them or less”??? What I said is that elastic gains should last until those cells had been “recycled” vian one’s DNA - this has nothing to do with the length of time that it took to deform those tissues.

See, reading articles about rat tail tendons can be more useful than misunderstanding abstracts about priapism.

So keep reading them.

Look, I can go on and on…you mention fibrosis, yet the article specifically states that he did not experience that, but that he had NORMAL FUNCTIONING of the penis.

no one supports your hypothesis that penis can grows only by ‘elastic deformation’.

With that statement, I see your delusionality. Many here agree with me. I’ve seen posts in the forum that specifically stated that MY view is the one that makes sense. I’ve also received a number of PMs to that effect.

If you can’t/won’t understand what I wrote in 50+ pages then 500+ posts won’t matter. Keep reading your unrelated extracts and, as you’ve habitually done, grossly misrepresenting what I’ve said.

I’m done with this political bullshit. This was never a part of the forum before; now, you get more politics here than on all the Sunday afternoon news programs.

Originally Posted by wadzilla
(3) I will concede that they seem to be employing a “generic” reference to hypertrophy, and not always the strict application associated with striated skeletal muscle. Because even though they claim the massive enlargement was due to “loss of elasticity,” they still employed the phrase “hypertrophy” (obviously in a loose manner). Yet the other, 134-yr old, study is far from modern science.

I think you are confusing the study you cited in your EtP thread (MEGALOPHALLUS AS A SEQUELA OF PRIAPISM IN SICKLE CELL ANEMIA) with the study marinera cited (AN UNUSUAL CASE OF PRIAPISM). The former doesn’t use the term hypertrophy at all, however the latter does, several times.

Authors of the former study conducted two tests: a penile color flow Doppler ultrasound scan and Blood oxygen level-dependent magnetic resonance imaging (BOLD-MRI).

BOLD-MRI detected the presence of deoxygenated hemoglobin in the corpora cavernosa.

Regarding Doppler imaging they state:

Quote
A penile color flow Doppler ultrasound scan revealed
good blood flow within the cavernosal arteries
and branches, with areas of high velocity

Quote
Fibrosis of the corpora cavernosa,
as previously hypothesized,2 should result
in low flow by Doppler imaging.

In the introduction they state:
Quote
Megalophallus has previously
been reported in association with sickle cell anemia
and is thought to result from fibrosis of the
corpora cavernosa.2

Since good blood flow within the CC seems to discount the possibility of fibrosis as a cause of enlargement, they proposed an alternative mechanism for this enlargement:
Quote
The increase in penile circumference follows
a sudden and permanent loss of elasticity of
the tunica albuginea, brought about by a particularly
intense priapism and a very engorged organ.
The loss of elasticity of the tunica albuginea releases
constraints on the corpora cavernosa, which
then expand like a sponge.

They claim that the plausibility of this mechanism of enlargement is supported by the “lack of increase in the circumference of the glans in our patient”, which according to them, is due to the fact that “the glans penis sinusoids are larger and the tunica albuginea is absent”. They do not mention any other evidence which would support their hypothesis.

If my understanding is correct, the tests they conducted simply show the presence of deoxygenated hemoglobin in the CC and good blood flow within the CC (which seems to invalidate the hypothesis of fibrosis as a cause of enlargement).

The latter study states that the glans and the CS “are not involved in priapism”, meaning they are not subject to engorgement. The conclusion that can be drawn from this study is there can be no priapism-induced enlargement of the glans or the CS simply because there is no priapism to induce enlargement in the first place. Priapism is confined to the CC.

Authors of the study marinera cited state the following regarding the possible mechanism of enlargement:

Quote

Furthermore, repeated episodes of mild

hypoxia resulting from the transient partial venous

obstruction in our patient might have been a stimulus

for the hypertrophy of corpora cavernosa, because

hypoxia is known to result in hypertrophy of tissues.4

Exactly, gjurob, thanks for saving some of my time. :)

Originally Posted by wadzilla
……..
marinera, I never said “gains last only 3 years.” Never. You are now clearly just being argumentative. I said - if you even care to know - that I kept my enlargement for 3+ years without any losses - then the losses came. Some like lil12big1 kept a percentage of their gains for even longer.
……….
You are backtracking Wad, don’t make me search because we all know what you wrote - it’s still on this site.

Originally Posted by wadzilla
………..
So why doesn’t this apply to weight training? Why not more tissue keeping those larger muscles for years after your last gym workout.
………
Because weight training is based mainly on hypertrophy of striatus muscles, where gains through PE are based on extracellular matrix rearrangement and hyperplasia of smooth muscle and connective tissue.

Originally Posted by wadzilla
….
(1) Who could “build unusual (tissue) enlargement” in 12 days? So why not just PE for 12 days then quit? Or the same with going to the gym? NO TISSUE GAINS can occur in 12 days - certainly not “unusual enlargement” unless there was deformation.

(2) Who said that elastic gains should last the same amount of time that is need to achieve them or less”??? What I said is that elastic gains should last until those cells had been “recycled” vian one’s DNA - this has nothing to do with the length of time that it took to deform those tissues.
…….
1) a guy with an unusual proliferative reponse to traumas, like could be the case for a man with sickle cell’s anemia, maybe;

2) >>Who said that elastic gains should last the same amount of time that is need to achieve them or less”???<<

That’s how elastic phenomena works in Physics, but maybe you want to change Physics laws also, now?

>>What I said is that elastic gains should last until those cells had been “recycled” vian one’s DNA - this has nothing to do with the length of time that it took to deform those tissues.<<

That doesn’t make any sense. ‘Elastic gains’ means that you are supposing cell’s don’t change in number or size as a consequence of stimuli - that’s why you supposed gains are just temporary. Introducing “recycling of cell’” (vian one’s DNA?!?!!) is contradictory with the idea of elastic gains.

Originally Posted by wadzilla
……
no one supports your hypothesis that penis can grows only by ‘elastic deformation’.


With that statement, I see your delusionality. Many here agree with me. I’ve seen posts in the forum that specifically stated that MY view is the one that makes sense. I’ve also received a number of PMs to that effect.

Don’t try this with me, Wad, do a better job when quoting:
Originally Posted by marinera
……I posted more than one study about those “massive penis enlargement”; no one supports your hypothesis that penis can grows only by ‘elastic deformation’.
……..
With “no one”, I was referring to studies, not to people.

Originally Posted by wadzilla
……..
I’m done with this political bullshit. This was never a part of the forum before; now, you get more politics here than on all the Sunday afternoon news programs.
Political bullshit?! Where you see politics here?


Last edited by marinera : 07-25-2009 at .
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