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My MaxVac Setup Longerstretch's Golf Weight and HTW setup My Log

Starting Size: circa 2003: 5 BPEL x 5.0 MSEG August 2007: 6 2/3 BPEL x 5.5 MSEG

04/22/08: 7.5 BPEL x 5.6 MSEG... On and Off again for a while... Restart PE in late 10/2013... 11/25/13: 7.75 BPEL x 5.75 MSEG

:)

collagenous tissue healing and contraction

Connective Tissues Contradiction in Wound Healing

An Experimental Study in Vivo and In Vitro

M. Reza Ghassemifar, MSe

Akademisk avhandling

som för avläggande av doktorsexamen i medicinsk vetenskap kommer att offentligt försvaras i Patologens föreläsningssal, plan 1 1, Hälsouniversitet, Linköping, fredagen den 8 mars, kL 09. 00. 1996

Contraction of connective tissue is an important part of tissue repair that reduces the wound space and helps to decrease the formation of scar tissue, both of which are needed to restore tissue integrity. In the present study, certain cellular mechanisms that are active during connective tissue contraction were assessed and the influence of transforming growth factor-ß1 on these mechanisms was evaluated in normal rat and protracted mouse contraction.

…….

In conclusion, the results have shed further light on various cellular activities during connective tissue contraction. …….The complex interaction of these mechanisms await to be further elucidated.

Department of Pathology II

Linköping University, Linköping, Sweden

Linköping 1996

Link

2 Healing by repair

If the injury occurred in cells that can’t regenerate (e.g. cardiac muscle or neurons), or if the collagen network has been damaged (e.g. by enzymes or physical destruction), or even if the collagen has collapsed (as can happen in an infarct), healing must happen by repair.

Repair starts happening soon after necrosis of the tissues, and ultimately results in a scar made of collagen, containing a small number of fibroblasts.

The first thing that happens is that the dead tissue is removed by macrophages. This is the process of demolition. As well as phagocytosis the tissue, macrophages release chemical factors that encourage fibroblasts and new capillaries.Capillaries are the smallest of the body’s blood vessels. They connect arteries and veins. Capillaries have walls composed of a single layer of cells, the endothelium. This layer is so thin that molecules such as oxygen, water and lipids can pass through to form.

Immature granulation tissue is the next thing to form. This contains plump active fibroblasts, producing lots of type III collagen very quickly. There are many new capillaries that are leaky and dilated, that are necessary to supply nutrients to the new cells.

Granulation tissue moves, as a wave, from the border of the injury towards the centre of the necrotic area. As the granulation tissue matures the fibroblasts produce less collagen, and are much more spindly in appearance. The collagen they produce is the much stronger type I collagen. Some of the fibroblasts contain actinMicrofilament Actin is a contractile protein filament important for cell movements. It is expressed in all body cells, but especially in muscle cells. Actin can polymerize into microfilament, which are essential for the cytoskeleton, for cell motility, an and myosinMyosin is a contractile protein filament found in muscle tissue. Together with actin filaments, myosin provides the mechanism for muscle contraction, utilizing energy from ATP. Muscle is composed of muscle cells (sometimes known as “muscle fibers”). Withi bundles, like smooth muscleSmooth muscle is a type of non- striated muscle, found within the ” walls” of hollow organs; such as blood vessels, bladders, uteri. gastrointestinal tracts, Smooth muscle is used to move matter withintraction|contraction]]; it generally operates ” involu which enables them to contract.

Eventually, the vessels of granulation tissue disappear, and there is a lot of type I collagen with a few spindly fibroblasts. This, and contraction of the myofibroblasts, has left a small white scar on the tissue.

Link

Impaired function of postoperative macrophages from zinc-deficient rats decreases collagen contraction. Brief report.

Zinc deficiency impairs connective tissue contraction in the perforated rat mesentery model. Since the rat mesentery is almost avascular, free peritoneal macrophages are important for mesenteric repair. Impairment of contraction may thus be caused either by a direct effect of zinc deficiency on tissue cells or by hampered macrophage function. To further elucidate the role of macrophages in tissue contraction, we studied their effect on lattice contraction. A number of typical functions of macrophages in zinc deficiency were also investigated. Lattice contraction was significantly impaired by conditioned medium from zinc-deficient macrophages…………….Conditioned medium from zinc-deficient macrophages was shown to impair lattice contraction in vitro and the results are compatible with impaired macrophage function as a cause of decreased connective tissue contraction in vivo.

Ghassemifar, M R : Olsson, M G : Agren, M S : Franzen, L E

APMIS. 1995 May; 103(5): 395-400

Link

So:

a) collagenous tissue does contracts, at difference from some believe;

b) this contraction is an important mechanism in wound healig;

c) figthing the contraction leads to a bigger formation of scar tissue;

d) deficiency of Zinc could impair the healing process.

Fatigue is More Damaging than Creep in Ligament Revealed by Modulus Reduction and Residual Strength

Gail M. Thornton1, 2, 3, Timothy D. Schwab2 and Thomas R. Oxland2

Abstract …….
Normal ligaments are exposed to static (creep) and cyclic (fatigue) loading from which damage can accumulate at these higher than normal stresses. This study tracked damage accumulation during creep and fatigue loading of normal rabbit medial collateral ligaments (MCLs) over a range of stresses, using modulus reduction as a marker of damage. Creep tests were interrupted occasionally with unloading/reloading cycles to measure modulus. Test stresses were normalized to ultimate tensile strength (UTS): 60%, 30%, and 15% UTS. Not all creep and fatigues tests progressed until rupture but were stopped and followed by an assessment of the residual strength of that partially damaged ligament using a monotonic failure test. Fatigue loading caused earlier modulus reduction than creep. Modulus reduction occurred at lower increases in strain (strain relative to initial strain) for fatigue than creep. In other words, at the same time or increase in strain, fatigue is more damaging than creep because the modulus ratio reduction is greater. These findings suggest that creep and fatigue have different strain and damage mechanisms. Ligaments exposed to creep or fatigue loading which produced a modulus reduction had decreased residual strength and increased toe-region strain in a subsequent monotonic failure test. This finding confirmed that modulus reduction during creep and fatigue is a suitable marker of partial damage in ligament. Cyclic loading caused damage earlier than static loading, likely an important consideration when ligaments are loaded to higher than normal magnitudes following injury of a complementary joint restraint.

Annals Of Biomedichal Engineering
Vol. 35, N. 10, October 2007
pages 1713-1721

Link

This study was posted before, but only in abstract. I think the whole document is interesting:

AN UNUSUAL CASE OF PRIAPISM

Mehdi Jam, MD, Nand S. Datta, MD, and Asghar Askari, MD

Los Angeles, California

J Nati Med Assoc. 1993;85:473-474

A 24-year old black man was diagnosed to have

sickle cell disease (SS hemoglobin) at the age of 2

years. He developed the first episode of priapism at the

age of 17 years when he was seen by our service for the

first time. This episode of priapism was associated with

vaso-occlusive crisis. ……..Since then he

has had 62 more episodes of priapism. Of these, 24

episodes were associated with other vaso-occlusive

crises, whereas 39 were isolated episodes of priapism.

…….

The range of duration of priapism was 2 to 8 days,

the average being 4 days. ……..

Successful resolution of the initial episodes of

priapism with medical management and no loss of

potency had convinced him that he did not need surgical

treatment.

Initial physical examination revealed normal-looking

external genitalia. However, subsequently the penis

gradually showed excessive growth and at the last visit

the penis measured 18 cm in length (from the pubic symphysis

to the tip of the penis) and 161/2 cm in circumference

in flaccid state. The hypertrophy was confined to

the corpora cavernosa. The glans penis and the scrotum

were of normal size. During an episode of priapism, the

penis further increased in size and got very tender.

…..

The exact mechanism of priapism is not well understood.

However, in sickle cell disease, it is believed to be due to blockage of venous

drainage by sickled cells. This results in ischemia of

the cavernous tissues of the corpora cavernosa. If

priapism is not treated within a reasonable period of

time, the ischemic injury to the delicate cavernous

tissue results in subsequent fibrosis and impotence.

Our patient did not develop impotence despite the

fact that he had several episodes of priapism. On the

contrary, he developed hypertrophy of his penis. The

exact reason for such occurrence is not clear. It appears

that the degree of venous obstruction in our patient was

such as to produce filling and engorgement of the

cavernous spaces resulting in prolonged erection and at

the same time the obstruction was not complete so that

the circulation through the cavernous spaces continued

to the extent that ischemic injury did not occur. Lack of

ischemic injury to the cavernous tissue was possibly

responsible for the preservation of potency.

When sickling occurs within the cavernous spaces of

the corpora cavernosa in sickle cell disease, it appears to

result in a spectrum of hemodynamic changes. On the

one end of the spectrum is total venous occlusion

resulting in priapism, cavernous ischemia and subsequent

fibrosis, and impotence, and on the other end is

the minimal venous occlusion with no priapism and no

ischemic changes. In the middle of the spectrum, there

appears to be various degrees of partial venous

obstruction, resulting in priapism associated with

adequate oxygenation of the cavernous tissue because

of continued circulation in the presence of incomplete

venous occlusion. Our patient represents such an

example. 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 It

is interesting to note that the penile hypertrophy was

confined to the corpora cavernosa and that the glans and

the corpus spongiosum were of normal size. It is well

known that the latter structures are not involved in

priapism5-7 and hence they are not subjected to hypoxic

stimulus to under hypertrophy.

Literature Cited

1. Tarry WF, Duckett JW, Synder H. Urological complications

of sickle cell disease in a pediatric population. J Urol.

1987; 1 38:592-594.

2. Edmond AM, Holman R, Hayes RJ, Serjeant GR.

Priapism and impotence in homozygous sickle cell disease.

Arch Intem Med. 1980;1 40:1434-1437.

3. Datta NS. Megalophallus in sickle cell disease. J Urol.

1977;1 17:672-673.

4. Florey L. General Pathology. 4th ed. Philadelphia, Pa:

WB Saunders Co; 1970:638-640.

Link

Originally Posted by marinera

… 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 …

Link

Could that be the case for clamping? Not that much of expansion by pressure, but the hypoxia due to venous obstruction to be responsible for girth gains?


Starting BPEL: 6.9" (Dec.1st, 2008)

Current BPEL: 8.11" NBPEL: 7.63" BPFSL: 9.09"

Current MEG : 5.6"

That’s the hypothesis I’m sustaining, cervix, here, for example. Or, to say it better, I thing both expansion by pressure and lack of oxygen are responsible factors.

A thought at some point that I’ve read most of the important threads on this forum. Then I realized that it’s just the tip of the aisberg. It’s hard to find a really new idea, that hasn’t been thought earlier!

This starvation of oxygen resulting in hypertrophy may also be responsible for the benefits reported for edging. Positive PI of night and morning woods are also associated with more/longer erections. As erection is also a mild deprivation of oxygen compared to flaccid state, longer erections should also lead to hypertrophy. Things make sense…


Starting BPEL: 6.9" (Dec.1st, 2008)

Current BPEL: 8.11" NBPEL: 7.63" BPFSL: 9.09"

Current MEG : 5.6"

Originally Posted by cervixhunter
A thought at some point that I’ve read most of the important threads on this forum. Then I realized that it’s just the tip of the aisberg. It’s hard to find a really new idea, that hasn’t been thought earlier!
……..

Holy words! :)

Originally Posted by cervixhunter
……..
This starvation of oxygen resulting in hypertrophy may also be responsible for the benefits reported for edging. Positive PI of night and morning woods are also associated with more/longer erections. As erection is also a mild deprivation of oxygen compared to flaccid state, longer erections should also lead to hypertrophy. Things make sense…

It should. Problem is: I never have seen any proof of gains by edging. Maybe the degree of oxygen deprivation doesn’t reach the minimal level required to start hypertrophy. Or maybe the erections should last longer. It could be interesting to know if priapism does cause harder AND longer than normal erections, or just longer.

Priapism is considered an erection lasting at least 4 hours. Even if it’s not harder than a standard erection, deprivation of oxygen can do irreversible damage to the tissues.

For sure edging is never so long and neither continuous erection!


Starting BPEL: 6.9" (Dec.1st, 2008)

Current BPEL: 8.11" NBPEL: 7.63" BPFSL: 9.09"

Current MEG : 5.6"

So, is there a trade-off between intensity of erection (force applied with the clamp, to speak), and time of blood occlusion? I mean, could a more complete blood-occlusion cause in less time the same hypertrophy than a mild continous erection could cause after hours? My guess is yes. I’d like to hear what other people thinks.

This part is also interesting:
“Initial physical examination revealed normal-looking
external genitalia. However, subsequently the penis
gradually showed excessive growth and at the last visit
the penis measured 18 cm in length (from the pubic symphysis
to the tip of the penis) and 161/2 cm in circumference
in flaccid state.”

It sounds like there was a delay between stress and growth - we’d say : after rest, the penis was grown. It doesn’t accords well the Etpt theory, I think. If the penis could only grow through elastic deformation, than only quasi-instantanous changes in size were possible.

Originally Posted by marinera

So, is there a trade-off between intensity of erection (force applied with the clamp, to speak), and time of blood occlusion? I mean, could a more complete blood-occlusion cause in less time the same hypertrophy than a mild continous erection could cause after hours? My guess is yes. I’d like to hear what other people thinks.

That’s the logical conclusion. You should include in the trade-off also the more dangers that go with complete occlusion.


Starting BPEL: 6.9" (Dec.1st, 2008)

Current BPEL: 8.11" NBPEL: 7.63" BPFSL: 9.09"

Current MEG : 5.6"

If so, even constriction in a flaccid state should cause some degree of growth.

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