Revimmune

A board to discuss future MS therapies in early stage (Phase I or II) trials.

Postby Lyon » Thu Aug 02, 2007 1:47 pm

bromley wrote: I'm off for a couple of weeks, but will rely on Dignan and yourself to keep the show going.
Do you have a cell phone number that dignan and I should know........in case the cure for MS is announced within the next couple of weeks?

bromley wrote:I've arranged to meet Lori at an exclusive restaurant in Naples in two weeks time.
Has Lori already been warned that you are an "enlightened male" and that it will be up to her to foot the bill?

bromley wrote:I hope there won't be any welcoming party when I arrive in Miami on Friday morning. Only the sight of Harry Z and Chris55 at arrivals would make me get on the next flight home. Ian
I decline comment because I'm not sure of your definition of "welcoming party". Anything like what we in the US term "lynch mob"?
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Postby viper498 » Thu Aug 02, 2007 3:36 pm

(for some reason my message didn't post?? wierd.)

As I was saying...

Ian,

It looks as though I am in luck. At the current time, I weigh 336 lbs. This means that I am 14 lbs. under the British Bed Weight Limit (BBWL). Luckily you won't have to worry about this for quite some time. Hopefully I do make it to London someday, sooner than later.

Best Regards,
Brock
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Postby viper498 » Thu Aug 02, 2007 3:37 pm

Oh, perhaps by the time I actually make it to London I will be @ or over 350 lbs. Lets hope not!!!!

Brock
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Postby Jean » Fri Aug 03, 2007 12:41 am

Hi Bob

Lyon wrote: which it doesn't seem that something as specific as Tovaxin (at least in its current form) is going to alleviate, where it seems that the Campath and HDC "sledgehammer" approach, in theory, should remove all aspects of all autoimmune diseases.


I think Campath and HDC have different mechanisms of actions : HDC is an immunisuppressant, which prevent some cells to replicate and to be produced, including pathogenic white cells but also hair cells, for instance (many people treated with HDC lose partially their hair). HDC blocks DNA replication and prevents mitosis. White cells naturally die within a relatively short period, and are not replaced because of HDC.

Campath is a monoclonal antibody, which directly attacks one particular cell clone (that's why it's called "monoclonal"). It binds to specific receptors on cell surface and kills it.


Lyon wrote: Considering that only killing the lymphocytes is much less dangerous and more effective, I'm not sure why, in the case of MS, anyone would continue to consider the greatly added risks of stem cell transplant. Sure, I can see it with cancer where the problems are generated in the bone marrow but it's looking as if with MS the process is reciprocated after that point.


The aim of cell transplant is to reset your body once for all : researchers believe if you are transplanted with that clean system, the disease will be cured, at least attacks will stop and the body will regenerate itself. That's why they're considering that one-time treatment option. With HDC only, you kill pathogenic cells, but perhaps you don't tackle the real cause of the disease : maybe what's going wrong is behind white cell production. For instance, if the problem comes from bone marrow or whatever else taking part in white cell production, if you simply kill faulty white cells, you are likely to still have faulty cells to be produced, and need lifetime HDC treatment (with all its side effects). Moreover, some specific white cells which "remember" dangerous antigens (like myelin proteins in MS) can live several months or years (I've heard about 72 years for some of them). If you don't destroy them, they can teach again other white cells how to attack myelin.

Very interesting topic, I've found no place to discuss those issues in France (where I live). This forum is really a great place.
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Postby finn » Fri Aug 03, 2007 4:47 am

Bob,
Lyon wrote:That's one of the reasons I'm cautiously optomistic about Campath. Something which is supposed to be alleviating the total immune system should alleviate all the autoimmune diseases and NEVER increase the risk of another autoimmune disease.

In case you didn't know, in 2005 the Campath trial was suspended after three patients developed an autoimmune disease called ITP.

Lyon wrote:There are already lots of things which could lead us to believe that progression without inflammation is a myth, but in the world of MS the direction of one's opinion totally depends which studies they decide to place their faith.

That is a bold statement. You know I have links to several imaging and pathologic studies showing that removing inflammation with an aggressive treatment hasn't been able to stop the progression of neurodegeneration. Do you happen to have any data suggesting that treating inflammation would have prevented neurodegeneration for good?

btw, I'm just curious. How would you define "total reboot" of the immune system, and how do you think it could be done?

Jean,
thanks for your posts.

-finn
"The great tragedy of science - the slaying of a beautiful hypothesis by an ugly fact.” -Thomas Henry Huxley
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Postby Jean » Fri Aug 03, 2007 6:04 am

finn wrote:In case you didn't know, in 2005 the Campath trial was suspended after three patients developed an autoimmune disease called ITP.


You're right, in ITP, white cells attack platelets, and since their number decreases, abnormal bleeding occurs.

finn wrote:That is a bold statement. You know I have links to several imaging and pathologic studies showing that removing inflammation with an aggressive treatment hasn't been able to stop the progression of neurodegeneration. Do you happen to have any data suggesting that treating inflammation would have prevented neurodegeneration for good?


A question would be : how do you define inflammation, and how would you define neurodegeneration ?

For me, inflammation is a mechanism allowing mass recruitment of immune defenses, and allowing those cells to pass through blood vessels barriers to destroy what's they've been recruited for.

And I define neurodegenration as neuron or axon death. The second question is : why do they die ? Because they're still attacked ? Because they are doomed to die on the long term lacking protective myelin ? Because they're more sensitive to toxins without their myelin ? Because someting else ? I've searched the web about causes of neurodegeneration in MS, but I couldn't find any consensus about what caused it, except the following one : inflammation is partially correlated with neurodegeneration at the beginning of the disease (RRMS), but seems to be independant of inflammation later on. Discovering processes involved in axonal injury would maybe help finding a cure.

finn wrote:btw, I'm just curious. How would you define "total reboot" of the immune system, and how do you think it could be done?


I define total reboot as :
- recruiting clean hematopietic or marrow stem cells (the problem is of course : how do you define "clean")
- Destroying all white cells
- Destroying all bone marrow and lymphoids tissues. (irradiation)
- Reimplanting stem cells
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Postby Lyon » Fri Aug 03, 2007 6:09 pm

finn wrote: In case you didn't know, in 2005 the Campath trial was suspended after three patients developed an autoimmune disease called ITP.
Hi finn,
Because I don't have MS it's impossible to be certain what my convictions would be if I did have MS, but I like to think that I would agree with bromley and Raven in that the risk of ITP and Grave's disease are acceptable risks when compared to the other treatments currently offered. That isn't to say that Campath 1H is perfect or that it should be considered anything more than a work in progress.
Lyon wrote:There are already lots of things which could lead us to believe that progression without inflammation is a myth, but in the world of MS the direction of one's opinion totally depends which studies they decide to place their faith.
finn wrote: That is a bold statement. You know I have links to several imaging and pathologic studies showing that removing inflammation with an aggressive treatment hasn't been able to stop the progression of neurodegeneration. Do you happen to have any data suggesting that treating inflammation would have prevented neurodegeneration for good?
I'm not sure I totally agree that was a "bold" statement. Maybe if I'd said "it's certain" or "almost certain" or "a predominance of information" but I only said "lots of things which could lead us to believe".

With that said, hopefully to open ears and open minds, I do think there are a lot of reasons to consider that progression without inflammation could very easily be a respected and widely held myth. I've read accounts which attribute the primary reason researchers originally considered "progression without inflammation" to the results found in the Campath trials (poor results on progressive MS).

If so, my personal questions regarding exactly which lymphocytes Campath eliminates and how effectively it eliminates them doesn't allow confidence that Campath is the perfect medium to base such an important conception as progression without inflammation.

Additionally, the resolution of the imaging machines commonly used to determine inflammation wasn't/aren't discerning enough to determine whether inflammation is non existent, has just gone deeper or has become less intense but more widespread...etc...

Additionally, lately I've been repeating like a broken record about the unheralded role of plasticity in every phase of MS and I think plasticity plays a big part in what, at face value, "seems" to us like the transition into the progressive phase, might instead represent the point in which a form of plasticity has reached it's capacity to mask neurodegeneration as it had been able to previously.
finn wrote:Do you happen to have any data suggesting that treating inflammation would have prevented neurodegeneration for good?
That would have been an excellent place to insert that "evil" smile emoticon. I hate to turn this thing around but your comment reflects exactly the point I was trying to make in my last post. You are familiar with the Campath, HDC and Tovaxin results. I'm aware of the Prineas and Barnett studies. Yet we both read completely different things into those results and it defies us to understand how the other doesn't accept the obviousness of it.

finn wrote:btw, I'm just curious. How would you define "total reboot" of the immune system, and how do you think it could be done?
ME?
First, "total" is a very serious word. All or nothing and nothing between. I don't think I'm the first to coin the term "total reboot" but in regards to leukemia it's very important that it consists of "total" elimination of the lymphocytes and "total" elimination of the bone marrow of the large bones which creates the lymphocytes.

Considering the inconceivable task of eliminating every last lymphocyte in the entire body and eliminating every cell in the enclosed bone marrow, I find it hard to believe that a true total reboot is possible. But since oncologists have been doing this procedure for 40 years with increasing success, I would have to guess that they're either perfected the process or have realized that it's not essential to kill every last cell.

After that, (so I've read) stem cells which are "seeded" back into the bones have been the patient's own cleansed cells, those from a closely matched donor or those derived from cows. Regarding leukemia this entire process is essential because it is certain that the faulty cells originate in the bone marrow.

It seems that researchers coincidentally noticed that patients with MS who were enduring this leukemia treatment process, fairly consistently experienced relief from their MS. At that point I think it was commonly accepted that the MS process was driven by the bone marrow and that the entire "total reboot" process was also necessary with MS. As we all know, results weren't stellar.

Regarding what we (on this site) have been calling "partial reboot" (chemotherapy with the specific intention of eliminating the lymphocytes, yet sparing the bone marrow), as far as I can tell this situation http://tinyurl.com/2ta34m seems to have been the hint that eliminating the lymphocytes alone might pose much less risk for the patient, shorter recovery time and result in higher effectiveness.

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Postby finn » Sat Aug 04, 2007 8:54 am

Bob,

Lyon wrote:I like to think that I would agree with bromley and Raven in that the risk of ITP and Grave's disease are acceptable risks when compared to the other treatments currently offered.

Yes. It is wise to compare possible risks vs. benefits of a drug treatment. Like Dr. Agnell said in an interview: "a drug has no side effects, it has multiple effects."

Lyon wrote:I do think there are a lot of reasons to consider that progression without inflammation could very easily be a respected and widely held myth.

Well, the theory of inflammation being the primary driving force of MS has been the widest held myth in MS research for 40 years, and most treatments in clinical trials at the moment are based on it (including Tovaxin). That is why I do understand your point of view.

Lyon wrote:I think plasticity plays a big part in what, at face value, "seems" to us like the transition into the progressive phase, might instead represent the point in which a form of plasticity has reached it's capacity to mask neurodegeneration as it had been able to previously.

I believe there is plasticity in MS brain, too, but I doubt its ability to modify the neurodegenerative process of this disease. Of course it may have a modest effect on the clinical course of MS. Animal studies suggest that it takes 15-30% axonal loss before first permanent symptoms appear, and reorganizing pathways in the brain may be able to delay the process.

Lyon wrote:I'm aware of the Prineas and Barnett studies.

The paper by Prineas et al was controversial and its results were quite mixed, but it opened the gate to a bunch of new imaging and pathological studies with innovative results showing that neurodegeneration is already happening at the clinical onset of the disease, and there can be neurodegeneration without inflammation (also outside lesions). I'd say those are the studies one should be aware of.

Lyon wrote:eliminating the lymphocytes alone might pose much less risk for the patient, shorter recovery time and result in higher effectiveness.

HDC with a drug like CFX seems safer than SCT (by the amount of abbreviations used in this thread, I'd say most of you guys are probably engineers), but one can question its long term efficiency. This quote is from a meta-analysis done by unbiased and reliable Cochrane group:
    "Intensive immunosuppression with CFX (alone or associated with ACTH or prednisone) in patients with progressive MS compared to placebo or no treatment (152 participants) did not prevent the long-term (12, 18, 24 months) clinical disability progression as defined as evolution to a next step of Expanded Disability Status Scale (EDSS) score. However, the mean change in disability (final disability subtracted from the baseline) significantly favoured the treated group at 12 and 18 months, but favoured the control group at 24 months. We were unable to verify the efficacy of other schedules. Five patients died; sepsis and amenorrhea frequently occurred in treated patients.
Jean,

Jean wrote:I define total reboot as : ...

You and Bob both defined total reboot as autologous stem cell transplant (ASCT). Thanks! Now I know what you're talking about.

Jean wrote:Discovering processes involved in axonal injury would maybe help finding a cure.

I agree.

-finn
"The great tragedy of science - the slaying of a beautiful hypothesis by an ugly fact.” -Thomas Henry Huxley
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Postby Lyon » Sat Aug 04, 2007 4:49 pm

finn wrote:Well, the theory of inflammation being the primary driving force of MS has been the widest health myth in MS research for 40 years, and most treatments in clinical trials at the moment are based on it (including Tovaxin). That is why I do understand your point of view.
Hi finn, I can't guess what the creator of Tovaxin had in mind other than to determine if and for how long the vaccine effect would remove the myelin reactive T cells from the system. And after that point to determine what effect removing those self-reactive T cells would have on MS.

Because for so long our vocabulary regarding the MS process was restricted to "permeable bbb, inflammation, neurodegeneration, lesions and atrophy" I think it got lost in the shuffle that something in the disease process precedes those things.

I have no idea what the future holds, but if in the future it is determined that Campath, HDC and/or Tovaxin stops MS in it's tracks, would it be completely correct for me to say they work by controlling inflammation, or you to say that they work by controlling neurodegeneration? I don't think so because they act at a point prior to the instigation of either inflammation or neurodegeneration. Kind of like removing the fuel before a fire can start as opposed to only concerning ourselves with inflammation and neurodegeneration is like attempts to dampen a fire which is already out of control.

finn wrote:I believe there is plasticity in MS brain, too, but I doubt its ability to modify the neurodegenerative process of this disease. Of course it may have a modest effect on the clinical course of MS. Animal studies suggest that it takes 15-30% axonal loss before first permanent symptoms appear, and reorganizing pathways in the brain may be able to delay the process.
Of course, anything I or anyone else on this site says should always be taken with a grain of salt. Over and above that, I'm about to say things, which I personally think are of a higher logic but which don't align with traditional MS "wisdom"

I don't hint that plasticity has any effect or direct relationship, positive or negative, with inflammation or neurodegeneration but that plasticity has a VASTLY greater ability to mask neurodegeneration than it has ever been given credit. Especially when progression is at a rate which plasticity can match, or almost match.

I think it's always important for us to keep in mind that with MS, involving the brain, spinal cord and optical nerves which for the most part are directly inaccessible to us, we have always been in the position of having to base opinions on what "seems" and not necessarily what "is". Although MRI helps, it isn't perfect and we still can't directly observe the MS process. Postmortem analysis lets us directly observe, but obviously after death and after the end of the MS process and decomposition has begun.

NONE of the information has ever been direct and this really is a situation in which common sense and logic should be aided by, but not directed by research results. That isn't what happened and that's why MS has remained so illusive for all these years.


I think there are at least two kinds of plasticity involved. One involves networks in the brain inherently having far more capacity than normal situations require. For our purposes allows ongoing damage to be masked without the brain actually having to “rewire” itself but instead, slowly obstructing the normally available pathways until reaching a point in which “traffic” (electrical impulses) is so congested that the effects are noticeable (what “seems” to us to be the first symptoms of MS and what would lead someone to seek diagnosis and which currently “seems” to us to be the beginning of the MS process). For some reason my mind always wants to consider this "quick plasticity".

It seems evident that most people only consider plasticity as "re-routing" of the circuits of the brain and is the type of plasticity we are most familiar in the rehabilitation of stroke and brain damage from car accidents, etc.... This is a slower process and is considered to REQUIRE intentional effort to implement. While it seems that intentional nurturing does insure a higher degree of completeness in rehabilitation and does speed rehabilitation, I'm convinced that through the use of necessity this type of plasticity does unintentionally and invisibly happen, especially in younger people.

At least two types of plasticity, each with their separate reservoirs of capacity and types of masking ability.

Hopefully you will consider my ideas on plasticity within the realm of possibility, maybe even within the realm of likelihood.

If you do and if you also agree that the entire accumulated knowledge base of MS “conventional wisdom” is based on indirect knowledge (based on what the picture “seems” to be) then you are ready to consider that, in addition to the traditional ways, there are other logical, possibly more logical, ways to view every aspect of MS.

Consider the RRMS phase. Although researchers admit they don’t know what is responsible for the symptoms and reversal of symptoms, it seems universally accepted that demyelinisation and remyelinisation is the driving force, despite the fact that it is obvious that remyelinisation is a slow process, which might even be slower in those with MS. The idea that remyelinisation might align with the timeline necessary to explain reversal of symptoms in RRMS is illogical.

Although when I mentioned it earlier it was appreciated like a fart in church, it seems much more logical to believe that in the RRMS phase, inflammation itself is initially responsible for the interruption of the nerve’s electrical impulses-the noticed symptoms. There is always permanent damage being done but, dependant on the severity of the inflammation, there are varying degrees of injury. Immediately fatally damage to some axons, mortally wounded but not immediately fatal and damage within the ability to heal. I think this is the reason why during initial relapses certain symptoms completely disappear during remission but after subsequent relapses almost inevitably become permanent. Underlining that, it seems most logical that a relapse portrays inflammation surpassing the combination of speed and ability of plasticity to mask symptoms.

It seems most logical that remission is the elimination or lessening of inflammation, again allowing efficiency of the electrical impulses of the nerves and subsequently allowing the masking ability of plasticity to keep pace.

Continuing the “Lyon hypothesis” into the progressive phase of MS, it might be accurate to consider that plasticity and inflammation still play a part, but like myself they are little worn out and don’t have the capacity they did in the past.

This seems to be an opportune time to point out that after MS has run it’s course for a certain amount of time, at some point in the progressive phase, it’s often been noticed that progression slows. That was a consideration when forming this hypothesis. What could possibly be the reasoning behind that?

Because any process we don’t understand and can’t explain, necessarily seems random, with further knowledge we most often find that it wasn’t really random at all. In the case of why and where inflammation and subsequent lesions form on the brain, at this point let’s go with the flow and consider it totally random because at this time we have no other options.

(of course this isn’t an accurate representation, but it might contain some degree of truth) Consider a brain in the beginning of the MS process as a spinning brain suspended on a string and we are the “monster” throwing darts at it, with the goal of always hitting a previously unaffected spot. In the beginning (the RRMS phase) this game is very successful but with enough time (the SPMS/PPMS phase) it becomes progressively harder to hit an unaffected area with a dart.

The truth in this might involve the fact that lesions are scar tissue, damaged tissue which (talking somewhat out of my arse here) might not lend itself to inflammation as well as
“virgin” tissue, in combination to the likelihood that the progressive phases align with a time when plasticity is reaching the end of certain capacities. I guess my point might be that it’s possible that the progressive phase might not signal an actual change in the disease process, as it “seems” to, but might instead, more sensibly, might be a visual sign that certain capacities have reached or are reaching their limits.

I admit that this is an imperfect hypothesis, which can’t be documented, but it continues to be a work in progress.

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Postby finn » Sun Aug 05, 2007 12:10 am

Bob,
Lyon wrote:...if...might...

Boy, it was a long post. Have you concidered running for politics?

Btw, maybe instead of "plasticity" it might be better to use the term "regenerative potential" more often in your hypothesis. Or did I get it wrong?

-finn
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Postby Lyon » Sun Aug 05, 2007 5:12 pm

finn wrote:Boy, it was a long post. Have you concidered running for politics?
Hi finn,
Sorry about the length of that last post, but I think that topic is really important as it implicates possible misconceptions permiating MS research and might play a big part in the fact that "nothing makes sense about MS".

I had considered going into politics but my children are young and I don't want my occupation to embarrass them. After they finish school maybe I'll quit driving the garbage truck and go into politics then :lol:
finn wrote:Btw, maybe instead of "plasticity" it might be better to use the term "regenerative potential" more often in your hypothesis. Or did I get it wrong?
Yes, "regenerative potential" is an accurate description of the common conception of "plasticity" (as in “rewiring” such as promoted in stroke and brain damage rehabilitation efforts) but my point is that there is another aspect of "plasticity" which likely dwarfs the potential of what is commonly considered plasticity. This other form doesn’t portray the image of being regenerative but instead starts early and causes damage (neurodegeneration) to be invisible or not nearly as bad as it is.
finn wrote:Animal studies suggest that it takes 15-30% axonal loss before first permanent symptoms appear
THAT is EXACTLY the type of plasticity I’m talking about!

Now consider that, compared to other animals, the human brain is a wonder of overcapacity and instead of 15-30% the figure is closer to 60-70% Additionally, in your above quote I think you can replace the word permanent with the word noticed.

I consider that to explain why, soon after diagnosis, it is often noticed that there is “already” WM and GM neurodegeneration and atrophy. In other words, the MS process has been going on for years, unnoticed, in people newly diagnosed with MS. Additionally, for the same reason I think that people diagnosed with PPMS in reality have had their entire rrms phase "hidden" by the above mentioned type of plasticity.

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Accentia Ann Investigational New Drug Application for Revimm

Postby thinkingoutloud86 » Mon Oct 08, 2007 4:29 pm

Accentia Biopharmaceuticals has met with the FDA for a scheduled pre-investigational new drug meeting on Revimmune, the company’s potential therapeutic for refractory relapsing-remitting multiple sclerosis (MS).

The FDA has indicated support for Accentia’s submitting an investigational new drug application for a pivotal Phase III trial of Revimmune, Accentia said.

The Revimmune MS study will enroll subjects in a one-year study comparing baseline disability with disability at month 12 with an interim data analysis. The company expects to commence the study in the first half of 2008.
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Postby Lyon » Tue Oct 09, 2007 3:05 pm

Thanks for the info thinkingoutloud!
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Postby Bandy » Thu Apr 21, 2011 9:36 am

In June of last year I also underwent the High Dose Cytoxan procedure without stem cell rescue. The procedure was performed at Rush Medical Center in Chicago with my entire stay within the bone marrow transplant ward. The Cytoxan was given over a 4 day period after which my red and white cell counts dropped dramatically. My white cell counts dropped to 0.002 and after 13 days rapidly increased after which time I was released. Major improvements were noted in my sense of smell and allergies. I previously was always congested due to allergies, but with my new immune system all allergies were gone and I regained my sense of smell. As a result of just this I have been able to be more fully rested and have additional energy. I also stopped taking Copaxone shots daily saving my insurance company $36,000 annually. It should also be noted that my insurance picked up the entire procedure and ended up paying Rush exactly $35,000. So just to be off the shots was a bargain for the insurance company. In July it will have been 12 months and I can honestly say I have not had any relapses. I still have symptoms due to nerve damage but look forward to improvements over the next few years. From my perspective the procedure was a success and stemmed from my moving from England to the South US when I was 14 years old and had an immature immune system. I have soken with many people who have had improvements in their EDSS scores and if I can achieve a 40% improvement it would be worth the temporary setbacks (loss of hair and weight). Now that the disease process has been halted my body is working to rewire/restore lost functions and while slow there is light at the end of the tunnel. I had RRMS for 16 years and my EDSS was 3.0 and even if it improves to 1.5 it will have been worth it. I have made it my personal mission to increase awareness so that we can get rid of the CRABS that just delay relapses but do not halt the disease process. It is also worthy to note that the same procedure could effectively heal/cure all 80 auto-immune diseases.
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