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- Feb 11, 2007
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As per a continued discussion hitherto haven taken place in the 'Hang-off' thread, I performed some preliminary biological investigations as to the mechanisms of cellular repair, especially the cellular repair of the types of cells as found in the tissues of the penis. As we all know, or rather, for all we care, the penis is composed of three anatomical bodies (four if you consider the corpora cavernosa as two seperate anatomical entities), essentially: the corpora cavernosa penis, the corpus cavernosum urethrae, and the tunica albuginea (the septum, as we colliquially term it, is simply the juncture of the lateral fibers of the tunica albuginea (there are, anatomically speaking, two distinct types of fibers which constitute the tunica, the first type are the superficial, longitudinal fibers which form a sheath around the corporas, the second group are lateral fibers which encircle, widthwise, the corporas and combine at a median juncture called the septum.)). ( The Penis - Gray's Anatomy of the Human Body - Yahoo! Education ). However, all of this is irrelevent to the treatment of our central concern which we have acknowledged, in the beginning, as the biochemical mechanisms of cellular repair and damage signaling in the penis. Now, it is here that we begin to encounter considerable difficulties which we may not be able, without considerable cost, to clear away. The biology texts which I still possess only speak about cellular damage and reconstitution in two different contexts: (1) the context of the inflammation response, and (2) the context of cellular communication. I shall speak about each of these in turn.
THE INFLAMMATION RESPONSE
The inflammation response is a thouroughly examined histological response to damage. Conjecturally, it consists of 5 varied elements each with their own adaptive functional utility. They are: swelling, redness, heat, pain and loss of function. According to Frederic H. Martini's 'Fundamentals of Anatomy and Physiology', "the restoration of homeostasis after a tissue injury involves two related responses" (139). He is insistent that all damage to vascular tissue responds to disruptions in homeostasis in this fashion, and, considering the accolades lauded upon this textbook, some degree of trust must inevitably be placed in the author's rather erudite opinion. Yet, do we as hangers notice any of these classic symptoms of the inflammation response? Concerning the first mentioned congenial symptom of inflammation, swelling, it is mentioned in a wikipedia aritcle on the matter that the swelling of the organ affected need not necessarily be visible ( Inflammation - Wikipedia, the free encyclopedia ). It is possible, however, that the periodically observed instances of momentary increases in BPFSL size are attributable to penile inflammation. It would be interesting to see as to whether or not the adminstration of known anti-inflammatory analgesics, such as aspirin, would combat post-hang BPFSL increases. Concerning redness, if we are indeed succeeding, in our various hanging regimens, to stress the ligaments and/or the tunica albuginea and not, as it where, the superficial skin, the redness itself would not be noticeable as the inflammation response would be directly affecting these subcutaneous tissues. Concerning pain, this is, itself, rather a recondite subject, for, what exactly is the difference between pain and general tissue fatigue? Certainly the difference is a matter of degree much in the same fashion as the difference between personal idiosyncracy and neurosis is itself little more than a matter of degree. Indeed, although the traditional ideologies rightly informed us to avoid pain, they do pedantically instruct us to quest after fatigue. Fatigue is a part of the inflammation response. Concerning loss of function, some hangers have, historically, reported a temporary incapacity to acheive erection following a hanging session. However, considering that we sensible hangers are not pushing ourselves to pain, we are neither pushing ourselves to complete tissue failure, which could, itself, present a rather serious medical problem ( Penile fracture - Wikipedia, the free encyclopedia ). Consequently, then, those of us not pushing the envelope beyond the pale of reason should not logically expect complete organ failure as a consequence of our practice. If you do, though, experience such an unhappy symptom, I'd recommend that you slow the fuck down and take a good old-fashioned time-out for yourself. Fine then, so the inflammation response is present. That is all well and good, yet, what does this portend for us? We shall discuss this in detail later.
CELLULAR COMMUNICATION AND TISSUE DAMAGE
Well, I'm getting really damned bored of writing all of this, so... all of you are going to have to wait until tomorrow before I finish it (if I do then....).
CELLULAR COMMUNICATION AND TISSUE DAMAGE
Intracellular communication occurs, in every instance, vis-a-vis chemical signaling molecules (not necessarily, in every cause, a macromolecule such as protein) which act as a ligand and bond to a protein receptor either on the cell-surface or in the cytoplasm of the cell. Whether or not a signaling molecule binds to receptors on the cell membrane or in the cytoplasm of the cell depend on a number of factors such as the extent of the chemical's hydrophobia or lipophilia, its mass etc; however, in keeping with the issue at hand, we needn't concern ourselves with tangential details such as this. Yet, it is obvious that it must be a concern of ours as to what actually causes cell communication such as we are beginning to describe. Cells respond only to a limited number of varying stimuli, a few of which are the following: light, pressure, specific chemicals (that is, chemicals which the cells are themselves evolutionarily adapted to recognize and recieve), electric potential variation. When hanging, it is obvious that we are directly affecting cells by simultaneously stretching their internal cytoskeletons and stressing intracellular bonds (as affected, say, by CAMs); obviously, we are destroying pre-existing cellular homeostasis. In biology, any such disruption of homeostasis is termed 'stress' and our friend the cell possesses a peculiar method of reacting to stress which has been inculcated in it over the course of evolutionary time.
However, for the time being, let us return to our consideration of cytoskeletons and how we hypothesize them to be affected by the violent stresses of hanging. Cytoskeletons are composed of three different types of filaments (the filaments themselves are composed of actin and myosin proteins): microfilaments, intermediate filaments, and microtubules. Each of these cellular constituents are vital for the function of the cell as these filaments are directly involved in cell mitosis (cell division), intercellular transport (without the cellular autobahn they form, intercellular transport in large complex cells would be impossible), cell shape and integrity etc. Consider the last cellular function they possess that I mentioned - cell shape and integrity. When hanging, it is generally said, penile tissue is being stretched and deformed. Fine. This is too macrobiological of an explanation for us as we understand something more complex is at hand, and, if perhaps we come to understand it, a more thorough theory of hanging can be formulated - a universal paradigm. Cells in penile tissue are attached to each other by CAMs (cell adhesion molecules). Obviously, it is not precisely the CAM facilitated intracellular meshwork we are conniving to destroy via Penis Enlargement, but rather, temporarily, the cytoskeletons of the myriad cells composing whatever gross anatomical structure we are targeting (whether it be the suspensory ligaments, the tunica albuginea etc.). When hanging, then, the cells themselves which constitute the targeted penile structure are being stretched and deformed; in particular it is their cytoskeletons (especially the microfilaments and microtubules). When these vital components of the cell are distorted, destroyed or otherwise damaged, the cell itself, being violently tossed from the comfortable world of homeostasis, releases bundles of excitatory chemical signals via exocytosis which trigger the development of the 'cellular stress response'. Indeed, it is precisely this cellular response that we thoughtful hangers are aiming for when hanging, for, as a consequence of these released ligands, the cells respond in a roughly two-fold manner: (1st) to deal with the acute stress at hand and to restore, as quickly as is possible, homeostasis, (2nd) to begin the inflammation response (described assiduously above) so that cellular healing can occur. Of course, as long as weight is attached to the penis, homeostasis can never be re-established irrespective of the poor frightened cells' desperate efforts. They do, however, try; in fact, we witness this very often - we call it turtling. Turtling is the concerted act of cells to prevent extensive distortion of their internal cytoskeletons. When we take the hanger off, or, as we have discussed concerning the ineluctable, though somewhat mysterious shrinking BPFSL, the cells contract, immediately shrinking their cytoskeletons, shirking, as it were, from the punisHydromaxent they have recieved at our hands. Indeed, this overcompensation has functional utility, as all natural biological operations do: it makes it easier for the cell to repair its damaged framework, and, what's more, it makes it all the more difficult to immediately further stretch the unwilling microfilaments and microtubules. At this point, it must be seen, we must diametrically oppose traditional die-hard hanging theories in that, continual exertion upon damaged cellular structures will lead to cellular shock which results, typically, in apoptosis (cellular suicide). Obviously it is not in our plan to loose cellular mass. It is here also that much can be learned from 10inchadvantage's (that fearless trailblazer!) fateful experimentation with all day and all night stretching. The cells, constantly denied even brief respite from homeostatic disruption, orchestrated mass apoptosis. What is more is that, much to his chagrin, his has managed to develop a case of what must called chronic inflammation ( Chronic inflammation - Wikipedia, the free encyclopedia ). Once the cell has incurred cytoskeletal damage, it can endure but little more; as we have said, the cytoskeleton is imperative for every vital cell function. Out of all of the stresses that can be levelled against a cell, it is difficult to imagine one which is more immediately threatening. Consequential of our understanding of the biochemical mechanisms involved up to this point, it is obvious that it is within our best interests to cease the application of stress at exactly this point. Any further application will lead to a level of damage either incapable of being endured by individual (or collectives of) cells and will incur their apoptosis, or, on the other hand, the inflammation response and cellular healing will be so protracted that, if not given long respite (days), extant cellular stress will cumulate to the extent that the culminated level of stress, actualized over several days or weeks of hanging, will either (depending on the level of this stress) retard cellular reconstitution or, in the extreme cases, destroy the cells we so wish to cosmetically alter.
It is true that the reconstitued cytoskeletal structures shall be more difficult to deform in the future, yet, it is imebcilic to pine rather for apoptosis or excessive levels of cellular stress. Yet, as we have mentioned above, with an increased weight-load (which, it is obvious from these considerations must be increased conservatively, in staid increments, over weeks) fatigue can ALWAYS be acheived. However, in our favor, concurrently with the the strengthening of the cytoskeleton, the cytoskeleton of the cells composing the targeted tissue structure shall grow back permanently elongated. Consider, for instance, the tunica albuginea, the tunica constricts the parameters of an erection (see the Gray's anatomy link above). If the tunica is the targeted tissue struture, the tunica structure itself, then, becomes permanently elongated. Obviously then, as a result, our usable erect length becomes greater. The implications of all of this writing should be rather obvious.
THE INFLAMMATION RESPONSE
The inflammation response is a thouroughly examined histological response to damage. Conjecturally, it consists of 5 varied elements each with their own adaptive functional utility. They are: swelling, redness, heat, pain and loss of function. According to Frederic H. Martini's 'Fundamentals of Anatomy and Physiology', "the restoration of homeostasis after a tissue injury involves two related responses" (139). He is insistent that all damage to vascular tissue responds to disruptions in homeostasis in this fashion, and, considering the accolades lauded upon this textbook, some degree of trust must inevitably be placed in the author's rather erudite opinion. Yet, do we as hangers notice any of these classic symptoms of the inflammation response? Concerning the first mentioned congenial symptom of inflammation, swelling, it is mentioned in a wikipedia aritcle on the matter that the swelling of the organ affected need not necessarily be visible ( Inflammation - Wikipedia, the free encyclopedia ). It is possible, however, that the periodically observed instances of momentary increases in BPFSL size are attributable to penile inflammation. It would be interesting to see as to whether or not the adminstration of known anti-inflammatory analgesics, such as aspirin, would combat post-hang BPFSL increases. Concerning redness, if we are indeed succeeding, in our various hanging regimens, to stress the ligaments and/or the tunica albuginea and not, as it where, the superficial skin, the redness itself would not be noticeable as the inflammation response would be directly affecting these subcutaneous tissues. Concerning pain, this is, itself, rather a recondite subject, for, what exactly is the difference between pain and general tissue fatigue? Certainly the difference is a matter of degree much in the same fashion as the difference between personal idiosyncracy and neurosis is itself little more than a matter of degree. Indeed, although the traditional ideologies rightly informed us to avoid pain, they do pedantically instruct us to quest after fatigue. Fatigue is a part of the inflammation response. Concerning loss of function, some hangers have, historically, reported a temporary incapacity to acheive erection following a hanging session. However, considering that we sensible hangers are not pushing ourselves to pain, we are neither pushing ourselves to complete tissue failure, which could, itself, present a rather serious medical problem ( Penile fracture - Wikipedia, the free encyclopedia ). Consequently, then, those of us not pushing the envelope beyond the pale of reason should not logically expect complete organ failure as a consequence of our practice. If you do, though, experience such an unhappy symptom, I'd recommend that you slow the fuck down and take a good old-fashioned time-out for yourself. Fine then, so the inflammation response is present. That is all well and good, yet, what does this portend for us? We shall discuss this in detail later.
CELLULAR COMMUNICATION AND TISSUE DAMAGE
Well, I'm getting really damned bored of writing all of this, so... all of you are going to have to wait until tomorrow before I finish it (if I do then....).
CELLULAR COMMUNICATION AND TISSUE DAMAGE
Intracellular communication occurs, in every instance, vis-a-vis chemical signaling molecules (not necessarily, in every cause, a macromolecule such as protein) which act as a ligand and bond to a protein receptor either on the cell-surface or in the cytoplasm of the cell. Whether or not a signaling molecule binds to receptors on the cell membrane or in the cytoplasm of the cell depend on a number of factors such as the extent of the chemical's hydrophobia or lipophilia, its mass etc; however, in keeping with the issue at hand, we needn't concern ourselves with tangential details such as this. Yet, it is obvious that it must be a concern of ours as to what actually causes cell communication such as we are beginning to describe. Cells respond only to a limited number of varying stimuli, a few of which are the following: light, pressure, specific chemicals (that is, chemicals which the cells are themselves evolutionarily adapted to recognize and recieve), electric potential variation. When hanging, it is obvious that we are directly affecting cells by simultaneously stretching their internal cytoskeletons and stressing intracellular bonds (as affected, say, by CAMs); obviously, we are destroying pre-existing cellular homeostasis. In biology, any such disruption of homeostasis is termed 'stress' and our friend the cell possesses a peculiar method of reacting to stress which has been inculcated in it over the course of evolutionary time.
However, for the time being, let us return to our consideration of cytoskeletons and how we hypothesize them to be affected by the violent stresses of hanging. Cytoskeletons are composed of three different types of filaments (the filaments themselves are composed of actin and myosin proteins): microfilaments, intermediate filaments, and microtubules. Each of these cellular constituents are vital for the function of the cell as these filaments are directly involved in cell mitosis (cell division), intercellular transport (without the cellular autobahn they form, intercellular transport in large complex cells would be impossible), cell shape and integrity etc. Consider the last cellular function they possess that I mentioned - cell shape and integrity. When hanging, it is generally said, penile tissue is being stretched and deformed. Fine. This is too macrobiological of an explanation for us as we understand something more complex is at hand, and, if perhaps we come to understand it, a more thorough theory of hanging can be formulated - a universal paradigm. Cells in penile tissue are attached to each other by CAMs (cell adhesion molecules). Obviously, it is not precisely the CAM facilitated intracellular meshwork we are conniving to destroy via Penis Enlargement, but rather, temporarily, the cytoskeletons of the myriad cells composing whatever gross anatomical structure we are targeting (whether it be the suspensory ligaments, the tunica albuginea etc.). When hanging, then, the cells themselves which constitute the targeted penile structure are being stretched and deformed; in particular it is their cytoskeletons (especially the microfilaments and microtubules). When these vital components of the cell are distorted, destroyed or otherwise damaged, the cell itself, being violently tossed from the comfortable world of homeostasis, releases bundles of excitatory chemical signals via exocytosis which trigger the development of the 'cellular stress response'. Indeed, it is precisely this cellular response that we thoughtful hangers are aiming for when hanging, for, as a consequence of these released ligands, the cells respond in a roughly two-fold manner: (1st) to deal with the acute stress at hand and to restore, as quickly as is possible, homeostasis, (2nd) to begin the inflammation response (described assiduously above) so that cellular healing can occur. Of course, as long as weight is attached to the penis, homeostasis can never be re-established irrespective of the poor frightened cells' desperate efforts. They do, however, try; in fact, we witness this very often - we call it turtling. Turtling is the concerted act of cells to prevent extensive distortion of their internal cytoskeletons. When we take the hanger off, or, as we have discussed concerning the ineluctable, though somewhat mysterious shrinking BPFSL, the cells contract, immediately shrinking their cytoskeletons, shirking, as it were, from the punisHydromaxent they have recieved at our hands. Indeed, this overcompensation has functional utility, as all natural biological operations do: it makes it easier for the cell to repair its damaged framework, and, what's more, it makes it all the more difficult to immediately further stretch the unwilling microfilaments and microtubules. At this point, it must be seen, we must diametrically oppose traditional die-hard hanging theories in that, continual exertion upon damaged cellular structures will lead to cellular shock which results, typically, in apoptosis (cellular suicide). Obviously it is not in our plan to loose cellular mass. It is here also that much can be learned from 10inchadvantage's (that fearless trailblazer!) fateful experimentation with all day and all night stretching. The cells, constantly denied even brief respite from homeostatic disruption, orchestrated mass apoptosis. What is more is that, much to his chagrin, his has managed to develop a case of what must called chronic inflammation ( Chronic inflammation - Wikipedia, the free encyclopedia ). Once the cell has incurred cytoskeletal damage, it can endure but little more; as we have said, the cytoskeleton is imperative for every vital cell function. Out of all of the stresses that can be levelled against a cell, it is difficult to imagine one which is more immediately threatening. Consequential of our understanding of the biochemical mechanisms involved up to this point, it is obvious that it is within our best interests to cease the application of stress at exactly this point. Any further application will lead to a level of damage either incapable of being endured by individual (or collectives of) cells and will incur their apoptosis, or, on the other hand, the inflammation response and cellular healing will be so protracted that, if not given long respite (days), extant cellular stress will cumulate to the extent that the culminated level of stress, actualized over several days or weeks of hanging, will either (depending on the level of this stress) retard cellular reconstitution or, in the extreme cases, destroy the cells we so wish to cosmetically alter.
It is true that the reconstitued cytoskeletal structures shall be more difficult to deform in the future, yet, it is imebcilic to pine rather for apoptosis or excessive levels of cellular stress. Yet, as we have mentioned above, with an increased weight-load (which, it is obvious from these considerations must be increased conservatively, in staid increments, over weeks) fatigue can ALWAYS be acheived. However, in our favor, concurrently with the the strengthening of the cytoskeleton, the cytoskeleton of the cells composing the targeted tissue structure shall grow back permanently elongated. Consider, for instance, the tunica albuginea, the tunica constricts the parameters of an erection (see the Gray's anatomy link above). If the tunica is the targeted tissue struture, the tunica structure itself, then, becomes permanently elongated. Obviously then, as a result, our usable erect length becomes greater. The implications of all of this writing should be rather obvious.
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