Acne.org Products
I copied and pasted this info and it appears to be replacing the 'beta' sign with AY for some reason.
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"Cytokines and growth factors are key elements in scarless wound healing
Recently, many experimental and clinical studies have demonstrated that wound healing is regulated by a panoply of cytokines, growth factors and their receptors. They influence cell migration, growth and proliferation in a complex, orchestrated manner and are involved in neutrophil and macrophage infiltration, angiogenesis, fibroplasia, matrix deposition, scarring and re-epithelialization. Besides platelets and macrophages, fibroblasts are the major cellular source of cytokines or growth factors during wound healing.
Recent data strongly suggests that scarless wound healing in fetal skin at early gestation is a result of the unique cytokine or growth factor profile. Of these, transforming growth factor-beta (TGF-AY) has been most widely studied as it is implicated in the transition between scarless healing and repair with scar formation.
Called growth factors for historical reasons, their main function is to control cell proliferation and differentiation and to stimulate the synthesis of extracellular matrix such as collagen.
Three highly homologue TGF-AY isoforms are known in humans: AY1, AY2 and AY3. Each form has been found by immunohistochemistry in unwounded fetal skin. However, low levels of TGF-AY1 and high levels of TGF-AY3 are expressed at gestational ages associated with scarless repair. In addition, it appears that the relative proportion of TGF-AY isoforms, and not the absolute concentration of any one isoform determines the wound repair outcome.
Exogenous application of TGF-AY1 to normally scarless fetal wounds resulted in scar formation [12, 13]. Moreover, an adult-like inflammatory response was observed. The profibrotic nature of TGF-AY1, and possibly TGF-AY2, was confirmed in wounds of adult rats as neutralizing TGF-AY1 and AY2 with antibodies partially reduced the amount of scarring. TGF-AY1 stimulates collagen I production, which is the predominant collagen type in adult skin. On the other hand, supplementation with TGF-AY3 reduced scarring and inflammation in adult wounds confirming its potential antifibrotic properties. The fact that scarless fetal wounds heal with little inflammation and the onset of scarring during fetal repair correlates with the presence of an acute inflammatory infiltrate [14] may be related to the pronounced anti-inflammatory properties of TGF-AY3.
On the other hand, TGF-AY1 and AY2 neutralizing antibodies do not entirely prevent scarring in the adult, and recent studies question the efficacy of TGF-AY3 in wound healing [15, 16]. This suggests that factors other than TGF-AY may also be important in scarless repair. For instance, extracellular matrix constituents fibromodulin or decorin, which are expressed as a function of gestation age in fetal skin, are known to modulate TGF-AY activity. This supports the hypothesis that differential expression of TGF-AY isoforms and TGF-AY activity modulators, rather than the mere presence or absence of TGF-AY has a role in the regulation of scarless repair.
Other growth factors differently expressed during the transition from scarless to scar-forming repair include epidermal (EGF) and platelet derived growth factor (PDGF) [17], as well as fibroblast growth factors (FGFs) [18]. High EGF levels were found in early-gestational age skin, which may help to rapidly reepithelialize after skin injury. In addition, rapid healing of fetal wounds may be also related to a higher level of vascular endothelial growth factor (VEGF) in scarless fetal wounds than in scarring fetal and adult wounds [19]. This high VEGF level may increase angiogenesis and vascular permeability early during healing.
Although known for its profibrotic role in wound healing inducing scar formation [20, 21], PDGF mRNA levels were higher in scarless wound healing. This suggests that its function may be isoform dependent and may relate in a more complex manner to the extracellular environment.
Fibroblast growth factors have a broad range of function. For example, FGF-2 (basic FGF) is a potent stimulator of angiogenesis, while FGF-5 regulates the hair cycle. FGF-7 (also known as keratinocyte growth factor 1, KGF-1) and FGF-10 (KGF-2) are produced by fibroblasts but act on keratinocytes to stimulate migration and proliferation. FGF isoforms are regulated in a complex manner during fetal skin development. Whereas some FGF isoforms did not change, FGF-7 and FGF-10 were found to be down-regulated in scarless wounds.
Summarizing, unique properties of fetal skin appear to contribute to perfect wound healing: (i) differential expression of TGF-AY isoforms together with other cytokines decreases scar formation and enhances re-epithelialization, (ii) fetal fibroblasts with high synthetic capabilities deposit collagen rapidly and scarlessly, and (iii) lack of pro-inflammatory signals may limit the inflammatory infiltrate early during healing.
Despite the great increase in knowledge gained over the past decade, the precise mechanisms of scarless healing remain unknown. Additional cytokines, growth factors or modulators, which may further participate in the complex orchestration of coordinated cellular responses leading to perfect skin repair, are currently being researched."
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Just found this quite interesting. There's evidence suggesting ACE inhibitors suppress TGF-beta1 but this article suggests that TGF-beta1 suppression on its own isn't enough for scarless healing to occur. So whilst ACE inhibitors may help to some degree I don't see how they could eliminate scars completely, yet in one of the research papers it said there was full resolution to one of the keloid/hypertrophic scars. Is there any evidence suggesting that ACE inhibitors can effect decorin levels or TGF-beta3?
I haven't managed to see my doctor yet but I'm still hoping to try enalapril. I think it could help but I don't see how it could offer full resolution if it only effects TGF-beta1.
Interested in hearing peoples thoughts.
IMO those photos are much better than the ones before, which 'some' IMO were good. And in no way can I see scar in this set.
He's pretending to expose the scalp wound in the last image. Look closer.
LOL
That image is funny, 3 thousand hair above the scar , i can't see anything.
hi. so with all this research into sacaless healing, stem cells and tissue engenering going on do u think thtat in 10 to 15 years time it is looking very posative that we can get rid on any scar on our body no matter how big or small the area and have perfect skin again or even better than igt was first time round. im very optimistic that in 15 years time it will definately happen. I even believe that by then a skin badly damage by burn can be regenerqated to perfection. Please give your opinion,thnks to all who gives up hope on this forum. Let all of us have bright happy and scar free future .
My response, I've just scanned the article so I may be ignorant here. I think they are trying to look at the mechanics of healing etc. Which will take a long time to uncover, even longer the more microscopic you look at it.
With regards to decorin.
What is scar? Lets say it is kind of tissue extracellular cement filler and it is a process that fills up collagen over time.
What enables the cement mixing and filling? Fibroblasts.
What makes the fibroblasts redundant or dormant?
Decorin makes the fibroblasts completely redundant and at the same time normal unscarred tissues are uneffected. Decorin is found by the bucket load in non wounded tissues, but in newly wounded tissues it is basically non existant.
Decorin completely stops fibrosis by the fact it stops the scar cement mixing and spreading of the scar over time inside collagen.
Decorin is the a a scar switch, it turns off and on scarring.
I copied and pasted this info and it appears to be replacing the 'beta' sign with ¯¿½…¸ for some reason.
__________________
"Cytokines and growth factors are key elements in scarless wound healing
Recently, many experimental and clinical studies have demonstrated that wound healing is regulated by a panoply of cytokines, growth factors and their receptors. They influence cell migration, growth and proliferation in a complex, orchestrated manner and are involved in neutrophil and macrophage infiltration, angiogenesis, fibroplasia, matrix deposition, scarring and re-epithelialization. Besides platelets and macrophages, fibroblasts are the major cellular source of cytokines or growth factors during wound healing.
Recent data strongly suggests that scarless wound healing in fetal skin at early gestation is a result of the unique cytokine or growth factor profile. Of these, transforming growth factor-beta (TGF-¯¿½…¸) has been most widely studied as it is implicated in the transition between scarless healing and repair with scar formation.
Called growth factors for historical reasons, their main function is to control cell proliferation and differentiation and to stimulate the synthesis of extracellular matrix such as collagen.
Three highly homologue TGF-¯¿½…¸ isoforms are known in humans: ¯¿½…¸1, ¯¿½…¸2 and ¯¿½…¸3. Each form has been found by immunohistochemistry in unwounded fetal skin. However, low levels of TGF-¯¿½…¸1 and high levels of TGF-¯¿½…¸3 are expressed at gestational ages associated with scarless repair. In addition, it appears that the relative proportion of TGF-¯¿½…¸ isoforms, and not the absolute concentration of any one isoform determines the wound repair outcome.
Exogenous application of TGF-¯¿½…¸1 to normally scarless fetal wounds resulted in scar formation [12, 13]. Moreover, an adult-like inflammatory response was observed. The profibrotic nature of TGF-¯¿½…¸1, and possibly TGF-¯¿½…¸2, was confirmed in wounds of adult rats as neutralizing TGF-¯¿½…¸1 and ¯¿½…¸2 with antibodies partially reduced the amount of scarring. TGF-¯¿½…¸1 stimulates collagen I production, which is the predominant collagen type in adult skin. On the other hand, supplementation with TGF-¯¿½…¸3 reduced scarring and inflammation in adult wounds confirming its potential antifibrotic properties. The fact that scarless fetal wounds heal with little inflammation and the onset of scarring during fetal repair correlates with the presence of an acute inflammatory infiltrate [14] may be related to the pronounced anti-inflammatory properties of TGF-¯¿½…¸3.
On the other hand, TGF-¯¿½…¸1 and ¯¿½…¸2 neutralizing antibodies do not entirely prevent scarring in the adult, and recent studies question the efficacy of TGF-¯¿½…¸3 in wound healing [15, 16]. This suggests that factors other than TGF-¯¿½…¸ may also be important in scarless repair. For instance, extracellular matrix constituents fibromodulin or decorin, which are expressed as a function of gestation age in fetal skin, are known to modulate TGF-¯¿½…¸ activity. This supports the hypothesis that differential expression of TGF-¯¿½…¸ isoforms and TGF-¯¿½…¸ activity modulators, rather than the mere presence or absence of TGF-¯¿½…¸ has a role in the regulation of scarless repair.
Other growth factors differently expressed during the transition from scarless to scar-forming repair include epidermal (EGF) and platelet derived growth factor (PDGF) [17], as well as fibroblast growth factors (FGFs) [18]. High EGF levels were found in early-gestational age skin, which may help to rapidly reepithelialize after skin injury. In addition, rapid healing of fetal wounds may be also related to a higher level of vascular endothelial growth factor (VEGF) in scarless fetal wounds than in scarring fetal and adult wounds [19]. This high VEGF level may increase angiogenesis and vascular permeability early during healing.
Although known for its profibrotic role in wound healing inducing scar formation [20, 21], PDGF mRNA levels were higher in scarless wound healing. This suggests that its function may be isoform dependent and may relate in a more complex manner to the extracellular environment.
Fibroblast growth factors have a broad range of function. For example, FGF-2 (basic FGF) is a potent stimulator of angiogenesis, while FGF-5 regulates the hair cycle. FGF-7 (also known as keratinocyte growth factor 1, KGF-1) and FGF-10 (KGF-2) are produced by fibroblasts but act on keratinocytes to stimulate migration and proliferation. FGF isoforms are regulated in a complex manner during fetal skin development. Whereas some FGF isoforms did not change, FGF-7 and FGF-10 were found to be down-regulated in scarless wounds.
Summarizing, unique properties of fetal skin appear to contribute to perfect wound healing: (i) differential expression of TGF-¯¿½…¸ isoforms together with other cytokines decreases scar formation and enhances re-epithelialization, (ii) fetal fibroblasts with high synthetic capabilities deposit collagen rapidly and scarlessly, and (iii) lack of pro-inflammatory signals may limit the inflammatory infiltrate early during healing.
Despite the great increase in knowledge gained over the past decade, the precise mechanisms of scarless healing remain unknown. Additional cytokines, growth factors or modulators, which may further participate in the complex orchestration of coordinated cellular responses leading to perfect skin repair, are currently being researched."
____________
Just found this quite interesting. There's evidence suggesting ACE inhibitors suppress TGF-beta1 but this article suggests that TGF-beta1 suppression on its own isn't enough for scarless healing to occur. So whilst ACE inhibitors may help to some degree I don't see how they could eliminate scars completely, yet in one of the research papers it said there was full resolution to one of the keloid/hypertrophic scars. Is there any evidence suggesting that ACE inhibitors can effect decorin levels or TGF-beta3?
I haven't managed to see my doctor yet but I'm still hoping to try enalapril. I think it could help but I don't see how it could offer full resolution if it only effects TGF-beta1.
Interested in hearing peoples thoughts.
IMO those photos are much better than the ones before, which 'some' IMO were good. And in no way can I see scar in this set.
He's pretending to expose the scalp wound in the last image. Look closer.
If you look at the area you selected it is way below the bald patch on his crown in the first photo, whilst his picture you've selected is closer to the bald spot like in the first picture.
However you ignored this image, which shows the lower part you say he ignored. (If you look at the set he actually does look at the area you highlighted) He looks higher up, and also little lower in the set.
Hello guys,
interesting stuff you are discussing here.
I have something about our old friend "Osteopontin". I don't know if somebody
did mention this before, but here is a report on the drug development based
on osteopontin.
http://www.science20.com/news_releases/ost...h_may_end_scars
Maybe you find it interestind and worth to be investigated.
There are so many products out there. If they would mix them up, what would be the results?
I'm still hoping for a scar-free future. And I hope that a huge increase in scar tissue can be achieved with the new treatments.
NEO
Just thinking out loud, what I'm wondering about is if you have a scar and you use say Juvista and the result is that you have a smaller scar...does that mean that the edges of what used to be the scar is now normal skin? And that the center is scar? And wouldn't that mean that if you then cut out the center and you use it again, you'd get an even smaller scar and that you theoretically can keep on doing this until the entire area that used to be scar is now normal skin? I hear people say things like "Well it didn't work so well as we ended up with a scar half the size of the original.". I mean wouldn't that mean that 50% of the area is now 100% normal again? Just wondering.
Anyway, I should listen to that Hitzig interview properly. I find it strange that this guy is taken seriously by Spencer Kobren who says he just might "write history" and then at the same time you've got Hitzig posting bogus photos and having a bad reputation. Weird... His statement about ACell being able to achieve scarless healing in six weeks is quite bold as well. I don't believe him. But other people seem too. I wonder what is the truth. 
so do you think we are near a breakthrough over next 10 to 15 years. I have scars all over my body due to skin picking. i hope by the furthest 2030 there will be something out there that can give me normal skin all over my body again. What is your opinion.im 23 now i hope to be 'normal' again by my early forties.
so do you think we are near a breakthrough over next 10 to 15 years. I have scars all over my body due to skin picking. i hope by the furthest 2030 there will be something out there that can give me normal skin all over my body again. What is your opinion.im 23 now i hope to be 'normal' again by my early forties.
I think so, yes. Well within the timeline you mentioned. Just what I think. Other people may disagree.
His statement about ACell being able to achieve scarless healing in six weeks
Look at the acell website, look at the hand picture were a full thickness wound 3 by 7 got complete site specific tissue in 2month.
Also look at the FAQs on Acellvet, cat gut actually spoils the remodelling process.
IMO I'll say it again, the biggest problem Acell faces is the getting the protocols. If they fuck that up...
His statement about ACell being able to achieve scarless healing in six weeks
Look at the acell website, look at the hand picture were a full thickness wound 3 by 7 got complete site specific tissue in 2month.
Also look at the FAQs on Acellvet, cat gut actually spoils the remodelling process.
IMO I'll say it again, the biggest problem Acell faces is the getting the protocols. If they fuck that up...
I still think solo_premium did basically the same thing as Hitzig says is the right way to approach it... I know there's the powder vs. sheet thing and all but nevertheless... I also think that what he said was very bold. He basically said "If you do it this way you've got your skin back in 6 six weeks." without ambiguity. Without a "probably" or a "possibly" or a "if you're lucky". And that, is something I don't think any good doctor would say as I think you'd give a percentage of your patients false hope. But who knows, Hitzig may be telling the truth. Anyway, I'm going to listen to that interview again.
In my topic 'Juvista' , i put the first photo of juvista in revision of scar, phase 3.
http://www.renovo.com/itemdetails.asp?c_id=31&news_id=73
Some news from Renovo. Preliminary results will be shown on December the 14th.
So stay tuned.
NEO
In my topic 'Juvista' , i put the first photo of juvista in revision of scar.
Aren't acne scars more complicated than a scar from a scratch, cut, burn etc like they are showing in those pictures? I really think other types of scars are easier to get rid of or improve than acne scars.
In my topic 'Juvista' , i put the first photo of juvista in revision of scar.
Aren't acne scars more complicated than a scar from a scratch, cut, burn etc like they are showing in those pictures? I really think other types of scars are easier to get rid of or improve than acne scars.
I dunno... One would think a wound is a wound regardless of what has been excised. But this apparently isn't the case. You're right. E.g. Juvista isn't going to be able to be used for keloids yet if it/when comes out next year...although it CAN be used for sunken scars. I don't get why, really.
I also think that what he said was very bold. He basically said "If you do it this way you've got your skin back in 6 six weeks." without ambiguity. Without a "probably" or a "possibly" or a "if you're lucky".
Why should he be economical with what he knows as the truth? Just so it eases in with your or someone elses reality? Why should anyone bend the truth just so it gives 'ambiguity' and someone a chance to spin it with a bias to their reality? Not very scientific is it?
I also think that what he said was very bold. He basically said "If you do it this way you've got your skin back in 6 six weeks." without ambiguity. Without a "probably" or a "possibly" or a "if you're lucky".
Why should he be economical with what he knows as the truth? Just so it eases in with your or someone elses reality? Why should anyone bend the truth just so it gives 'ambiguity' and someone a chance to spin it with a bias to their reality? Not very scientific is it?
You misunderstood. I don't believe any treatment is a sure fire one, garuanteed to work every time. Treat 100 people with ACell the best way possible, you possibly won't get 100 ideal results. You can maximize the possibility of an ideal outcome for every patient but you can't promise every one of those 100 people an ideal outcome. And that's what he seems to be doing which I think is something that most doctors wouldn't do.
This isn't entirely relevant but I found certain parts interesting. I've quoted the main part that interested me.
"Excessive production of TGF-I has been linked to fibrotic diseases. Enhanced TGF-I1 expression and an associated increase in the production of collagen I, III, and VI have been documented in tissues of patients with systemic sclerosis, postburn hypertrophic scar tissue, and keloids. Conversely, inhibition of TGF-I has been shown to decrease collagen deposition and scarring. The application of neutralizing antibodies to TGF-I in rat incisional wounds successfully reduced cutaneous scarring."
http://www.orthosupersite.com/view.aspx?rid=76427
So here is yet another source saying that TGF-beta1 suppression improves scaring. I assume that the neutralizing antibodies used on the rats was just a one off application (or only done for a short period of time) and it says scarring was reduced. If this is the case then long term use of ACE inhibitors in theory would provide even better results.
Has anybody managed to get hold of an ACE inhibitor yet?
seabs you sure do know a lot about decorin lol. In your opinion do you think enalapril could work or at least help?
Looking at the cites put up on this thread, which show the resolution of a hypertrophic caesarian scar in 3 to 4 month, reduction of keloid in months, how the inhibitor resolved internal scarring. I'd say it would work.