Stephen Davies Update

[GRAMMY]

Since Decorin is effective in the acute phase of SCI, there is early evidence that it may also be effective in the chronic phase as well. Testing of Decorin in the chronic phase of SCI is presently taking place in chronic rats and results should be available by the end of 2006.
/forum/showthread.php?t=66029

I asked Wise's opinion of Dr. Davies work last weekend in Austin. His only comment to me focused on the lack of data associated with contusion to the spinal cord, strongly implying transection to be less relevant in his opinion.
/forum/showpost.php?p=1018250&postcount=590

Based on published results, there is still no information concerning the efficacy of Decorin for chronic spinal cord injury or the contusion model of spinal cord injury. Most of the data has been generated by one laboratory.
/forum/showpost.php?p=1207326&postcount=6

Whilst decorin treatment did not improve functional recovery after SCI, and did not enhance the marked improvements in recovery after hBMSC transplantation, it may serve best in combinatorial repair strategies by prolonging donor cell survival, reducing the inflammatory response and enhancing tissue sparing after SCI. Functional recovery is not significantly improved in animals subjected to decorin infusion via pump (either isoform) compared to control (injury only) animals in both acute and chronic SCI.
http://www.stepahead.org.au/pages/research-focus/partnershipscurrent-projects/project-1.php

Astrocytes in vivo are totally plastic. In fact, Dr. Jerry Silver started the immature astrocyte story many years ago. They have a published paper showing that the affect of immature astrocytes by themselves only allow axons to regenerate into the lesion and not beyond. Dr. Fischer made the assessment that GRP never promoted regeneration. He examined the properties of astrocytes derived from a population of stem cells called GRP and tested their ability to promote regeneration in a SCI model. The results of his studies were different than Davies results. He found that all populations of astocytes derived from GRP were permissive and promoted regeneration but the regeneration was limited to growth into the injury only. With only modest effects of astrocyte transplantation there would need to be a whole lot more development before planning a clinical trial. This also underscores my point about replications needing completed by contracted NIH labs to confirm the data. There would also probably need to be a clinically relevant model such as contustion so it could be relevant for a trial when considering SCI therapy. In addition, with what little information and data that has been acquired so far, I just consider this work to be very basic research so far. It of course is nowhere near close to any type of translation and will take many many years for anything even remotely close to develop towards translating to the clinic.
http://www.drexelmed.edu/home/abouto...akfischer.aspx

Charlie, I'm glad you're interested in the research on chronic spinal cord injury!

[Charles Hansen]

Since Decorin is effective in the acute phase of SCI, there is early evidence that it may also be effective in the chronic phase as well. Testing of Decorin in the chronic phase of SCI is presently taking place in chronic rats and results should be available by the end of 2006.

This was from the earliest visit of a CC member to Dr. Davies' lab. I know that Dr. Davies alternates between using GRP's and Deocorin in his experiments, although I don't know why. On several occasions (such as Work2Walk) he has said that the thinks the best results will come from a combination of the two therapies.

Much of the delay in this specific case is that it takes at least a full year to run tests on chronic injuries. Rats have a typical lifespan of two years. They are two months old before they are mature enough to train (for the grid-walk test, the most indicative test available -- at lest until we learn to speak to rats). Then they must be surgically injured, and kept alive for another nine months (equivalent to a decade or two in humans), then finally treated for their injuries and re-tested. Finally the rats must be dissected so that photomicrographs can be made showing the amount of regrowth, et cetera. Only then can the paper be written and submitted for publication, which typically takes another year.

Dr. Davies began his work at Baylor in Texas. Then the University pf Colorado opened a new facility and mad Dr. Davies an offer he couldn't refuse. When he relocated his lab to Colorado he had to euthanize all of he rats and start all over again.

I asked Wise's opinion of Dr. Davies work last weekend in Austin. His only comment to me focused on the lack of data associated with contusion to the spinal cord, strongly implying transection to be less relevant in his opinion.

This is exactly the opposite of Dr. Davies opinion. Although techniques for introducing contusions are constantly improving, it is still extremely difficult (if not absolutely impossible) to make identical injuries in all of the test subjects during an experiment. Additionally Dr. Davies has indicated that his opinion is that a transsection is a much more difficult injury to heal, and therefore a better test all the way around. I don't think that anybody (and certainly not myself) can say that one view or the other is the correct one at this point in time. Clearly a contusion is much more representative of a typical SCI in a human.

This is the kind of "infighting" that I find extremely annoying. If Dr. Davies has developed techniques that will heal a transsection, I cannot see any reason why they wouldn't also heal a contusion, which after all is clearly a less severe injury. Again, I am far from an expert and could be completely wrong. But the impression I am left with is one of nit-picking that is hardly constructive.

Based on published results, there is still no information concerning the efficacy of Decorin for chronic spinal cord injury or the contusion model of spinal cord injury. Most of the data has been generated by one laboratory.

Well if that is the objection, it is very easy to address. If a particular researcher feels that the problem is that the experiments should be done with contusions and by additional labs, then that is exactly what they should do. But to criticize Dr. Davies for running the experiment in a slightly different manner than Dr. Young thinks best is just silly to my way of thinking. Remember, all of these articles have been published in peer-reviewed journals. None of the reviewers felt that using transsections was a flaw or they would have rejected the papers and they never would have been published.

Astrocytes in vivo are totally plastic. In fact, Dr. Jerry Silver started the immature astrocyte story many years ago. They have a published paper showing that the affect of immature astrocytes by themselves only allow axons to regenerate into the lesion and not beyond. Dr. Fischer from Drexel made an assessment that GRP never promoted regeneration. So, perhaps Stephen's labeling technique was inappropriate and he was most likely was labeling spared axons. I say this because the Fischer study examined the properties of astrocytes derived from a population of stem cells called GRP and tested their ability to promote regeneration in a model of spinal cord injury. It followed published studies from the Davies lab reporting that a specific population of of astrocytes (but not others) can promote robust regeneration through and beyond the injury. The results of the study showed significant differences from the Davies results. In particular, all populations of the astrocytes derived from GRP were permissive and promoted regeneration, but the regneration was limited with growth into the injury only. The modest effects of astrocyte transplantation suggested that the Davies strategy would need more development before planning any clinical trials. The testing would at least need done in a more appropriate model such as a contusion that Dr. Young implied because it would be more clinically relevant. It would probably also need to be combined with an additional treatment.

I don't feel comfortable commenting on this until I have read the paper, something I won't have time for in the foreseeable future. To me it seems that there are two likely possibilities:

a) Dr. Davies is a scam artist, inventing non-existent results.

b) The lab trying to replicate his work overlooked some detail that affected the outcome of their experiments.

I think these topics and links explain my previous comments about the importance of replication studies that should be completed by a contracted NIH lab.

Yes, of course. The question in my mind is why no other labs have tried to replicate Dr. Davies' work. As I implied in previous posts, as near as I can tell most of this is strictly for "political" reasons. A lab that has been pursuing a certain course for decades is unlikely to say, "Gee I guess we were wrong. We'll try a completely different approach that was not invented here." (The famous NIH - not National Institutes of Health - syndrome.)

Charlie, I apologize for the lack of specifc links. I'll sort through all of the exact ones I'm making reference to when I have time and send them to you. Much of the astrocyte work I follow takes place at Drexel. http://www.drexelmed.edu/home/abouto...akfischer.aspx

Thank you for the kind offer, but honestly I am far too busy to spend time reading these at the moment. I was in the hospital for seven months after a serious bout with food poisoning, and am completely behind on just about everything there is to be behind on.

Personally I think the Davies lab is doing very very basic research at this point and will need much more time to mature anything into a viable therapy to translate to the clinic. (But that is just my personal opinion).

Again, we are 180 degrees apart on this. I personally think that the Davies lab is doing the most advanced research with best results of any lab in the world. But everyone is entitled to their own opinion. I do agree that more work needs to be done to translate this into clinical trials. I can't see how this could NOT be the case, as otherwise Dr. Davies would already be running clinical trials. But my strong impression is that most of the hurdles here are political ones and not scientific ones.

Warm regards,
Charles Hansen

[GRAMMY]

Ok, all my best wishes to you Charlie, but the replication work done at the Drexel lab wasn't about politics though, nor a hurdle. It's a necessity and a serious one. Dr. Fischer is all about the science. Check out his credentials and publications on Neural Stem Cells, Bone Marrow Stromal Cells, Gene Therapy, Modified Fibroblasts and Matrices, Neuronal Cytoskeleton and Review Articles sometime when things aren't so hectic for you.
http://www.drexelmed.edu/home/aboutourfaculty/itzhakfischer.aspx

http://www.drexelmed.edu/Home/AboutTheCollege/DepartmentsCentersandInstitutes/BasicScienceDepts/NeurobiologyandAnatomy.aspx

The hemi transection model is not particularly good for accessing behavior since most chronic hemisected rats are walking almost normally. It's a tiny strategically placed nick in the cord that essentially do not paralyze the animal at all. Most people with paralysis don't walk near normally and have suffered contusion injuries. There is a big difference when presenting data to move a therapy into the clinic. That is why people have asked repeatedly "where is the contustion model?" Many posts in this thread have discussed the lack of appropriate model. Dr. Davies was also repeatedly asked at W2W2011 about it... (the reason he was asked at the 2011 symposium is because he posted this here and was presenting data yet again on rats walking near normal before treatment.)

"We are now appying what we have learned with transection injuries and working on contusion injuries with several collaborating labs".

Davies 11/07/07 Response to Poon: Answer: Yes. Given the robust and multiple benefits of GDA BMPs for acute SCI, we will be testing the effects of these cells in chronic SCI rats in the next few months. As mentioned by Schmeky we are also working hard to develop human GDA BMP cells and their GMP production. These human cells will also of course be tested both in acute and chronic SCI rats. Answer: We have set up a collaboration with the Miami Project (at their request) to test rat GDA BMP cells in rat contusioninjuries, at the Miami Project. Initial experiments will be conducted in acute contusion SCI rats to verify our acuteSCI results. The first experiments testing rat GDA BMPs and chronic SCI injured rats will be conducted in my lab here in Colorado with transection injuries. As my lab also has a rat SCI contusion device, we may also first test GDA BMP cells in chronic contusion SCI rats before collaborating with other labs on these chronic experiments. We have also set up GDA related collaborations with other top labs that have experience with measuring recovery of bladder, bowel and sexual function in contusion SCI in rats. We are now set to apply what we have already learned with transection injuries to both acute and chronic contusion injuries.


Charlie, it's 2012. I'm a hardass but not unreasonable. Researchers need to get in the batters box and start swinging for the team. If not they sit the bench and become part of the problem instead of part of the solution. Resources and funding needs to be focused on promising productive sci research labs. I'll never be able to quantify this scenerio as advanced research with the best results of any lab in the world. Not even close...

He has the capability and equipment to do a contusion...but we don't get that. BBB scores are not hard to acquire...but we don't get that either. Replication labs mentioned in this thread already consisted of Yale, UCSF, Miami Project, Drexel, University of Birmingham, University of Western Australia to name a few. That's why I just don't buy the political NIH syndrome excuse. It's about good quality research and production. It's not personal nor politics. It's about the latency not urgency.

[kz]

In one of my post while ago, i asked Dr. Jerry Silver about decorin and if it does the same thing as chondroitinase does for treatment of spinal cord injury , his reply was " the decorin story has not been independently replicated as far as i know but from the limited amount of data its effect are meagre compared to those of chase "(chondroitinase) .

[GRAMMY]

In one of my post while ago, i asked Dr. Jerry Silver about decorin and if it does the same thing as chondroitinase does for treatment of spinal cord injury , his reply was " the decorin story has not been independently replicated as far as i know but from the limited amount of data its effect are meagre compared to those of chase "(chondroitinase) .

@kz Here's the SFN Abstract – New Orleans, LA 2012 you might be interested in about "Super Chronics".
http://spinalcordinjuryresearchandad...-at-super.html

[kz]

Hi GRAMMY ,
Thanks for the link .

[Charles Hansen]

Ok, all my best wishes to you Charlie, but the replication work done at the Drexel lab wasn't about politics though, nor a hurdle. It's a necessity and a serious one. Dr. Fischer is all about the science. Check out his credentials and publications on Neural Stem Cells, Bone Marrow Stromal Cells, Gene Therapy, Modified Fibroblasts and Matrices, Neuronal Cytoskeleton and Review Articles sometime when things aren't so hectic for you.

Thank you very much for the links. Unfortunately given my situation at the time I don't anticipate reading them even by the end of the year. My time situation is extremely tight currently and I don't see it easing up at all this year, although I am sure that eventually I will read the links you have posted. I probably will need to stop posting for a while as that can chew up a lot of time also that I currently do not have. However I have greatly appreciated our dialog, and have also gained a lot from your posts, so thank you for taking the time to respond to my questions.

The hemi transection model is not particularly good for accessing behavior since most chronic hemisected rats are walking almost normally. It's a tiny strategically placed nick in the cord that essentially do not paralyze the animal at all. Most people with paralysis don't walk near normally and have suffered contusion injuries.

Most of what you say is clearly true. But it is hard enough to keep a human alive with BBS problems. Trying to keep rats alive for 10 months with enough damage to the spinal cord to create severe BBS problems is virtually impossible. To the best of my knowledge, no company makes foley catheters for rats, and I cannot even imagine trying to maintain a bowel routine on 36 paralyzed rates. (If I recall correctly he normally does three batches of six treated rats and the same number of "control" animals.)

(Remember that before the development of many plastics during WW II, the survival time for quads was measured in days, while the survival time for paras was measured in weeks.)

What Dr. Davies does is create the "tiny nick" in the cord so that the rat's hind legs are severely disabled. He then can quantify the degree of recovery with a process called a "grid walk". There is some sort of equipment that can tell exactly where the rat places each of the four paws as it walks. This is a very exacting test, as it doesn't simply indicate that the rat can move its hind paws again. Instead the rat must be able to place the hind paws in exactly the correct spot as it did before the injury. This is referred to as "volitional foot placement" and is roughly the equivalent of a paralyzed person being able to walk again without limping and walking with the same stride as before (length and width between the right and left feet).

There is a big difference when presenting data to move a therapy into the clinic. That is why people have asked repeatedly "where is the contustion model?" Many posts in this thread have discussed the lack of appropriate model. Dr. Davies was also repeatedly asked at W2W2011 about it... (the reason he was asked at the 2011 symposium is because he posted this here and was presenting data yet again on rats walking near normal before treatment.)

There are many advantages to Dr. Davies approach:

a) It becomes possible to keep the rat alive and active for the 10 months to both classify the injury as "chronic" and then measure its foot placement.

b) There is no subjectivity involved in determining how well the rat walks. The number of errors in foot placement is easily quantified both pre- and post-injury. This makes it much easier to determine the effectiveness of any given treatment.

At the same time there is also clearly a need to study contusion injuries and also more severe injuries than the ones inflicted by Dr. Davies. In the case of rats this will likely be limited to acute injuries, simply because it is difficult to keep a severely injured rat alive for the length of time required for the study of chronic inuries. This is one of the reasons that Dr. Davies research goes more slowly than we would like -- he is very methodical and very careful.

Davies 11/07/07 Response to Poon: We have set up a collaboration with the Miami Project (at their request) to test rat GDA BMP cells in rat contusion injuries, at the Miami Project. Initial experiments will be conducted in acute contusion SCI rats to verify our acute SCI results.

I remember asking Dr. Davies about the collaboration with the MP several years.ago. Unfortunately my memory is not as good as it used to be after a bout with viral meningitis. I simply don't remember his answer. However I also know that if had been something disappointing to me that caused me to lose faith in Dr. Davies' research and approach that I would have remembered it. It may have been that the Decorin manufacturer wouldn't donate the Decorin or something equally as frustrating, but certainly not something that had me question the effectiveness of Decorin or Dr. Davies.

I have found that in life, for all of us our greatest strength is usually also our greatest weakness. So the fact that Dr. Davies tends to be extremely thorough and methodical (a great asset) can also lead to his research taking much longer that either he had planned or that we would like (an unfortunate weakness).

Charlie, it's 2012. I'm a hardass but not unreasonable.

Grammy come visit me so that I can give your bottom a squeeze. I'll let you know if you are a hard-ass or not!

As for the rest, I really don't know who has done what in terms of replication. The few times i have spent time with Dr. Davies, I have never been less than satisfied with his answers to any of my questions. I'm sure that if we were to spend some time with him on these specific issues that we would both be more than happy with his answers.

However I really make every effort I can to limit my contact with him. I don't know if it is due to Dr. Davies, myself, or a the combination of the two, but we end up speaking for far longer than either of us planned. In his case he probably ends up being late for meetings and such. In my case my time is normally not so regimented, but I end up feeling guilty about taking so much time that he could be spending on research that would benefit all of us.

Keep the faith,
Charlie

[GRAMMY]

Catalent provided the Decorin for the Davies snf 2011 poster. http://www.catalent.com/index.php/ne...al-With-Euclid It is not expensive nor exclusive and is readily available as a research reagent. Last year Davies did show at SFN that using a "lateral" contusion model at C4-5, intrathecal decorin treatment administered 12 days after injury restored a measure of locomotor ability. But again Charlie, the lesion is being carefully crafted. He's not using a larger centrally placed lesion that is more human-like. They also only waited 12 days. Why didn't he wait longer so the animals are truly chronic? Considering the amount of donation money raised here for chronic studies, I would have hoped that luxury would have been granted to us. With the lack of chronic data and pace of the work it leads me to think there's probably minimum efficacy with Decorin at chronic stages. Remember 5 years ago he stated the chronic experiments were underway. He stated that here himself many times right from the beginning. But yet, the papers we view are all about acutes. No excuses, just the facts.

I've seen grid walk tests being run in addition to watching surgeries being performed on rats to paralyze them in the lab setting. Hundreds of animals are being heavily contused with Infinite Horizon impactors in many labs. They are then cared for and some for up to extremely long periods of time (1 year to 1.5 years super chronic stage) to work the necessary chronic spinal cord injury experiments. Granted it takes extra equipment and staff, but it's all a necessary piece of providing good solid research data for the chronic sci community. The injury Stephen uses is a quadrantic lesion that minimally effects locomotor behavior. Over ground walking is essentially normal, so that is why he reverts to a gridwalk test to just pick up small differences in footfalls. Because the lesion is so small, there's many spared fibers in the rubrospinal tract that can sprout to compensate for the lost connections. These animals are not "severely" paralyzed at all Charlie.

(Incidentally, cathaters are not used for chronic rats so don't worry about the plastics). Chronic paralyzed rats have their voids carefully measured for bowel and bladder outputs in metabolic cages so the data can be recorded to analyze their return of B&B function during treatments to be clinically relevant. It is not impossible or as difficult as you've been led to believe. It's all being done every day, all day long, month after month with hundreds of rats in the very best progressive sci labs.

The University of Western Australia with Giles Plant did replication experiments but failed to see any behavioral improvements in the animals. In fact, they spent nearly one million dollars over the course of 3 years in this study. Replication studies are an essential part of putting out good research and data. It's not about being disappointed if the experiments do not produce the desired results. It's about producing worthwhile data that can be utilized in future research forward to cure chronic paralysis. I don't give a scientist any free passes with excuses or worry about wasting their time. I worry about them wasting ours. Take care now Charlie.

[Schmeky]

Mr Hanson,

I respectfully request you show anything Davies claimed 6 years ago that has come to fruition.

He used this forum, mis-represented his intentions, took who knows how much in donations this forum generated, and turned his back on the constituents he purported to be helping.

Davies, at a minimun, should have provided some updates (as he indicated he would do) once or twice a year.

If you believe in his methodologies, then by all means, send all the spare change you have.

[Charles Hansen]

Catalent provided the Decorin for the Davies snf 2011 poster. http://www.catalent.com/index.php/ne...al-With-Euclid It is not expensive nor exclusive and is readily available as a research reagent.

The press release notes an agreement to work with with a commercial company on an "opthalmic clinical trial". Apparently what happens is the the patient wears a contact-lens-like device for a number of hours (possibly overnight) that has the proper shape to re-form the lens. The device is treated with Decorin, and this causes the lens to retain its new shape for 6 months or so. In this way, people that normally wear eyeglasses or contact lenses would instead only need treatments twice a year to have normal vision. It may even turn out that the effect is cumulative, and not necessary to continue treatments after a few years. That is nice for eyeglass wearers, but of course that doesn't help people with SCI's.

The press release did not mention Dr. Davies or SCI research. My understanding is that they were providing free Decorin for his work with rats, but they were going to charge in excess of $100,000 per patient for human studies. There may be other companies that also make it for less money, but not necessarily with the same purity and consistency of quality (GMP) as Catalent. Dr. Davies was deeply disappointed by this decision from Catalent, as it would require many millions of dollars just for the Decorin to run even a small human trial.

He had tested the Catelent product and found it to be over 95% pure, while some of the other companies had only achieved a purity of less than 40%.So unless something has changed radically in the last year or two, Decorin suitable for research on humans is *not* "inexpensive" nor "readily available".

Last year Davies did show at SFN that using a "lateral" contusion model at C4-5, intrathecal decorin treatment administered 12 days after injury restored a measure of locomotor ability. But again Charlie, the lesion is being carefully crafted. He's not using a larger centrally placed lesion that is more human-like. They also only waited 12 days. Why didn't he wait longer so the animals are truly chronic? Considering the amount of donation money raised here for chronic studies, I would have hoped that luxury would have been granted to us. With the lack of chronic data and pace of the work it leads me to think there's probably minimum efficacy with Decorin at chronic stages. Remember 5 years ago he stated the chronic experiments were underway. He stated that here himself many times right from the beginning. But yet, the papers we view are all about acutes. No excuses, just the facts.

Years ago the experiments *were* underway at Baylor, but these were interrupted by his move to the University of Colorado,

As far as the contusions, I don't have enough knowledge to comment one way or the other, so I won't even try. All I can say is that this is not the first time that experts in any given field, disagree on the best way to do things and that is not necessarily bad.

For example there was a general consensus in the scientific community for nearly 100 years that smell worked by the "lock and key" model, where specific receptors in one's nose were shaped to bond to specific shaped molecules, creating our sense of smell.

Spend $12 at Amazon for a book called "The Secret of Scent" by Luca Turin. In the last 20 years he has pretty much proven that our noses work in a completely different fashion altogether. Not only is it an interesting read, but the politics behind the science were fascinating. His first paper was published in an obscure journal. Eventually he had one published in "Nature", considered one of the top two most prestigious scientific journals in the world. But there was so much opposition from the "competing" researchers, that Nature took the unprecedented step of having the editor precede the article with an editorial saying that this research was only speculative and blah, blah, blah. Since then the editor has had to eat his words, as more and more evidence mounts to show that the new theory is the correct one.

I've seen grid walk tests being run in addition to watching surgeries being performed on rats to paralyze them in the lab setting. Hundreds of animals are being heavily contused with Infinite Horizon impactors in many labs. They are then cared for and some for up to extremely long periods of time (1 year to 1.5 years super chronic stage) to work the necessary chronic spinal cord injury experiments. Granted it takes extra equipment and staff, but it's all a necessary piece of providing good solid research data for the chronic sci community. The injury Stephen uses is a quadrantic lesion that minimally effects locomotor behavior. Over ground walking is essentially normal, so that is why he reverts to a gridwalk test to just pick up small differences in footfalls. Because the lesion is so small, there's many spared fibers in the rubrospinal tract that can sprout to compensate for the lost connections. These animals are not "severely" paralyzed at all Charlie.

Again, I am simply not qualified to judge which of the competing claims by various researchers is the truth. And if you get a chance to read "The Secret of Scent" you will quickly find that many of the researchers themselves are not qualified either! At the time that Turin did his research, probably 98% of all researchers working on the sense of smell believed the lock-and-key model was correct. But it was this vast majority that turned out to be wrong. Only time will tell.

(Incidentally, catheters are not used for chronic rats so don't worry about the plastics). Chronic paralyzed rats have their voids carefully measured for bowel and bladder outputs in metabolic cages so the data can be recorded to analyze their return of B&B function during treatments to be clinically relevant. It is not impossible or as difficult as you've been led to believe. It's all being done every day, all day long, month after month with hundreds of rats in the very best progressive sci labs.

First of all, please don't blame my errors on Dr. Davies. This has been a problem whenever I post. For whatever reason many forum participants seem to think that I am a spokesperson for Dr. Davies, or at the very least "parroting" what he says. This is absolutely not true.

For example in the case of paralyzed rats, catheters are completely unnecessary. I actually already knew this as one of my sons had two pet rats. They make absolutely wonderful pets except for two things:

a) They only live around two years. It is long enough to become extremely attached to them, but too short to seem like they had a long and happy life. Our entire family was heart broken when the first one died rather suddenly. The second one lived another six months but with increasing health problems (apparently breast cancers that are extremely common in rats). She was so ill for so long that it was something of a relief when her suffering ended.

b) They have no bladder. This means that as their kidneys produce urine that it immediately leaks out. When you take them out to play with them or hold them, you also need to have a towel handy to wipe up the (very small amounts) of urine that is constantly being excreted.

Dr. Davies has never even mentioned anything regarding the care of rats with chronic injuries to me. So any errors I have made here are purely my own (based on my own difficulties with establishing a workable bowel routine) and should not blamed on Dr. Davies in the slightest degree.

The University of Western Australia with Giles Plant did replication experiments but failed to see any behavioral improvements in the animals. Replication studies are an essential part of putting out good research and data. It's not about being disappointed if the experiments do not produce the desired results. It's about producing worthwhile data that can be utilized in future research forward to cure chronic paralysis. I don't give a scientist any free passes with excuses or worry about wasting their time. I worry about them wasting ours. Take care now Charlie.

Again, I don't have enough knowledge to make a definitive comment. You can view Dr. Davies' CV at:

http://www.ucdenver.edu/academics/co...20Feb%2008.pdf

This is apparently somewhat out of date, but at the time it was prepared he had only published two papers on the use of Decorin, with one more submitted for review, and a fial one in preparation. I don't know how the replication process works, but it seems unlikely to me that a lab could duplicate another lab's research just by reading a published paper. (Kind of like learning to fly an airplane just by reading books.) It seems to me that it would require the original researcher to work directly with the other lab in order properly validate the results.

Again, I have zero knowledge of how this process works. Perhaps Dr. Davies has already done this to no avail. Perhaps he was not in a position to do so. Or perhaps this is not considered to be the "proper" protocol. Without knowing a great deal more about the situation, I wouldn't even attempt to comment. Again, the only thing that I can report is that I have a much stronger-than-average background in biochemistry and biology. And every time that I asked Dr. Davies a pointed question regarding his work, he has always answered me in a satisfying manner. I have never felt that he was holding anything back, trying to avoid uncomfortable topics, or being deceitful in any way. Quite the opposite, in fact.

Am I disappointed that he hasn't published any of his work with chronic injuries? Of course. Am I disappointed that it has been well over a year since his last paper was published? Yes. Am I disappointed that human trials appear to be years (rather than months) away? Absolutely. Am I disappointed that he doesn't have a working cure yet? Every single day of my life.

And yet I personally feel that he is one of the best and brightest, and until and unless something better comes along that he is our best hope. Just my opinion. YMMV.

Best,
Charlie

[Charles Hansen]

I respectfully request you show anything Davies claimed 6 years ago that has come to fruition.

As a famous person once said, "It depends on your definition of fruition." If you mean that we can walk into a hospital and be cured of our SCI's, then clearly the answer is "no". If you mean that he has done important research to will lead to a cure, I believe the answer is "yes". YMMV.

He used this forum, mis-represented his intentions, took who knows how much in donations this forum generated, and turned his back on the constituents he purported to be helping.

I disagree completely. First of all, I don't believe for a moment that he ever "misrepresented his intentions". I think he saw this forum as opportunity for two things:

a) Communicate his findings to the SCI community.

b) Reach out to potential donors to help raise money to fund his hab.

In his case it didn't turn out as planned. For part (a), it seemed that he had many more critics and people that wanted to argue with him people than appreciated his reporting on his work. In the end, the trouble-to-worth ratio in making posts of any kind went completely off the charts. He made a conscious decision to stop using this forum and focusing instead on the research itself.

For part (b), most of the forum participants are unable to work and are unable to give much money. He told me one time the total amount of donations he had received from the CC forum was less than $10,000. (My memory is terrible and this may be off significantly. Once more, before someone makes a post saying that they alone donated $50,000, blame me and my poor memory and not Dr. Davies. Any errors on this point are purely mine.) Again, the trouble-to-worth ratio made it an untenable situation.

He was literally generating something between $2 and $5 per hour when he was actively posting. He had just moved, was setting up a new lab, had a newborn son, and was trying to do ground-breaking research all at the same time. Even if he were generating $1000 an hour in donations by posting on CC, he simply couldn't keep it up. There are other researchers posting on CC that make generate far, far more money than that, but Dr. Davies was certainly not one of them.

Davies, at a minimum, should have provided some updates (as he indicated he would do) once or twice a year.

On the one hand I agree completely, as it wouldn't really take up much of his time. On the the other hand I completely understand his decision to simply stop posting. Financial issues aside, it ended up being much more like the old Monty Python skit:

http://www.youtube.com/watch?v=kQFKtI6gn9Y

He simply didn't need the abuse he received here.

If you believe in his methodologies, then by all means, send all the spare change you have.

Thanks, Schmeky, I do. And I know that you do the same for the researchers you believe in. That's the only way we'll get out of our wheelchairs.

[6 Shooter]

a) Communicate his findings to the SCI community.

b) Reach out to potential donors to help raise money to fund his hab.

In his case it didn't turn out as planned. For part (a), it seemed that he had many more critics and people that wanted to argue with him people than appreciated his reporting on his work. In the end, the trouble-to-worth ratio in making posts of any kind went completely off the charts. He made a conscious decision to stop using this forum and focusing instead on the research itself.

He simply didn't need the abuse he received here.

This is so sad. The back-biters on this forum have been warned repeatly over the last 5 years of my CC reading and postings about attacking others. You know who you are and this is your accomplishment!!

[nrf]

This is so sad. The back-biters on this forum have been warned repeatly over the last 5 years of my CC reading and postings about attacking others. You know who you are and this is your accomplishment!!

If he's not posting his amazing progress here, then where? Are all publications full of back biting attackers? Is the NIH nothing more than a mob of antagonistic back biters? Save your sanctimony for religious figures.

[nrf]

As a famous person once said, "It depends on your definition of fruition." If you mean that we can walk into a hospital and be cured of our SCI's, then clearly the answer is "no". If you mean that he has done important research to will lead to a cure, I believe the answer is "yes". YMMV.



I disagree completely. First of all, I don't believe for a moment that he ever "misrepresented his intentions". I think he saw this forum as opportunity for two things:

a) Communicate his findings to the SCI community.

b) Reach out to potential donors to help raise money to fund his hab.

In his case it didn't turn out as planned. For part (a), it seemed that he had many more critics and people that wanted to argue with him people than appreciated his reporting on his work. In the end, the trouble-to-worth ratio in making posts of any kind went completely off the charts. He made a conscious decision to stop using this forum and focusing instead on the research itself.

For part (b), most of the forum participants are unable to work and are unable to give much money. He told me one time the total amount of donations he had received from the CC forum was less than $10,000. (My memory is terrible and this may be off significantly. Once more, before someone makes a post saying that they alone donated $50,000, blame me and my poor memory and not Dr. Davies. Any errors on this point are purely mine.) Again, the trouble-to-worth ratio made it an untenable situation.

He was literally generating something between $2 and $5 per hour when he was actively posting. He had just moved, was setting up a new lab, had a newborn son, and was trying to do ground-breaking research all at the same time. Even if he were generating $1000 an hour in donations by posting on CC, he simply couldn't keep it up. There are other researchers posting on CC that make generate far, far more money than that, but Dr. Davies was certainly not one of them.



On the one hand I agree completely, as it wouldn't really take up much of his time. On the the other hand I completely understand his decision to simply stop posting. Financial issues aside, it ended up being much more like the old Monty Python skit:

http://www.youtube.com/watch?v=kQFKtI6gn9Y

He simply didn't need the abuse he received here.



Thanks, Schmeky, I do. And I know that you do the same for the researchers you believe in. That's the only way we'll get out of our wheelchairs.

In your topic b) is "hab" short for "habit".

[eks]

In your topic b) is "hab" short for "habit".

You're such a clever girl.