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Repairing the long-term damage from Accutane

vitamin d vitamin a vitamin e biotin garlic milk thistle depression

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#6641 yetanotheraccutanevictim

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Posted 21 May 2015 - 11:33 AM

What differences have you noticed with the probiotic?

No ill effects like constipation or diarrhea. Perfect, large bowel movements. Less undigested particles in the stool. Perhaps more frequent bms. Less bloating in colon. And of course the unseen systemic benefits of repopulating the colon with beneficial organisms (better nutrient assimilation and production, less depression, less brain fog, more energy, better sleep etc..)

But I've tried a lot of probiotics that have caused distress. One probiotic might work for me but will not work for you and vice versa. Personally the pure encapsulations and prescript assist work great for me.



#6642 Accutazed

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Posted 21 May 2015 - 11:58 AM

I haven't posted on here in quite awhile but I might as well discuss the theory I am working on at the moment.

Here's a quick run down of case and symptoms:

Accutane - 20mg twice a day for 4 months.

Symptoms during:
Dry skin
Cracked lips
Brain Fog
Depression

After:
All of the above +
Bleeding gums
Acne continued
Dry flakey skin on face / scalp (exacerbated in winter)
Social anxiety
Eye floaters
Lack of energy
Apathetic
Loss of personality
Stammer / slurred speech
Poor libido

What I have tried so far:
Candida detox
colon cleanse
liver flushes (7)
low sugar diet
leafy green + meat diet (green smoothies etc)
PMO reboot (anxiety related)
4x adrenal saliva test
endocrinologist test
b12 and testosterone testing
b12 and T injections
heaps of supplements
parasite cleanse
pregnenolone creams
weekly clay masks


Its safe to say I have tried plenty in the 3 years I have been dealing with these symptoms

I always persisted and stuck as close to the requirements of each attempt I've made at alleviating my symptoms.

Anyway, I feel like I may have found the answer now. Its been discussed on these boards in small amounts and google searches seem to show only a few documented reports of people actually discussing this idea, it seems it can be found in other drug related ailments which are similar to those of accutane.

So the other weekend I was out for a night out with some mates, I never really do drugs due to how crappy I feel most of the time and being scared of what they may actually do to me that accutane hasn't already done or if anything make my problems worse. But then I thought yolo fuck it whatever.

So I had 2x caps of some MDMA that a friend of mine bought off the internet, Apparently the source is credible and the quality insured by hundreds of reviews on the deep web. Needless to say I had fun, blah blah blah, The night ended early so I got home and just lay in bed thinking. When all of a sudden i realized, boom! no eye floaters. not even one. I've had them for 2 years constantly and can even see them when I sleep. I was utterly shocked. I turned on my light in my room which normally makes them become so large and obvious I get a little angry. Nothing at all. I literally went from being in pitch black to as bright as I could in my rooms (2 sources of light plus white screen on TV) just to test this properly. seriously nothing at all.

So then I did a little research on MD and broke it down into the chemical sequence it initiates in order for you to have so much fun. It basically causes large amounts of serotonin to be released from tissue inside the brain. It also block the receptors which regulate serotonin in order to control mood, so basically you just have tons of serotonin in your head and you feel good because of that. Obviously this is dumbed down and I'm sure people can elaborate on this but thats not the point.

In 2013 I had a hair mineral analysis done and noted on the results that my copper in soft tissue was of the flipping charts. This is because Accutane increases estrogen which in turn allows copper to build up. It piles up in the liver as that is already getting bombarded witch Vitamin A and cannot function. So it over flows and stores itself in soft tissue, like the brain and joints in order to bail from killing the liver. (a little theory of mine here is that those who have suffered accutane effects in the extremities often have a weak liver to begin with either genetically or though poor diet, I myself ate thousand of sweets/lollies as a kid and also binge drank alcohol during my accutane course as I was young and naive, and also ill-informed by a rouge doctor)

Further research of copper shows that when in the brain soft tissue it has a dramatic effect on serotonin and how it is produced. It basically make it redundant by oxidizing it. So although you may be able to make it, you never really get to see the benefits of it, eg. sharp memory, mood, cognitive functions, focus etc etc.

So in conclusion. The accumulation of copper in the brains soft tissue, as a result of accutanes effect on estrogen and the liver, results in the stunting of serotonin production.

CURE:

From what I gather Nutritional balancing seems to be the most discussed way of getting copper out of soft tissue. This is anecdotal and just seems to be what I read about the most on the internet.
It seems this can take months and even years depending on the severity of your case. A correct diet limiting certain foods and focusing on foods that maintain the zinc / copper balance seem to be critical.
In my own research I have heard good things about 5-HTP and the benefits it can have on serotonin production, It seems it may just get eaten up with copper but its probably worth a try just to experiment.

I believe there is equally as much money in alternative medicine as their is practical. And while I don't think any practitioner really consciously wants to deter anyone from their health, I am sure they are subconsciously biased to what they recommend to clients as far as money and repeat business goes.

This idea is open to discussion and I greatly welcome it. Obviously this is the path I am now taking and seeing as I am determined as fuck I will stick with this idea if only to rule it out.

KOI 


^.

My skin looks amazing on MDMA ;) . I believe and think that our sides are fully dependent on our serotonin levels and possibly dopamine production.

Mdma, Weed, Liquor, Mushrooms, NoFap, and **High dose SSRI** are the only things that have drastically lowered symptoms and made me feel normal and beautiful. 

**I started on a low dose (5mg) SSRI Cipralex and worked my way up to 20mg. @ 20mg almost all symptoms were completely gone however i just felt way too speedy in my mind to continue on it. I stopped the SSRI's and went with NoFap which is a longer and harder approach but gets me close to the same results.

I am going to discuss with my doctor about trying other SSRI's that don't make me feel so speedy ><. 

Koi go to a doctor and talk about getting prescription SSRI meds. They will make your skin beautiful like it is on MDMA. ;) 
 



#6643 Modeaa

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Posted 21 May 2015 - 01:45 PM

accutane can deplete folate and b12. this can cause depression.

probiotics might not work without siga. some sais they can be bad for someone who has sibo, i would think this also has to do with siga.
---------------------------------------------------------------------------------------------------
http://en.wikipedia.org/wiki/Vitamin_A
Vitamin A also functions in a very different role as retinoic acid (an irreversibly oxidized form of retinol), which is an important hormone-like growth factor for epithelial and other cells.[2][5]

http://www.ncbi.nlm....les/PMC3142734/
Retinal is the form involved in vision, whereas retinoic acid is involved in growth and cellular functions
......Retinol and retinyl esters (palmitate shown) are the dietary forms of preformed vitamin A. Retinal is essential in vision, and retinoic acid is involved in growth and cellular differentiation.
...

http://www.news-medi...-Vitamin-A.aspx
Another form of Vitamin A, retinoic acid, is a key hormone-like growth factor for epithelial cells and other cell types in the body


http://en.wikipedia....sis_A#Mechanism

Retinoic acid suppresses osteoblast activity and stimulates osteoclast formation in vitro,[23] resulting in increased bone resorption and decreased bone formation. It is likely to exert this effect by binding to specific nuclear receptors (members of the retinoic acid receptor or retinoid X receptor nuclear transcription family) which are found in every cell (including osteoblasts and osteoclasts).

This change in bone turnover is likely to be the reason for numerous effects seen in hypervitaminosis A, such as hypercalcemia and numerous bone changes such as bone loss that potentially leads to osteoporosis, spontaneous bone fractures, altered skeletal development in children, skeletal pain, radiographic changes,[20][23] and bone lesions.[29]

http://en.wikipedia..../strong></span>
Osteoblast are cells with single nuclei that synthesize bone.
Osteoblasts are specialized, terminally differentiated products of mesenchymal stem cells.[1]They synthesize very dense, crosslinked collagen, and several additional specialized proteins in much smaller quantities, including osteocalcin and osteopontin, which comprise the organic matrix of bone.
-----------------------------------------------------------------------------------------------------------------------------------------------------------------------------------------

brilliant. accutane and telomeres
http://www.acne.org/...r-if-hes-right/

http://www.ncbi.nlm....les/PMC3485670/
Retinoic acid signalling is known to be important for a wide variety of physiological processes, including immunomodulatory functions, though its role in immune responses to parasitic infections is not yet fully understood. The precursor of this metabolite, vitamin A or retinol, is an essential nutrient obtained from the diet, and deficiency in this vitamin can lead to an increased susceptibility to infectious diseases (1).

http://en.wikipedia.org/wiki/RIG-I
'' RIG-I (retinoic acid-inducible gene 1) is a RIG-I-like receptor dsRNA helicase enzyme that is encoded (in humans) by the DDX58 gene. RIG-I is part of the RIG-I-like receptor family, which also includes MDA5 and LGP2, and functions as a pattern recognition receptor that is a sensor for viruses........RIG-I and MDA5 are involved in activating MAVS and triggering an antiviral response ''

http://www.ncbi.nlm....pubmed/24495389
 ''The results indicated that ATRA reduced the percentage of EV71-infected cells and protected cells against EV71-induced apoptosis. Correspondingly, ATRA increased the production of IFN-α one of the most important antiviral cytokines, at both mRNA and protein levels in EV71-infected cells. In addition, the expression of RIG-I mRNA and its downstream genes was up-regulated by ATRA in EV71-infected cells. Ro 41-5253 abrogated the inhibitory effects of ATRA on EV71. The present findings suggest that ATRA is an interferon-inducing agent with antiviral activity against EV71 in vitro and that its actions are mediated at least in part by RAR-α activity and the RIG-I signalling pathway''

this immune response can happen with larges amounts of retinoic acid even witout a presence of infaction? as wiki state- RIG-I (retinoic acid-inducible gene 1) functions as a pattern recognition receptor that is a sensor for viruses........RIG-I and MDA5 are involved in activating MAVS and triggering an antiviral response '' maybe this mechanisem is out control cause the drug bombed the body with 13-cis retinoic acid? so there is no infection but the body act as if there is?

lets think how an immune system response to infection due to accutane can cause the side affects.
some thaghs i have: isn't the first place to defend against infection is the skin? where the infection will first  reach you?also the intestine.the outest layers of the body. would that cause the immune cells to attack the ''infected cells'' so they won't infect the rest of the body- it will make the immune cells to atack the infection with ROS. the drug administraed again and again and with high dose comparing to regular diet vitmain A, so this infection alert state remains and cells kepp dying and replaced by others(or it cycle somehow speeded), becuase every cell being treat as if it is infected, this is the cell prolifiration mechanisem that accutane induces? after all the cell divisions the telomerese get too short and chromosomes/histone/whatever reach it replication limit-hayflick limit, and since
http://en.wikipedia....8px;">29</span>With critically shortened telomeres, further cell proliferation can be achieved by inactivation of p53 and pRb pathways. Cells entering proliferation after inactivation of p53 and pRb pathways undergo crisis. Crisis is characterized by gross chromosomal rearrangements and genome instability, and almost all cells die.
 

maybe then the body finally reach to the point where it fighthing the accutane, which mean it fighting against itself for stoping itself atacking itself due to a false belive it cells are infected:
what that confusing is that if it is the case then it semms that the retinoic acid itelf induce this defend acording to what i read. maybe more correctly is that that the body induces this defenf as a consequence of retinoic acid toxicity? if not then that's not understood- retinoic acid make the immune system to act against infection and on the same time shuts the immune system down?
http://www.ncbi.nlm....les/PMC3485670/
Retinoic acid has multiple effects on innate and adaptive immunity, including promoting the differentiation of T and B cells (9,10), modulating cytokine production (11), driving Th2 responses (12,13) and inducing immune tolerance through induction of Foxp3+ regulatory T cells (Tregs) (14),

http://www.ncbi.nlm....ubmed/17620363/

All-trans retinoic acid mediates enhanced T reg cell growth, differentiation, and gut homing in the face of high levels of co-stimulation. Under conditions that favor the differentiation of A-Tregs (transforming growth factor-beta1 and interleukin 2) in vitro, the inclusion of RA induces nearly all activated CD4(+) T cells to express FoxP3 and greatly increases the accumulation of these cells
In the absence of RA, A-Treg differentiation is abruptly impaired by proficient antigen presenting cells or through direct co-stimulation. In the presence of RA, A-Treg generation occurs even in the presence of high levels of co-stimulation, with RA attenuating co-stimulation from interfering from FoxP3 induction. The recognition that RA induces gut imprinting, together with our finding that it enhances A-Treg conversion, differentiation, and expansion, indicates that RA production in vivo may drive both the imprinting and A-Treg development in the face of overt inflammation.



http://www.ncbi.nlm....les/PMC3485670/
'The regulatory T cells (Tregs), formerly known as suppressor T cells, are a subpopulation of T cells which modulate the immune system, maintain tolerance to self-antigens, and abrogate autoimmune disease. These cells generally suppress or downregulate induction and proliferation of effector T cells. Additional regulatory T cells known as Treg17 cells have recently been identified

those Foxp3+ regulatory T cells (Tregs) , guess who is a good friend of them? FOXO

http://www.sciencedi...074761310004620
''In this issue of Immunity, Kerdiles et al. (2010) report that Foxo transcription factors are essential for the development and function of Foxp3-expressing regulatory T (Treg) cells via controlling the expression of genes associated with Treg cell function.''


SO all this make me wonder if that drug caused the body to act agains infection over and over on cells and repalacing them with non infected cells which again persumed as infected  till the the telomeres shortened so much that cells reached it replication limit, or befor it?
then foxo took its role so no more infection like fighting will happen cause it will be deadly, or that the cells can't diviede and cell cycle stack so thats also or alone whay foxo is up.
dont know how much of all that is close to the truth and scientific the way i said it,
maybe all the cell death/cell cycle arrest happen cause the body fight pressived infection? by down regulate htert?
 

hTERT gene produce telomerase which reapir telomeres. accutane can shut htert down. is it for fighting assumed infection?
http://www.pnas.org/...2/6662.full.pdf
A second pathway of hTERT regulation,identified in the RAR-responsive, maturation-resistant NB4-R1 cell line, results in a down-regulation of telomerase that develops slowly during two weeks of all-trans retinoic acid (ATRA) treatment. This pathway leads to telomere shortening, growth arrest,and cell death, all events that are overcome by ectopic expressionof hTERT

https://www.mskcc.or...>vitamin</span>''ATRA halts telomerase activity and exerts antitumor effects via a rapid decrease of H3-K9 acetylation at the hTERT promoter (39). The protective effect of supplemental retinol against melanoma may be mediated by sunlight exposure (25). http://www.nature.co...l/1207093a.html Retinoic acid receptor and retinoid-X receptor-specific agonists synergistically target telomerase expression and induce tumor cell death http://www.ncbi.nlm....icles/PMC34517/
We identified two levels of regulation of telomerase by retinoids and showed that retinoids can regulate telomerase and telomere length independently of cell maturation, leading ultimately to extinction of the tumor cell clone
Therefore, the inhibition of telomerase activity correlated with the induction of growth arrest and/or the attainment of a maturated state.''
bringing foxo?



these is confusing.
http://www.nature.co.../1206063f4.html
''Note the appearance and subsequent increase of SOD-2 message after 60 h of infection, whereas there is no significant change in expression of alpha-actin. © The relative increase of hTERT binding to telomeres and SOD-2 expression. The estimation of hTERT binding to telomeres is relative to the p21 binding to genomic DNA and the estimation of SOD-2 gene expression is relative to alpha-actin expression. Note an increase in telomeric DNA levels coimmunoprecipitated with the increase in postinfection time, suggesting that TERT protein binds to telomeres. The intensities were quantitated by the procedure described in the Methods section. Note that the increase in the interaction of hTERT with telomeres precedes the increase in SOD-2 gene expression''


 

Edited by Modeaa, Yesterday, 04:38 AM.


#6644 unbroken94

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Posted Yesterday, 02:36 AM

I'm not really sure where to start with this , the last year has been a living hell for me that's as I'm sure you can understand the only way you can describe the turmoil caused by accutane , for a while I believed it was all the doctors fault but after a certain number of depressive months 2 suicide attempts and a stay in a phychiatric hospital here in Australia I came to realise the majority of the blame could only be placed upon myself , I'd like to say that I commend all of you for coming through this and still been alive and willing to fight the problems you have been faced with , that in itself takes enormous courage when faced with the variety of situations we are , some worse or even slightly better than my own . There are perhaps some clues im struggling to make sense of , and I am hoping you maybe able to shed some light on these for me . So basically whilst on accutane for 5 and a half months I was Also taking lexapro an ssri that some of you may not be familiar with , anyway long story short as I'm sure you can imagine after my experience with accutane and finding the truth behind it ( not just clear skinned people on YouTube ) , I decided enough was enough with medication , I wouldn't pollute my body any longer , ; now during this withdrawal from lexapro which I am currently five months into I have noticed some very interesting things ,

1, my skin is back to been as dry as I was on accutane , (eyes included )

2) the flushing has returned how ever not as bad as when on accutane (yet)


3) muscle pains all over the body


And many other symptoms since coming off lexapro which could both be withdrawal from that drug or accutane catching up with me , I find interesting that lexapro made my skin oily though , surely this may support what some of you have said about are hormones though or testosterone receptors , anyway I'm no scientist , maybe like a lot of you just trying to get out this mess the best we can , I often fantasise that all of us around the world who have been effected could pool our money and resources and build a place full of equipment and finally find the reasons are body's are acting this way and maybe one day find a cure , But apart from that to be surrounded by people who truely , truely understand what you have been through ,, that is my dream most nights apart from dismembering my doctor , good luck to you all and best wishes and if you are reading this and considering takeing accutane do not play Russian roulette with this dastardly substance , to those suffering stay strong , a thank you I believe is in order to Stefan for creating this thread and allowing me to know I'm not going crazy , I'm originally from the uk to It was only after accutane I saw the documentary you were involved in , it's fantastic that you are spreading the message about the destruction this can cause , and also a thank you to all of you that contributed suggestions and your research , each sufferer and victim we get one day closer to getting the answer we need , I hope before I'm dead there will be an explanation , fuck the big pharm

Edited by unbroken94, Yesterday, 02:45 AM.


#6645 ciaobella

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Posted Yesterday, 03:02 AM

I took Accutane in 2009. If you look through my posting history, I actually kept a log of my course on this site.

My skin cleared up, I got into my dream university, everything seemed wonderful. And then I got really, really depressed. Let me say that there's no history of depression or anxiety on either side of my family. I also haven't had any extremely distressing or negative events happen to me in the last several years, so logically there's no explanation for why I became depressed.

My grades tanked because some days I couldn't even bring myself to get out of bed. My bedroom was a mess because I couldn't ever find the motivation to clean it. I'd stay locked up in my room for days on end, sleeping while the sun was up and laying in bed doing nothing at night. This was a stark contrast from the person I was before I took Accutane - a straight-A student and extrovert. I went to my GP and got a psych referral because she believed I was severely depressed. The psychiatrist agreed with her assessment, and I've been on antidepressants ever since.

6 years after Accutane, if I don't follow a strict high-fiber, low-dairy diet, I get IBS symptoms and anal fissures that don't heal. 6 years after Accutane, I'm taking 300mg of antidepressants each day just to get by. But hey, at least my skin's clear, right?

you were an island and i passed you by...
my accutane log :)


#6646 macleod

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Posted Yesterday, 03:21 AM

yea, its kind of funny. I was thinking about this earlier. it was like ok, im fucked. but the only way to live with my fuckedness is to go to a doc and take some more pills that will fuck me even more, therefore i am ultimately fucked. my only solution is to fuck off to an island, where i'll live out the rest of my days fucked. i dunno...i thought it was kind of funny when i first thought of it

6684 replies to this thread. this is the biggest thread on this site. calculate that with the total posters on the entire forum. the percentage of people affected by this drug is through the roof. 10% of 5 - 10 million. That's a lot of people. Roche is hoping we don't start putting 2 and 2 together and taking them to court. Retinoids isn't a viable therapy for the general public. Wonder how much data they hid from regulators.

Edited by macleod, Yesterday, 03:32 AM.


#6647 unbroken94

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Posted Yesterday, 05:03 AM

If any of you have chronically annoying symptoms such as dry skin , flushing , muscle pain , erectile dysfunction , dry eyes , , dry hair , I honestly feel that you should look at look at accutazed post on page on 319 as it correlates with my post earlier today I don't know what the connection is between these ssri's helping accutane side effects , they also cured my raynauds and in most cases help with the flushing mine was under control while I was on it , I also should note though that these medications carry they're own risk as I'm sure you know however if someone is desperate enough I'm sure they might help , after reading through all this im honestly considering going back on my own but at a much lower dose simply to help me comfortabally live my life , I am convinced 250% these will alleviate your e.d as I was prescribed them after a short course of accutane at 16 (1month long before the last one) which left me with that particular side effect :/ there is hope

#6648 Modeaa

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Posted Yesterday, 07:57 AM

maybe this apply for seretonin depletion from accutane.
http://www.ncbi.nlm....les/PMC3485670/
Retinoic acid has multiple effects on innate and adaptive immunity, including promoting the differentiation of T and B cells (9,10), modulating cytokine production (11), driving Th2 responses (12,13) and inducing immune tolerance through induction of Foxp3+regulatory T cells (Tregs) (14),

http://www.ncbi.nlm....les/PMC3485670/
'The regulatory T cells (Tregs), formerly known as suppressor T cells, are a subpopulation of T cells which modulate the immune system, maintain tolerance to self-antigens, and abrogate autoimmune disease. These cells generally suppress or downregulate induction and proliferation of effector T cells. Additional regulatory T cells known as Treg17 cells have recently been identified


trypthophan is needed for making seretonin.(right?), acording to the next it's look like those regulatory T cells (Tregs), may use/need tryptophan for their creation. also retinoic acid mentioned and some more.

http://www.cellandbi...5-3701-1-20.pdf
       ndoleamine 2,3-dioxygenase in DCs drives iTreg
differentiation
DC populations expressing indoleamine 2,3-dioxygenase
(IDO) can play a critical role in immune tolerance by
promoting iTreg induction [47]. IDO catalyzes trypto-
phan metabolism via the kynurenine pathway and there-
fore depletes the local environment of tryptophan.
Tryptophan catabolism likely plays an important role in
suppressing T cell proliferat
ion by arresting T cells in
G1 phase of cell cycle [48]. However, recent studies
have highlighted an important role of tryptophan cata-
bolites in mediating iTreg i
nduction by exerting their
effects directly on DCs. During HIV infection, IDO
activity is critical in regulating Treg/Th17 balance with
increased IDO levels produced by DCs, associated with
a chronic inflammatory state in progressive HIV disease
due to a breakdown of mucosal barrier [49].''

DCs=dendric cells

http://en.wikipedia..../Dendritic_cell
Dendritic cells
(DCs) are antigen-presenting cells (also known as accessory cells) of the mammalian immune system. Their main function is to process antigen material and present it on the cell surface to the T cells of the immune system. They act as messengers between the innate and the adaptive immune systems.

Dendritic cells are present in those tissues that are in contact with the external environment, such as the skin (where there is a specialized dendritic cell type called the Langerhans cell) and the inner lining of the nose, lungs, stomach and intestines. They can also be found in an immature state in the blood. Once activated, they migrate to the lymph nodes where they interact with T cells and B cells to initiate and shape the adaptive immune response

whats that means?
https://www.ecco-ibd...in-t-cells.html
Effects of isotretinoin treatment on epigenetic programming in T cells
Results

Analysis of epigenetic modifications in naive and regulatory T cells revealed potential long-term effects in both T cells subsets. In regulatory T cells mainly the methylation pattern was altered in T cells isolated four weeks after cessation of treatment. In naive T cells on the other hand predominantly microRNA expression was altered in T cells isolated after four weeks without treatment. Pathway analysis by Meta Core® revealed that pathways of immune responses, concerning antigen presentation and T helper cell differentiation were affected. Further functional analysis of affected pathways is currently under investigation.


Edited by Modeaa, Yesterday, 08:07 AM.



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