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If I hire a company to do an independent review, they can't publish that. I have to publish the work. That's how it works in science. I publish the millipore study... that I fund. If I don't like the findings, I suppose I could suppress it. That's what bad scientists do. But that's not what happened here. The Study was reported by Intellicell because it was helpful... just like happens throughout the pharmaceutical industry every DAMN day.
This post deserves a sticky!!! Read this. If it doesn't convince you that Intellicell is in the infancy of a really major technological and financial breakthrough, nothing will. Great post!!!
No one has this kind of crystal ball. I think we'd be lying to you if we told you it's going to be "X." If realistically I KNEW it was going be 10 cents in 1 year, I'd own half the company stock at the the current value. I can't predict it. It depends on too many factors. However, if they get their finances in order (and they are) they get a management team organized to move training and research forward (this is in rapid evolution), the IP comes through (I think that will happen any moment now), and revenues start to rise while debt drops, this stock will climb.
Now... I which they'd take on IR. But in the minds of the the expert jurists hired by SVFC, another decision may have been made. I just think the IR deserves to be really taken out behind the woodshed (figuratively).
ALL IMO.
I believe in this company. So I buy when I can. I bought 1/2 million today. I have enough background in science and medicine to know when something is stupid and looks like snake oil. This isn't.
I also think that Vic is slow...BUT he's hiring the right folks. He hired the right attorneys to represent our needs (and resources) and he's being transparent in the filings (which believe will come on time now).
Ego: Hell yes he's got one. Show me a leader of new company that takes on the crap he has to, world wide, including lectures, finances, etc. that doesn't need a healthy ego. I'm damned glad he's got a strong one. Otherwise, this would have folded like bad pasta a long time ago and everyone here knows that.
So, I think the PPS is not reflective of the value. It's reflective of the difficulty in building a biotech company in the current environment. But, those of us holding this stock are at the very ground level of what looks like a serious change in how stem cells could be collected. He'll need time, money and a team to market and teach the method. Trials to prove it. With those things done, after we've faced the vicissitudes of the market makers, I believe this stock will rise dramatically.
So, like other longs, I'm buying and accumulating. I'm also voting Y_Razz for the SVFC Board. Probably PhitheBuilder too!
PR is coming. Here's my bet in order: CFO, PATENT, new clinical data. Somewhere tucked in all this will be the new 10Q showing some new revenues and reduced debt.
This is a great post. Thank you. Do you have any idea of it's reader impact?
Are these new?
Jonathan Schwartz No Relationships Executive Vice President 55
Robert J. Sexauer No Relationships Executive Vice President of Clinical Development 60
As I read Oing's order, only SVFC has the right to file for punitives at this time.
Thank you for this reply. The float is still the same. I wish poeple would pay attention to this. The remainder of the shares is for a purpose... yet to be determined.
Y-Razz, you clearly understand stem cell stocks. Thank you!
If the pps goes up, revenues go up, investors get rich...I don't care if he becomes a billionaire.
No, that's wrong. It's not hype. Wait.
Anyone can post an opinion. I'm position mine after some DD. The silence is on purpose and the reason will be reported.
In the interim, I'm accumulating and holding.
Yes, I think it's been correctly stared that SVFC is quiet on purpose. There is a reason.
It will be reported.
Back to buying and accumulating.
There is a lot going on. If he is going to do this on his own, given it's scope, he's chosen to run quiet right now for a reason. Now we think we understand the reason.
Eventually, this will open up, but it's quiet and that ok for me. Very Long SVFC Accumulate and Hold.
Exactly. Some have new information that point to the stock doing exactly what we have been discussing. Time to load up!
Roller 150, I think you're right. I think we are right on the verge of making all of the red days' headaches a thing of the past.
Something very big is happening.
Ohhhh.... you gotta love this.
I'm betting on the people with the bigger wallets and LONGER vision!
This sounds like it has all the makings of a bear trap.
Will you describe the interaction w quotes please. This is very important to all of us. Thank you.
License =\= patent
I was thinking differently. I was looking forward to the inclusion of a CFO/CEO and European patents, revenue generation and PPS upwards of $1.00. In that scenario, does Dominion and YA profit. Futhermore, if the PPS really vaults because the others recognize the value of cavitational methods to extract stem cells and the PPS goes to 15$, does Dominion and YA benefit even more, despite the 10 bil shares we've already noted?
Pardon me, I meant significantly rising share values (PPS).
Is there a circumstance where YA, Dominion, shareholders and the doc would mutually benefit MORE from significantly rising valuse shares versus the scenario being played out in the previous post?
Comparison of human adult stem cells from adipose tissue and bone marrow in the treatment of experimental autoimmune encephalomyelitis
Julie A Semon1, Catherine Maness2, Xiujuan Zhang1, Steven A Sharkey3, Marc M Beuttler1, Forum S Shah4, Amitabh C Pandey1, Jeffrey M Gimble4, Shijia Zhang13, Brittni A Scruggs13, Amy L Strong1, Thomas A Strong1 and Bruce A Bunnell13*
* Corresponding author: Bruce A Bunnell bbunnell@tulane.edu
Author Affiliations
1 Center for Stem Cell Research and Regenerative Medicine, School of Medicine, Tulane University, 1430 Tulane Avenue, SL-99, New Orleans, LA 70112, USA
2 Department of Cell and Molecular Biology, School of Science and Engineering, Tulane University, 6400 Freret Street, New Orleans, LA 70118, USA
3 Department of Pharmacology, School of Medicine, Tulane University, 1430 Tulane Avenue, SL-83, New Orleans, LA 70112, USA
4 Stem Cell Biology Laboratory, Pennington Biomedical Research Center, Louisiana State University System, 6400 Perkins Road, Baton Rouge, LA 70808, USA
For all author emails, please log on.
Stem Cell Research & Therapy 2014, 5:2 doi:10.1186/scrt391
<SNIPPED>
Discussion
MSCs are a promising therapy for the treatment of CNS-related autoimmune diseases due to their immunomodulatory and neuroprotective effects. However, the source and availability of MSCs is becoming a crucial issue for their clinical application. BMSCs, the most studied MSCs, have demonstrated the ability to ameliorate both chronic and relapsing-remitting EAE [38-40]. Although BMSCs have demonstrated promising results, the invasive nature of bone marrow biopsies may limit their practicality for wider clinical applications. [color=red]Adipose tissue has become an appealing cell source for regenerative medicine and tissue engineering, since it contains a large number of ASCs, is easy to obtain in large volumes, and is easily accessible [41-44].[/color] ASCs have been shown to hold many of the same properties as BMSCs, such as the ability to differentiate, inhibit T-cell activation and proliferation, produce anti-inflammatory molecules, and aid in tissue repair through the secretion of cytokines [45].
Despite the promising potential of ASCs, the need for ex vivo cellular expansion still presents a significant challenge for human applications. The uncultured counterpart of ASCs, the SVF, is a particularly promising candidate for regenerative medicine because the cells can be isolated within hours of obtaining the lipoaspirate and no culture expansion of the cells is required, which would reduce any potential risks associated with growing cells in vitro and remove the need for specialized laboratories. In addition to the clinical risks of ex vivo expansion, the variables used in cell culture, such as percent and source of serum used, type of basal media, media supplements, culture surface substrate, cell seeding density, passage number, and confluency of culture, are undoubtedly giving way to contrasting and confusing results in research.
Adipose tissue comprises one of the largest organs in the body and serves as an important endocrine organ regulating many facets of homeostasis [26,46,47]. Comprised of mature adipocytes and other nonadipocyte cells, adipose tissue can be manually disrupted and/or treated with collagenase to isolate the SVF. Although not a fully defined cell population, the SVF includes vascular smooth muscle cells, fibroblasts, mast cells, macrophages, lymphocytes, endothelial cells, pre-adipocytes, and ASCs [48-52].
SVF cells have been used clinically to treat acute and chronic diseases afflicting a range of tissues and organs, including soft tissue defects, breast reconstruction, and autoimmune diseases such as graft-versus-host-disease, rheumatoid arthritis, and Crohn’s disease [27,30,41,46,53]. To date only one group has demonstrated improved function in MS patients treated with SVF; however, mechanisms behind the improvements were not explored [30]. Similarly, only one study showed that culture-expanded murine ASCs had a significant beneficial effect on chronic EAE by acting simultaneously in the lymphoid organs as well as the inflamed CNS and causing a dramatic change in antigen-specific T cells [33]. This present study is the first to investigate human ASCs and SVF cells in the treatment of EAE. Although SVF cells had similar mean maximum disease scores and time of disease onset to ASCs, the SVF had lower cumulative disease score. We previously compared the ability of murine SVF with ASCs in the same EAE model and showed that the SVF effectively inhibited disease severity and was statistically more effective than ASCs [54]. Unlike the human SVF, which had a disease incidence of 10 out of 12 mice (Table 1), the murine SVF only had 3 out of 12 mice demonstrate clinical signs [54]. EAE mice treated with human SVF had a disease onset of 9.3?±?1.6 (Table 1) while EAE mice treated with murine SVF had a disease onset of 15?±?4.5 days post disease induction (unpublished findings). The disparate results between human and mouse SVF may be due to species differences or some undefined mechanism(s). The current results show that uncultured SVF can ameliorate clinical symptoms as well as reduce spinal cord inflammation, demyelination, and axonal damage without the dangers associated with ex vivo cellular expansion.
Furthermore, SVF treatment had a similar effect on the systemic immune response in EAE mice. IFN? is a cytokine associated with a number of autoinflammatory and autoimmune diseases, due to its role in Th1 cell stimulation, differentiation, and function via STAT1 and STAT4 pathways [37]. These autoreactive T cells play a central role in the direct regulation of T-cell activation and survival during autoimmune inflammation in the pathogenesis of MS and EAE [37,55]. In this study, IFN? was reduced comparably between treatment groups. These results point to the ability of SVF cells to play an effector role similar to that of both ASCs and BMSCs, which would occur during the early inflammatory phase of disease, supporting the possibility that uncultured SVF cells could also affect the generation of encephalitogenic effector T cells. Although BMSCs have been shown to reduce levels of IFN? by direct contact, it is unclear whether ASCs and SVF cells utilize the same mechanism [56]. Although the mechanisms mediating such effects are still only partially understood, it is likely that they involve both direct cell-to-cell contact and paracrine signaling through soluble factors.
In addition to IFN?, IL-12 is responsible for Th1 cell stimulation, differentiation, and function and plays a central role in the pathology of MS [37]. In this study, IL-12 was reduced in the BMSC-treated group and further reduced in the SVF-treated group. Although this is the first study to show that SVF treatment reduced the levels of IL-12, BMSCs have been shown to reduce levels of IL-12 in a chronic EAE model [56,57]. Interestingly, murine BMSCs were shown to exert opposing effects on Th1 cells depending on the time of disease onset and the level of effector T-cell activation, suppressing all T cells when administered early during T-cell activation and able to decrease IFN? and increase IL-17 once T cells become activated [58]. These results indicate that IL-12 may play an important mechanistic role during the increased potency of SVF-based therapy. It is possible that the SVF cells, beyond their ex vivo expanded ASC counterpart, have the ability to further reduce the level of effector T-cell activation, keeping the disease in a more naïve state by reducing IL-12, and therefore Th1 stimulation and differentiation. Whether this is a result of the ASCs being uncultured and retaining more of their in vivo properties, is a result of the SVF being administered in a heterogeneous population, or is a product resulting from the interaction of ASCs with one of the other cell types present remains unclear.
Although BMSCs have been shown to reduce TNFa levels by direct contact in vitro, this study showed that intraperitoneal injection of neither BMSCs, ASCs, or SVF cells affected TNFa levels in an EAE model [48]. This may be due to the BMSCs being injected locally, murine BMSCs utilizing a different mechanism, or the studies being administered at a different time points during T-cell activation and differentiation. This also reiterates the speculation that the timing of stem cell interaction with T cells may drastically change immunomodulatory results and, therefore, disease progression.
These results point to the ability of all three cell types to play an effector role, which would occur during the early inflammatory phase of disease. Although the mechanisms mediating such effects are still only partially understood, it is likely that they involve both direct cell-to-cell contact and paracrine signaling through soluble factors. Further work needs to address whether the treatments utilized similar or unique mechanisms. This work also reiterates the speculation that the timing of cell therapy may drastically change immunomodulatory results and, therefore, disease progression. Further work needs to address cell therapy efficacy and cytokine response during the course of the disease, paying particular attention to cytokines that change quickly after cell treatment, such as T-helper type-17 cells. Although these data demonstrate that BMSCs, ASCs, and the SVF could affect the generation of encephalitogenic effector T cells, whether they can affect viability and function of the encephalitogenic effector T cells in established disease still needs to be determined.
I'm a bit confused... are convertible debentures always bad? Aren't they common in the early development of new companies. Can't they actually benefit a company? Are they always toxic? Can them sometimes work to the benefit of both the company and the shareholder? Are all of SVFC's debts "toxic??
SVFC- this is the time to accumulate and Buy!!! Hold your shares. Many of us are staring this down. Our time is coming.
Is there a way to know how many shares short sellers have sold/purchased of SVFC at the end of a given day?
BTW, should you have questions re: SVFC and the SEC, here's the info re: Clayton Parker. http://www.klgates.com/clayton-e-parker/#overview He takes all questions re: SVFC and forwards them to Intellicell for review.
Clayton Parker advised me this evening that his role with SVFC is"I am US SEC counsel." and not having anything to do with investor relations. FYI.
What was clay Parker's number?
I understand the sentiment. I'm really referring to filings that have been so thorough when, in fact, they didn't need to be so thorough. The addition of a professional athlete as a spokesperson who didn't need to lend his name if he thought it was a sham. Dr. Andrews involvement isn't a scam (and he wouldn't lend his name for whatever amount has been suggested) as it would destroy his legacy - no amount is worth that much. Instead, I'm chosing to attend the rather excellent manner in which Intellicell has defended itself against false claims (IR) and the skill applied in the depth of their filings. I'm not happy with the pace of their PR and would like to see this evolving more quickly, but I think that PR is coming and, frankly, believe the Patents are closer than you know. I'd say, that's the next big news. So, Rather than play Sierra and guess Roche, I'm guessing patents.
There is a reason why this keeps floating near it's double bottom. Everyone knows that PR is coming. It's not in YA's best interest for this to sink. Patience. The PR will come.
My personal opinion is that charts don't address reality well in in situations like these, other than to say we have held support.
No. It would have already been there if this were junk. It's not. So, no. I think if you ask others who have carefully looked at the fundamentals of the technology, they will mirror this.
Curious,
With all of the common characters missing.... why are we sitting at 19?????
Let's move this sucker!
I would suggest that the investing public, when considering investing or holding SVFC, remember the following tomorrow. It will be pertinent.
A BASHER HANDBOOK:
Do not underestimate a Bashers influence on a stock. The Pro's are good at what they
do and what they do is profit from your losses. Below is their "hand-book". Learn from it
or you will be donating your hard earned money to them!
Rules for Successful Bashing:
1. Be anonymous
2. Use 10% fact. 90% suggestion. The facts will lend credibility to your suggestions.
3. Let others help you learn about the stock. Build rapport and a support base before
initiating your Bashing routine.
4. Enter w/ humor and reply to all who reply to you.
5. Use multiple ISP's, handles and aliases.
6. Use two (2) or more aliases to simulate a discussion.
7. Do not start with an all out slam of the stock. Build softly.
8. Identify your foes (Longs) and the boards "guru" Use them to
your advantage. Lead them do not follow their lead.
9. Only Bash until the tide/momentum turns. Let doubt carry it the rest of the way.
10. Give the appearance of being open minded.
11. Be bold in your statements. People follow strength.
12. Write headlines in caps with catchy statements.
13. Pour it on as your position gains momentum. Not your personality.
14. Don't worry about being labeled a "Basher". Newbies won't know your history.
15. When identified put up a brief fight, then back off. Return in an hour unless your foe
is a weak in reasoning powers.
16. Your goal is to limit the momentum of the run. Not to tank the company or create
a plunge in the stock; be subtle and consistent.
17. Kill the dreams of profits, not the company or the stock.
18. Use questions to create critical thinking. Statements to reinforce facts.
19. DO NOT LIE, NAME CALL or USE PROFANITY.
20. Encourage people to call the company. 99% won't. They'll take your word for claims
made. If they do call you can always find something that is inaccurate in how they report
their findings.
21. Discourage people from believing Press Releases.Encourage them to call the company.
They won't out of laziness.
22. If the companies history/PR's are negative constantly point to that. Compile a list of
this data prior to beginning your efforts.
23. If the price rises blame it on the hype or the PR, temporary mass reaction, the market,
etc. Anything but the stock itself.
24. If other posters share your concerns, play on that and share theirs too.
25. Always cite low volume, even when it's not.
26. Three or four aliases can dominate a board and wear down the longs.
27. Bait the Longs into personal debates putting their focus/efforts on you and
not the stock or facts. Divert their attention from facts.
28. Promote other stocks that would-be investors can turn to
instead of the one your Bashing.
30. Do not fall for challenges on the "values" of what you are doing, it's a game and you
are playing it with your own rules.
I think that the investing public may be interested in the following article from 2014. I will cite the reference and quote the discussion below. In the discussion it references the efficiency of SVF in terms of obtaining stem cells versus marrow. Please remember that Intellicell is in the process of obtaining patents for what it holds out a MORE efficient manner of obtaining stem cells than is currently used, even in the report. It already has a US patent and is seeking a European patent. *If an article exists that specifically points to a static ceiling for *SVF extraction,*I haven't seen it. **
In any event, this new article is really worth reading and if you put the info into a google search, you'll find it online for free.
Caveat: when posting studies like this from an iPad , iHub often turns exponentials into three digit numbers (eg 10-5 becomes 105). Just be alert. :)
You'll need to know the following:
ASC = adipose stem cell
SVF= stromal vascular fraction
MSC = mesenchymal stem cell
BMSC = bone derived marrow stromal cells
EAE= experimental autoimmune encephalitis
CNS = central nervous system
Begin Article:
Comparison of human adult stem cells from adipose tissue and bone marrow in the treatment of experimental autoimmune encephalomyelitis
Julie A Semon1, Catherine Maness2, Xiujuan Zhang1, Steven A Sharkey3, Marc M Beuttler1, Forum S Shah4, Amitabh C Pandey1, Jeffrey M Gimble4, Shijia Zhang13, Brittni A Scruggs13, Amy L Strong1, Thomas A Strong1 and Bruce A Bunnell13*
* Corresponding author: Bruce A Bunnell bbunnell@tulane.edu
Author Affiliations
1 Center for Stem Cell Research and Regenerative Medicine, School of Medicine, Tulane University, 1430 Tulane Avenue, SL-99, New Orleans, LA 70112, USA
2 Department of Cell and Molecular Biology, School of Science and Engineering, Tulane University, 6400 Freret Street, New Orleans, LA 70118, USA
3 Department of Pharmacology, School of Medicine, Tulane University, 1430 Tulane Avenue, SL-83, New Orleans, LA 70112, USA
4 Stem Cell Biology Laboratory, Pennington Biomedical Research Center, Louisiana State University System, 6400 Perkins Road, Baton Rouge, LA 70808, USA
For all author emails, please log on.
Stem Cell Research & Therapy 2014, 5:2 doi:10.1186/scrt391
<SNIPPED>
Discussion
MSCs are a promising therapy for the treatment of CNS-related autoimmune diseases due to their immunomodulatory and neuroprotective effects. However, the source and availability of MSCs is becoming a crucial issue for their clinical application. BMSCs, the most studied MSCs, have demonstrated the ability to ameliorate both chronic and relapsing-remitting EAE [38-40]. Although BMSCs have demonstrated promising results, the invasive nature of bone marrow biopsies may limit their practicality for wider clinical applications. Adipose tissue has become an appealing cell source for regenerative medicine and tissue engineering, since it contains a large number of ASCs, is easy to obtain in large volumes, and is easily accessible [41-44]. ASCs have been shown to hold many of the same properties as BMSCs, such as the ability to differentiate, inhibit T-cell activation and proliferation, produce anti-inflammatory molecules, and aid in tissue repair through the secretion of cytokines [45].
Despite the promising potential of ASCs, the need for ex vivo cellular expansion still presents a significant challenge for human applications. The uncultured counterpart of ASCs, the SVF, is a particularly promising candidate for regenerative medicine because the cells can be isolated within hours of obtaining the lipoaspirate and no culture expansion of the cells is required, which would reduce any potential risks associated with growing cells in vitro and remove the need for specialized laboratories. In addition to the clinical risks of ex vivo expansion, the variables used in cell culture, such as percent and source of serum used, type of basal media, media supplements, culture surface substrate, cell seeding density, passage number, and confluency of culture, are undoubtedly giving way to contrasting and confusing results in research.
Adipose tissue comprises one of the largest organs in the body and serves as an important endocrine organ regulating many facets of homeostasis [26,46,47]. Comprised of mature adipocytes and other nonadipocyte cells, adipose tissue can be manually disrupted and/or treated with collagenase to isolate the SVF. Although not a fully defined cell population, the SVF includes vascular smooth muscle cells, fibroblasts, mast cells, macrophages, lymphocytes, endothelial cells, pre-adipocytes, and ASCs [48-52].
SVF cells have been used clinically to treat acute and chronic diseases afflicting a range of tissues and organs, including soft tissue defects, breast reconstruction, and autoimmune diseases such as graft-versus-host-disease, rheumatoid arthritis, and Crohn’s disease [27,30,41,46,53]. To date only one group has demonstrated improved function in MS patients treated with SVF; however, mechanisms behind the improvements were not explored [30]. Similarly, only one study showed that culture-expanded murine ASCs had a significant beneficial effect on chronic EAE by acting simultaneously in the lymphoid organs as well as the inflamed CNS and causing a dramatic change in antigen-specific T cells [33]. This present study is the first to investigate human ASCs and SVF cells in the treatment of EAE. Although SVF cells had similar mean maximum disease scores and time of disease onset to ASCs, the SVF had lower cumulative disease score. We previously compared the ability of murine SVF with ASCs in the same EAE model and showed that the SVF effectively inhibited disease severity and was statistically more effective than ASCs [54]. Unlike the human SVF, which had a disease incidence of 10 out of 12 mice (Table 1), the murine SVF only had 3 out of 12 mice demonstrate clinical signs [54]. EAE mice treated with human SVF had a disease onset of 9.3?±?1.6 (Table 1) while EAE mice treated with murine SVF had a disease onset of 15?±?4.5 days post disease induction (unpublished findings). The disparate results between human and mouse SVF may be due to species differences or some undefined mechanism(s). The current results show that uncultured SVF can ameliorate clinical symptoms as well as reduce spinal cord inflammation, demyelination, and axonal damage without the dangers associated with ex vivo cellular expansion.
Furthermore, SVF treatment had a similar effect on the systemic immune response in EAE mice. IFN? is a cytokine associated with a number of autoinflammatory and autoimmune diseases, due to its role in Th1 cell stimulation, differentiation, and function via STAT1 and STAT4 pathways [37]. These autoreactive T cells play a central role in the direct regulation of T-cell activation and survival during autoimmune inflammation in the pathogenesis of MS and EAE [37,55]. In this study, IFN? was reduced comparably between treatment groups. These results point to the ability of SVF cells to play an effector role similar to that of both ASCs and BMSCs, which would occur during the early inflammatory phase of disease, supporting the possibility that uncultured SVF cells could also affect the generation of encephalitogenic effector T cells. Although BMSCs have been shown to reduce levels of IFN? by direct contact, it is unclear whether ASCs and SVF cells utilize the same mechanism [56]. Although the mechanisms mediating such effects are still only partially understood, it is likely that they involve both direct cell-to-cell contact and paracrine signaling through soluble factors.
In addition to IFN?, IL-12 is responsible for Th1 cell stimulation, differentiation, and function and plays a central role in the pathology of MS [37]. In this study, IL-12 was reduced in the BMSC-treated group and further reduced in the SVF-treated group. Although this is the first study to show that SVF treatment reduced the levels of IL-12, BMSCs have been shown to reduce levels of IL-12 in a chronic EAE model [56,57]. Interestingly, murine BMSCs were shown to exert opposing effects on Th1 cells depending on the time of disease onset and the level of effector T-cell activation, suppressing all T cells when administered early during T-cell activation and able to decrease IFN? and increase IL-17 once T cells become activated [58]. These results indicate that IL-12 may play an important mechanistic role during the increased potency of SVF-based therapy. It is possible that the SVF cells, beyond their ex vivo expanded ASC counterpart, have the ability to further reduce the level of effector T-cell activation, keeping the disease in a more naïve state by reducing IL-12, and therefore Th1 stimulation and differentiation. Whether this is a result of the ASCs being uncultured and retaining more of their in vivo properties, is a result of the SVF being administered in a heterogeneous population, or is a product resulting from the interaction of ASCs with one of the other cell types present remains unclear.
Although BMSCs have been shown to reduce TNFa levels by direct contact in vitro, this study showed that intraperitoneal injection of neither BMSCs, ASCs, or SVF cells affected TNFa levels in an EAE model [48]. This may be due to the BMSCs being injected locally, murine BMSCs utilizing a different mechanism, or the studies being administered at a different time points during T-cell activation and differentiation. This also reiterates the speculation that the timing of stem cell interaction with T cells may drastically change immunomodulatory results and, therefore, disease progression.
These results point to the ability of all three cell types to play an effector role, which would occur during the early inflammatory phase of disease. Although the mechanisms mediating such effects are still only partially understood, it is likely that they involve both direct cell-to-cell contact and paracrine signaling through soluble factors. Further work needs to address whether the treatments utilized similar or unique mechanisms. This work also reiterates the speculation that the timing of cell therapy may drastically change immunomodulatory results and, therefore, disease progression. Further work needs to address cell therapy efficacy and cytokine response during the course of the disease, paying particular attention to cytokines that change quickly after cell treatment, such as T-helper type-17 cells. Although these data demonstrate that BMSCs, ASCs, and the SVF could affect the generation of encephalitogenic effector T cells, whether they can affect viability and function of the encephalitogenic effector T cells in established disease still needs to be determined.
I think the investing community may appreciate citations they can read, versus believing anyone holding themselves out to be an expert without support. See the last 2 paragraphs below for my conclusion.
The following comes from: Stem Cells International
Volume 2012 (2012), Article ID 812693,
Title:
Adipose-Derived Mesenchymal Stromal/Stem Cells: Tissue Localization, Characterization, and Heterogeneity
Authors, etc:
Patrick C. Baer and Helmut Geiger
Division of Nephrology, Department of Internal Medicine III, Johann Wolfgang Goethe University, 60590 Frankfurt, Germany
Received 10 January 2012; Accepted 12 February 2012
Academic Editor: Selim Kuçi
Copyright © 2012 Patrick C. Baer and Helmut Geiger. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
<SNIPPED>
"Adipose tissue contains a large number of multipotent cells, which is an essential prerequisite for stem-cell-based therapies. It has been described that stem and progenitor cells in the uncultured stroma-vascular fraction (SVF) from adipose tissue usually amount to up to 3% of the whole cells, and this is 2,500-fold more than the frequency of stem cells in bone marrow [21]. Others have also described that adipose tissue provides large numbers of stem cells compared to bone marrow. A bone marrow transplant contains approximately 6 × 106 nucleated cells per mL [22], of which only 0.001–0.01% are stem cells [23]. In comparison, the number of SVF cells that can be isolated from subcutaneous liposuction aspirates is approximately 0.5–2.0 × 106 cells per gram of adipose tissue [22, 24–27], whereby the percentages of stem cells range from 1 to 10% [26, 28, 29], most likely depending on the donor and tissue harvesting site. Therefore, approximately 0.5 × 104 to 2 × 105 stem cells can be isolated per gram of adipose tissue, varying among patients."
Please note that the authors state a range of stem cells available (0.5x x104 to 2 x 105) and more importantly, say.... APPROXIMATELY....VARYING among patients.
Anyway, I think that SVFC is saying that there method is more efficient at obtaining more cells. If that's true, it's a big deal and it's fair for the investing public to know this.
(I'm limited to one post per day, so unfortunately can't debate this in the way scholars should. )
Hmmmm....in response to an earlier comment:
I think the investment community benefits from independent validation of any of a company's statements.
The method used here should be analyzed via appropriate clinical and scientific method and when I met with Dr. Victor he discussed that. However, the method of use here makes biological sense since you are giving the pt his or own cells back and the long term negative sequelae for this should be nil. For the reason, the path for current use is broad.
The investment community will benefit if we bang this out in the literature, much the way we have done with vaccinations. I think it's noble to fight for a cause. In this case there are there are three: protect the public, provide the public with best available treatment, meet the obligations to the shareholders. Protection of the public should, of course, be paramount, but the methods for this can get very gray.
SVFC is going to make some mistakes along the way. It's CEO is not well trained as a businessman and should release the reins to someone who is or sell. My opinion. Otherwise he will hurt our investments, his and the distribution of this technology. However, I think that the technology as described is sound and worth support. That's why I'm here and investing (and I'm also a member of the medical/scientific community).
All this is obviously my opinion only,
What would the investment community consider sufficient validation?
Litigation sucks up resources. The technology remains, though. Glad I have so many shares now.
Deep breath. There have been a number of very thoughtful, non-hysterical posts that explain what's going on. Trebeg and others have taken the time to explain the landscape, there are post-litigation adaptations that are taking place and the European patents are on the horizon. Venture Cap's explanation of the hypothetical is pretty reasonable (and I'd agree with the ego comment), but the former information above is already known (SVFC is adjusting to post IR and moving forward with business plans as evidenced by SEC filings).
So, the shorts are having their day because some additional shaking is going on. If people will take a deep breath, stop, and remember why they bought into this technology at sub-penny value, hang onto their shares, the landslide will stop.
The sky is not falling.