Stephen Davies Update

[KofQ]

"When our new data is published this year - no one except maybe my scientific competitors (some of whom I'm told read my posts on this forum) are going to be disappointed."

this is a direct quote from dr. davies last post on care cure, the same one you went to the trouble of looking up. how could you misunderstand this quote to mean anything other than he's concerned with beating his competitors.

Most discoveries arise from competition. Do you really think that Wise, Davies or anyone else does this work without at least some thought of recognition or reward?

I don't think it's too much to ask for Davies or one of his subordinates to post a short paragraph or two every few months to keep everyone who donates informed. Not knowing is the cause of the anxiety here, I think.

[Charles Hansen]

Most discoveries arise from competition. Do you really think that Wise, Davies or anyone else does this work without at least some thought of recognition or reward?

Correct. Nobody wants to be left behind when a scientific revolution comes along. What happened to all of the conventional physicists when Einstein came along? (Not that his ideas were embraced immediately!)

There are also financial considerations. Many of the discoveries are covered under patent. Many of the large pharmaceuticals want to "obtain" intellectual property for the lowest possible price and sell the resultant product for the highest possible price. (That's actually their job.)

And it's even possible that both could be rolled together in one. It's not out of the question that the person/team that restored function in an SCI victim would win a Nobel prize. Of course, that takes at least ten years to make its way through the "machine", so often the prizes are posthumous...

I don't think it's too much to ask for Davies or one of his subordinates to post a short paragraph or two every few months to keep everyone who donates informed. Not knowing is the cause of the anxiety here, I think.

It seems like a reasonable request, but unfortunately that's not possible. Releasing any information in advance of publication by a scholarly journal means that it will never be published. Davies (and everyone else) have to follow the rules of the game.

It sucks.

[Charles Hansen]

"When our new data is published this year - no one except maybe my scientific competitors (some of whom I'm told read my posts on this forum) are going to be disappointed."

this is a direct quote from dr. davies last post on care cure, the same one you went to the trouble of looking up. how could you misunderstand this quote to mean anything other than he's concerned with beating his competitors. not to mention the fact that what year was he talking about his data being published,he said this year. he must have been pointing at a calendar from 2015 when he typed that line.

Yes, that was Dr. Davies' quote. He did miss his self-imposed deadline by a month -- the most recent paper was published in January of this year rather than last year. But that doesn't bother me very much.

The paper showed the HUMAN stem cells worked to cure SCI's in rats. This was the first time such an experiment had been done. Were you disappointed? I wasn't. Were some of his "competitors"? As Dr. Davies said, "Maybe."

That is a FAR stretch from saying that the only thing Dr. Davies is interested in is "beating his scientific $competitors$", as you did in an earlier post -- with the dollar signs implying that his other motivation is money.

Personally I think that it is far more likely that money is the main motivator for one of Dr. Davies' "scientific competitors" -- the one who drives a Ferrari.

[Charles Hansen]

Seriously? You've been here since 2008 and haven't figured out that Just A Dollar A Day goes to the SCINetUSA clinical trials? Dr. Young has been nothing but transparent, not to mention prolific, about both the trials and the fundraising process. Like, hundreds, if not thousands of posts, most in this little corner of the forum.

Yes, seriously. I simply haven't followed that closely at all. My bad. Maybe I'm missing out on some incredible stuff.

If you don't mind, could you just post a few sentences of the accomplishment highlights? If it's too much trouble, don't bother. Thanks.

[Charles Hansen]

Correction. Dr. Davies had directly/indirectly solicited funds from the CareCure community, and has acknowledged it. You might have forgotten but it was discussed earlier.

Dr Davies has made around 100 posts in various threads in CareCure. I haven't read them all. I did find an early one in this thread:

/forum/showpost.php?p=739653&postcount=139

In it he wrote,

"I have received several emails over the past few days requesting information as to how to make a donation, so here below are instructions for both wire transfers and personal checks."

I'm not sure if that's what you mean by "soliciting funds", but that's not what I would call it. YMMV.

What I have come to understand over years of following SCI cure research is that human injury models are contusion as a rule and transection (from knife/bullet injury) as an exception. So far, Dr. Davies' published research/papers have been based on transected spinal cord. Recovery from chronic contusion injury in mouse/rat models would be the analog for us chronics.

Here is what Dr. Davies had to say about transection studies versus contusion studies:

/forum/showthread.php?p=960957#post960957

The highlight being,

"Transection injuries make the absolute worst scar to try and overcome at the acute and particularly the chronic stages of SCI. We have seen indications that scarring spreads away from the injury site and is more extensive within white matter pathways of the chronically injured spinal cord in rats. Thus if you can overcome the effects of scarring on axon regeneration and / or plasticity (sprouting of intact circuits) in a transection injury model then the odds are that the therapy will be equally if not more effective in contusion injuries where it is generally thought that scarring is less robust.

"My lab is one of the few labs in the world that has actually quantified the levels of individual types of scar associated inhibitory molecules at acute through chronic (6 months out) stages of SCI and identified the cells that are making the inhibitors. We chose to first study transection injuries rather than contusion injuries because it is well known that the contusion injury models vary too much in size between animals to allow accurate quantification of scar associated molecules. In contrast transection injuries are highly reproducible AND RESULT IN LONG TERM DEFICITS IN LOCOMOTOR FUNCTION (THAT EVEN ACTUALLY APPEAR TO INCREASE IN SEVERITY AT CHRONIC STAGES)."

Please note that other labs may have attachments to using contusion injuries for other reasons.

He had started work on such mouse models with Decorin alone and in combination with type I astrocytes long ago. There has been no information on the results. In its absence speculation suggests that Decorin alone was probably not found to be effective enough in chronic contusion injury model. Then again it can be speculated that efforts (Decorin plus other things) are ongoing, and we will know in the next five years. Of course, if history is any guide, we will probably be repeating that every year.

I agree. The delays are extremely frustrating. But until something better comes along, I will continue to support Dr. Davies. Naturally, each of us is free to choose any lab, or no lab at all.

[Scaper1]

Yes, seriously. I simply haven't followed that closely at all. My bad. Maybe I'm missing out on some incredible stuff.

If you don't mind, could you just post a few sentences of the accomplishment highlights? If it's too much trouble, don't bother. Thanks.

You're kind of making me want to cry.

The SCINetUSA and China SCINet threads are both stickied. (They are collaborating.) A couple dozen CC posters link to the trials in our signatures.

Highlights: http://www.icontact-archive.com/9xHN...a8hh8Qtp_D?w=3

From Summer Open House: Clinical Trial Update
At the recent Summer Open House, Dr. Wise Young gave an update on the Phase 2 trials in Hong Kong. This Phase 2 trial is looking at the safety of escalating doses of injections of umbilical cord blood mononuclear cells into the spinal cord, with four people at each level. At each level, patients are observed for potential side effects. After the third increase in dosage, methylprednisolone will be added. Then in the final step of Phase 2, participants will be given the highest safe dose of cord blood stem cells plus a six-week course of oral lithium.

Seven patients already have been treated with no significant problems. Some have reported increased sensation and some recovery of function. However, results need to wait for the six-month independent examinations.

This Phase 2 Trial will be repeated in the fall in Kunming, China. In Kunming it will be accompanied by intense physical therapy, the so-called '6-6-6' program: six hours a day, six days a week, for six months.

The data from these trials will be submitted to the FDA for clinical trials in the United States. In September we will be meeting with people at our flagship hospital in Austin, Texas to continue planning there.

[nrf]

scaper1,

i fear charles hansen has selective vision rather than selective hearing.

[Quad62]

Dr Davies has made around 100 posts in various threads in CareCure. I haven't read them all. I did find an early one in this thread:

https://www.carecure.net/forum/showp...&postcount=139

In it he wrote,

"I have received several emails over the past few days requesting information as to how to make a donation, so here below are instructions for both wire transfers and personal checks."

I'm not sure if that's what you mean by "soliciting funds", but that's not what I would call it. YMMV.

CH,

You yourself agree to not have read through all his posts, forget about other direct/indirect solicitations. In any case, I see no point in bickering about it.

CareCure community has donated funds to Davies research, and therefore he should be held accountable. And I mean accountable to providing information, not positive results because results don't always turn out positive. Just clarifying so you don't think I'm frustrated simply because we haven't had that cure yet.

on July 18, 2006

Chronic Injuries
However as I have already mentioned we are also currently investigating whether Decorin can promote the breakdown or "degradation" of chronic scar tissue. We have recently shown that decorin can induce the spinal cord to make an enzyme called Plasmin which other labs have shown can breakdown molecules found in scar tissue that are known to inhibit growth of nerve fibers. The ability to modify or breakdown chronic scar tissue in a controlled manner that does not create an even bigger injury, should allow better integration of transplanted cells within or adjacent to sites of injury, and therefore hopefully increase recovery of spinal cord function.

Transplantation of GDAs alone to chronic injuries may promote recovery of function (next round of studies) however to my mind all transplanted cells be they GDAs, OECs, Bone Marrow cells or oligodendrocyte precursors will be far more effecient at promoting recovery if they do not find themselves within or next to dense, fibrotic scar tissue.

on December 2, 2008

Thus if you can overcome the effects of scarring on axon regeneration and / or plasticity (sprouting of intact circuits) in a transection injury model then the odds are that the therapy will be equally if not more effective in contusion injuries where it is generally thought that scarring is less robust.

My lab is one of the few labs in the world that has actually quantified the levels of individual types of scar associated inhibitory molecules at acute through chronic (6 months out) stages of SCI and identified the cells that are making the inhibitors. We chose to first study transection injuries rather than contusion injuries because it is well known that the contusion injury models vary too much in size between animals to allow accurate quantification of scar associated molecules. In contrast transection injuries are highly reproducible AND RESULT IN LONG TERM DEFICITS IN LOCOMOTOR FUNCTION (THAT EVEN ACTUALLY APPEAR TO INCREASE IN SEVERITY AT CHRONIC STAGES).

Note:We are also starting collaborations with other labs to study the effects of decorin on chronic contusion SCI rats.

Originally Posted by Wise Young:

As I have explained many times here and elsewhere, I disagree with the use of the word "scar" to describe what is happening at the spinal cord injury site. To me, scar means a fibrous collagenous tissue that is formed by fibroblasts (skin cells) to heal a cut in skin and other tissues. Normally, there are no fibroblasts in the spinal cord. Scar does form in the spinal cord when one uses a knife to cut the spinal cord and does not repair the dura afterward. The meninges do have fibroblasts but they usually do not invade into the spinal cord unless there has been a penetrating wound of the spinal cord. After contusion or compression injuries (which is what happens to a large majority of human spinal cords), there is no penetrating wound of the spinal cord and few or no fibroblasts in the spinal cord.

I know that many scientists use the word scar in their descriptions of spinal cord injuries and have made it a primary target of their research. I disagree with this use of the word and have publicly criticized the suggestion that "scar" is the main obstacle to regeneration. I believe it is an artifact of their spinal cord injury model where they cut into the spinal cord and then fail to close the dura. I think that this is why Dr. Davies and almost every scientist who use the dorsal hemisection, lateral hemisection, or transection models of spinal cord injury emphasize scar formation . When fibroblasts invade into the spinal cord, astrocytes proliferate to wall them off (because they are foreign to the central nervous system and it is the job of astrocytes to segregate the central nervous system from surrounding tissues). When this happens, I agree that scar is forming in the spinal cord and poses a significant barrier to axonal growth.

I have spent 30 years studying contusion injuries of the spinal cord. The vast majority of people with spinal cord injury have had contusions, compression, or ischemic lesions of the spinal cord. These types of injuries have little or no fibroblast invasion of the injury site. There is gliosis but these do not form physical barriers to axonal growth. In 1997, a group of 8 leading spinal cord injury centers in the United States (the Multicenter Animal Spinal Cord Injury Study) studied over 700 contused rat spinal cords (this is part of the multicenter animal spinal cord injury study). We found a majority (I believe >70%) of the contused spinal cords have a matrix of glial cells and Schwann cells at the injury center with many axons running through the middle of the injury site. Some of the spinal cords form cysts at the injury site. None had collagenous scars with fibroblasts.

There is a clear difference of opinion about the presence of fibrotic scar tissue and it being an obstacle to axonal regeneration. I have waited for evidence from Davies' research to confirm his opinion that the odds are that the therapy will be equally if not more effective in contusion injuries. No evidence provided so far for almost five years.

Please note that other labs may have attachments to using contusion injuries for other reasons.

Your conjecture above might apply to his lab regarding using transection injuries. Real chronic contusion trial results would be the only way to contradict it.

[KofQ]

I don't think it's too much to ask for Davies or one of his subordinates to post a short paragraph or two every few months to keep everyone who donates informed. Not knowing is the cause of the anxiety here, I think.

It seems like a reasonable request, but unfortunately that's not possible. Releasing any information in advance of publication by a scholarly journal means that it will never be published. Davies (and everyone else) have to follow the rules of the game.
It sucks.

I don't think anyone is asking for any trade secrets here, just a little periodic progress report. For example, Davies' experiments are being replicated at Yale right now. This was reported in the Step Ahead Australia newsletter and posted in this forum.

https://www.carecure.net/forum/showp...8&postcount=10

If Davies posted this on here himself, he would probably get a lot more suport (financial and otherwise) from those who are upset with him.

[Schmeky]

But until something better comes along, I will continue to support Dr. Davies

As far as peer reviewed publications is concerned, it has already happened.

[Han Solo]

Hey guys, I know its very frustrating not hearing anything from Dr Davies regarding how things are going. Believe me Ive posted in this thread before venting my frustrations toward Charles but the truth is hes just giving his honest opinion towards his beliefs in Dr Davies work. Anyone here would defend their friend when they believe people are unfairly bashing them. The truth is the only thing Charles is doing is trying to get others to keep hope in Dr Davies alive, and being as optimistic as he can. Its just sad because everyone is waiting for an answer from somebody to help ease the pain of what we are going through, but the fact is all the bickering and disagreeing still isn't bringing us any closer to the answer we seek. It isn't making Dr Davies post. We're all in this together so lets just cut each other some slack and keep preparing ourselves to be ready for the good news when it does come. Donate to whatever cause you believe in and keep yourselves healthy for future therapies. I believe Davies is onto something big but until he posts we need people like Charles and Susan to relay any messages of hope, as cryptic as they may seem. Just keep you heads up.

[Charles Hansen]

You're kind of making me want to cry.

Sorry for the tears. Your post kind of wanted to make me cry, too. It was of interest, no doubt. But there were far more questions than answers. I went to the link you gave and it looked like a press release. The sticky has over 400 posts -- too many to wade through for me.

Of the seven subjects, "some" have reported "increased sensation" and "some" recovery of function.

How many of the seven is "some"? Exactly how much "increased sensation" did "some" of the subjects report? Exactly how much "recovery of function" did "some" of the subjects report? What was the exact protocol? Just UCBMC in the spinal cord? Nothing else? No physical therapy? What was the patient population? How long post-injury? What level of injury? Complete or incomplete?

As I said, it is of interest but does not yet sound like the breakthrough that will get us out of our chairs. But maybe that will change with the introduction of lithium and/or exercise and/or methylprednisone. Even then it would be nice if it worked on SCI patients that are many years out with complete injuries. Definitely something to watch. Thanks for the pointer.

[nrf]

charles hansen,

why do you scrutinize every aspect of dr.youngs work but expect everyone to swallow your "Kool-Ade". what part of phase 2 trials can't you comprehend? you spew crap about researching labs to donate money wisely, then claim 400 posts are too many to read. i think you are either being dishonest in your posts, or have succumbed to your own "Kool-Ade".

every one of your "questions" is answered on this site with a fraction of the effort you have put into selling your "Kool-Ade" here.

[Charles Hansen]

There is a clear difference of opinion about the presence of fibrotic scar tissue and it being an obstacle to axonal regeneration. I have waited for evidence from Davies' research to confirm his opinion that the odds are that the therapy will be equally if not more effective in contusion injuries. No evidence provided so far for almost five years.

Your conjecture above might apply to his lab regarding using transection injuries. Real chronic contusion trial results would be the only way to contradict it.

Yes, reading Dr. Young's post and Dr. Davies' post shows that there is, at the very least, a difference in the definition of a "scar". I know that in my conversations with him Dr. Davies has always been careful to note that when he says "scar" that it is a convenient shorthand for some sort of chemical barrier that prevents neuronal regrowth across the site of the injury, and not the type of scar that is formed by, say, skin.

Whether the difference between these two approaches is simply a matter of semantics, or whether it involves methods of study that may produce errors in the results is not known to me.

I'm sure that either Dr. Young, Dr. Davies, or time will be able to tell us...

[Charles Hansen]

charles hansen,

why do you scrutinize every aspect of dr.youngs work but expect everyone to swallow your "Kool-Ade". what part of phase 2 trials can't you comprehend? you spew crap about researching labs to donate money wisely, then claim 400 posts are too many to read. i think you are either being dishonest in your posts, or have succumbed to your own "Kool-Ade".

every one of your "questions" is answered on this site with a fraction of the effort you have put into selling your "Kool-Ade" here.

I guess I just like to sell Kool-Ade...

PS -- Thanks for spelling my name correctly.