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Wow. 98 bucks!
BC will always have positive developments under way. This has been the case for at least 7 years. The question has always been how much are you willing to accept (or swallow).
I am sorry to say comments have dried up on the Silicon Investor and Raging Bull sites and I am happy to see these posts here.
Your guess is as good as mine.
http://finance.yahoo.com/q?s=grno.pk&d=c&k=c4&t=5d&l=on&z=m&q=l
FYI, BigCharts has GRNO's trading as well.
http://bigcharts.marketwatch.com/intchart/frames/frames.asp?symb=grno&time=20&freq=2
You can see trading several years ago and by using the controls on the left side of the site you can zoom in on recent trading.
GRNO had put out a news release about using tallow from mad cow disease cattle to convert to diesel. Due to the absence of any other comment on GRNO threads, I am posting this article on some science loosely related to MCD.
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Source:
Cornell University
Date:
2003-01-31
Mouse Genetic Model For Spongiform Brain Diseases
ITHACA, N.Y. -- Some mice with a genetic mutation for mahogany-colored coats also develop spongiform degeneration of brain tissue, similar to mad cow disease. Because of this oddity, the mice could be valuable animal models for human disorders, such as Parkinson's and Alzheimer's diseases, according to geneticists at Cornell and Stanford universities.
The surprising discovery in a mouse strain known to geneticists since the 1960s is reported in the latest issue of the journal Science (Jan. 31, 2003) by Teresa M. Gunn, Gregory S. Barsh and their collaborators as "Spongiform Degeneration in mahoganoid Mutant Mice."
"Just don't call them mad mice," pleads Gunn, an assistant professor of genetics in Cornell's College of Veterinary Medicine who began the research in Barsh's laboratory at Stanford. "We do see the same kind of tissue degeneration -- with fluid-filled vacuoles, or holes, where the gray matter should be -- in BSE cattle with bovine spongiform encephalopathy and in these mutant mice. But the mice don't have the same motor coordination problems as mad cows, and the condition is not lethal."
Rather, the mutant mice exhibit little more than a slight tremor when they begin to move, they live a normal life span for their species and are able to reproduce, Gunn says. Nor did the investigators find evidence of misshapen prion proteins (the cause of spongiform encephalopathies such as mad cow and mad elk diseases) in the mice, although they did see damage to the myelin sheaths around nerve cells. Among other distinguishing characteristics of the mutant mice are curly whiskers and slightly curly body hair, as well as the habit of clasping their hind feet together when lifted off the ground. Normal mice tend to splay their legs straight out when they are elevated, Gunn explains.
Furthermore, this form of neurodegeneration is not known to be contagious, Gunn says, noting: "A cat that eats a mahoganoid mutant mouse -- should one escape from the laboratory -- would not get spongiform encephalopathy."
The researchers were looking for effects that might be linked to mutations in pigmentation genes. They knew that a loss of function in the so-called Mahogunin gene causes a partial reduction in the amount of yellow pigment, so that the mice were left with only small patches of yellow hair on mostly black bodies. But they were surprised to learn that a complete loss of function in that gene produced all-black mice with brain neurodegeneration. Linkages between unusual pigmentation and neural defects are not unheard of in the animal world, Gunn adds, citing predominantly white dogs, such as Dalmatians, that sometimes are deaf.
As an animal model, the mahoganoid mutant mice probably will not be useful to study spongiform encephalopathies like mad cow disease, Gunn believes, because rogue prions are not the cause of the mouse condition. But as an example of defective ubiquitination -- a protein-related process involved in many neurodegenerative disorders, including Parkinson's and Alzheimer's diseases -- the mahogany-colored mice with spongy brains could have real value, according to the Cornell scientist.
And the mutant mouse probably isn't patentable because it has a naturally occurring defect that the researchers did not create and because the mice already are commercially available. However, Gunn suggests, further work with the gene responsible for the neurodegenerative condition might result in patent applications.
Gunn credits Cornell undergraduate student Aaron F. Jolly for his research assistance in the study. Jolly is one of eight co-authors of the Science report. The study was supported, in part, by grants from the National Institutes of Health and the American Heart Association.
Editor's Note: The original news release can be found here.
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Note: This story has been adapted from a news release issued for journalists and other members of the public. If you wish to quote any part of this story, please credit Cornell University as the original source. You may also wish to include the following link in any citation:
http://www.sciencedaily.com/releases/2003/01/030131072420.htm
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It looks to me like there are many articles available on MCD if you start looking a little.
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Source:
Stanford University Medical Center
Date:
2003-02-03
Prion Disease May Be Caused By Buildup Of Cellular Trash, Say Stanford Researchers
STANFORD, Calif. - Mutant mice whose brains gradually become peppered with small holes resembling those found in prion disease lack a protein involved in disposing of cellular trash, say researchers at Stanford University Medical Center. The finding may shed light on how diseases such as Creutzfeldt-Jakob, bovine spongiform encephalopathy (also known as mad cow disease), and scrapie wreak havoc in humans and other mammals, and lends further support to the growing notion that glitches in protein turnover may be the unifying element in many neurodegenerative disorders.
Although the scientists caution that the mutant mice don't accumulate the misfolded protein, or prion, associated with the infectious forms of spongiform encephalopathy, the rodents' brains are dead-ringers for the brains of people and cows who have died from the disease. They speculate that the mutation in a ubiquitin ligase - a protein that flags other proteins for destruction by the cell's recycling machinery - may represent a downstream step in the cascade of events that leaves the brain looking somewhat like a kitchen sponge.
"No one really understands how or why spongy degeneration develops," said Gregory Barsh, MD, PhD, professor of pediatrics and of genetics in the Stanford School of Medicine, in whose laboratory the research was conducted. "Now we have a molecular handle with which to study it." The research is published in the Jan. 31 issue of Science.
Ubiquitin ligases are just a few members of a complex team of proteins that make up the ubiquitin pathway. Together they identify and physically tag abnormal, misfolded or simply worn-out proteins for dismantling in the cell's recycling center. Until recently they were about as glamorous as garbage collectors.
The study of neurodegenerative diseases such as Parkinson's, Huntington's and Lou Gehrig's upped the ubiquitin ante, however, with the discovery that patients' brain cells share a common trait: large clumps of proteins seemingly begging in vain for destruction. Prion diseases such as Creutzfeldt-Jakob, scrapie (a fatal disease affecting the central nervous system of sheep and goats), or bovine spongiform encephalopathy are also associated with accumulation of a specific protein. However, a direct role for the ubiquitin pathway has been identified only in an early onset form of Parkinson's disease - until now.
"This is the first convincing evidence that links spongiform disease to a ubiquitin-dependent protein turnover defect," said Lin He, the graduate student who performed the work together with Teresa Gunn, a former postdoctoral fellow in the Barsh lab. "We're really excited about it."
He and Gunn studied a mutation, mahoganoid, which changes the hair color of laboratory mice from brown to black. Previous research by He, Gunn and Barsh had shown that mice with a mutation in another coat color gene, Attractin, developed spongiform degeneration and body tremor. Because mahoganoid mutants share their darkened coat color with Attractin mutants, He and Gunn wondered if they would also develop holes in their brains. They did.
"In many ways, mahoganoid or Attractin mutant animals develop a prion-like disease without prions," said Barsh.
When He and Gunn cloned the gene responsible for the mayhem, they found that the mutants were unable to express a ubiquitin ligase they named Mahogunin. Mahogunin was also identified late last year by scientists at Columbia University School of Medicine. Further experiments by the Stanford researchers suggested that the Attractin gene either activates or permits the activity of Mahogunin in the pathway of destruction, and confirmed that Mahogunin can function as a ubiquitin ligase in vitro.
He, Gunn and Barsh speculate that the absence of Mahogunin leads to the buildup of a protein or proteins in the neurons, which causes damage and eventual neuronal death. The finding confirms many researchers' long-standing suspicions that the removal of unwanted proteins is vital to the health of neurons in the brain.
"The theme has been there, but now here's a striking example of how protein stability is critical in this disease as well," said Peter Jackson, PhD, Stanford associate professor of pathology who, together with a graduate student in his lab, Adam Eldridge, collaborated on the work. Now He and her colleagues face their next research hurdle in their attempt to connect the dots leading to neuronal degeneration and death: identifying the natural target for Mahogunin.
Additional collaborators include Stanley J. Watson, Jr., MD, PhD, professor of psychiatry, and Xinyun Lu, PhD, research investigator, both from the University of Michigan School of Medicine; and Aaron Jolly, a student at Cornell University.
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Stanford University Medical Center integrates research, medical education and patient care at its three institutions - Stanford University School of Medicine, Stanford Hospital & Clinics and Lucile Packard Children's Hospital at Stanford. For more information, please visit the Web site of the medical center's Office of Communication & Public Affairs at http://mednews.stanford.edu .
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Note: This story has been adapted from a news release issued for journalists and other members of the public. If you wish to quote any part of this story, please credit Stanford University Medical Center as the original source. You may also wish to include the following link in any citation:
http://www.sciencedaily.com/releases/2003/02/030203075813.htm
It looks like 5/29/02 was 200 shares at 15 cents.
I hadn't been looking at freerealtime. Thanks for that.
I had been looking at pinksheets and edreyfus. I see that pinksheets agrees with freerealtime but edreyfus says another 100,000 shares at 10 cents registered before the 100 shares at 1 cent showed.
Chas, your March 18th data should have been dated March 19. In fact, recent trading seems to indicate buying at 10 cents. I looked at your data to find out whether the March 18 100,000 trade was at 5 cents or 10. I expect it must have been 10 cents because subsequent days were at 10. Ask Research no longer shows GRNO trading.
Here is the recent trading volume. I didn't show price data because on days when there is more than one trade at different prices, it doesn't indicate which trade was at what price.
3/26/2002 100,000
3/25/2002 100,000
3/19/2002 1,100
3/18/2002 101,000
3/15/2002 100,000
I think all the above 100,000 share trades were buys for whatever that is worth.
Charles
The price trend indicates that fresh hype is needed. The old stuff has developed the distinct aroma of failure.
It looks to me like 50,200 is the number.
Sorry, I got a double post. Anyway, I like to see how the Brits express themselves. So sue me.
Sure, but look at "whynag" and his use of English. Isn't it worth something to enjoy what he does with the Mother Tongue? Add that to the sound of the accent and at least we can enjoy that.
Chas, I would have replied to your question on SI but it no longer allows me to post there, even though I have been posting there since 1996. They are working with me to try to solve my problem.
If the plant is in production, I wonder how much revenue it
brings in? Maybe the Partners could find out?
Although the partners are or were legally required to learn information about the operation of the partnership, I as an LP never did except through a third party. I could go into a long sad story which includes a law suit, but I recently converted out of being a LP. As I understand it, all or almost all the partners have converted and the partnership no longer exists. One hold out may be a partner who simply dropped out of contact and no one seems to be able to tell that person that we are trying to make the partnership go away. The partnership is as worthless as the stock and it might be of some slight help to the company if we simply gave up expecting anything from it.
I could dig out and post some wonderful sounding stuff about the plant's operation in 1997 such as how they ran it up to X gallons an hour to check out the operation of pumps, but we all know it was just typical BS so why bother.
Silicon Investor is now indicating I must register to be able to do what I have been doing since 1996. I asked them for an explanation, but I am not holding my breath any more than I am holding my breath any more about GRNO.
Your guess is as good as mine but if they can't operate a plant at 400 gph right there on their lot, how could they operate an entirely different plant thousands of miles away. Theoretically, all they would have to do is scale all the parts such as thermal oxidizer, pumps, tanks, and the like. But if their story doesn't work as demonstrated by the lack of an operating plant in Charleston, despite their claim that it is such a wonderful business opportunity, then they can make any kind of claim that they want and get the same response. In other works, the sky is the limit as far as what they claim they can do in processing ability and they don't have to explain anything. That is why they can never get financing to land an order.
Blue sky PR is as nice a way to put it as I could think of.
I occasionally ask myself why they do what they do. The official story is from the business plan where they go abroad to get plant orders so that they get the capital to be able to build their own domestic operations. They announce the orders publicly. But looking back to the time we invested in GRNO, when there were all those deals and all that "backlog", the technology had all those show stoppers that prevented the plant from being operated at a profit for the suckers, I mean investors. They were actively selling and promoting the company and its technology, even though they had problems they didn't have a clue how to solve. If they couldn't solve them in Charleston, how could they solve them in remote corners of the world?
Scroll ahead to today and what do we see. News releases extolling orders for plants. And yet these orders are once again for plants that nobody has a clue whether they have any idea whether they can produce them or not. The difference between today and 6 years ago is that there is no bank that can be convinced that GRNO is not a rat hole. There is no source of financing that they have been able to come up with, only lists of banks that they are trying to work. You and I can walk into any bank and fill out loan forms but that doesn't mean we will get the loans.
So I ask myself why they do what they do. After several years, they have proven that what they do always fails, at least for investors. So why should anybody even consider putting a dime into GRNO? Could it be that this hype they put out is good enough to produce the results they get and they are satisfied with the results? The results being people like us putting money into these schemes, of course. But think of the alternative, that is being required to actually trying to produce another plant that works. That would present quite a nightmare to them.
Hope does spring eternal and we sure would like to see 6 again, but a lot has happened since then. No orders ever happened despite the news releases, the plant never returned a penny to investors, GRNO is no longer a reporting company on the BB, and GRNO has lost its credibility. The last news release looked wonderful as they all do, but financing for the Turkish deal was supposed to have been completed by this time. The following is an example of the steady stream of news releases we used to see as a reason we got into this.
Green Oasis Environmental, Inc., Announces Financing of Brazilian Orders
Charleston, SC - April 29, 1996 - Green Oasis Environmental, Inc., (OTCBB: GRNO) today announced that financing had been secured for the purchase of four of its EnviroEconomics (TM) processing plants by Specialty Recovery Systems, Inc., of San Palo, Brazil. Specialty Recovery Systems confirmed to Green Oasis that the Brazilian Development Bank will finance the purchase of these units as well as make a direct investment in Specialty Recovery Systems, Inc. The four EnviroEconomics (TM) facilities are scheduled for delivery the next 24 months.
William D. Carraway, President, stated that "This not only is our single largest order to date, but is also an endorsement of the economics of our process and the very rapid return on investment that the EnviroEconomics (TM) process provides. The fact that the Brazilian Development Bank intends a direct investment of one million dollars of its own funds will facilitate the purchase of our equipment in the future by other non-domestic entities."
Happy New Year yourself, Chas.
So much for the belated Santa Claus rally.
5,000 shares at 50 cents! The belated Santa Claus rally. When I first saw that 5,000 shares at 50 cents, I thought that one of GRNO's tales finally came true and somebody is actually funding a GRNO project. Then I saw the rest of the trading and realized somebody was just giving a market maker a belated Christmas present.
As the great philosopher once said, "It's more fun when there's no point."
I certainly did. That is one bitter individual. I visited his sites after making the necessary spelling change. Hits on web sites never did impress me. The only thing that ever impressed me was what should be the bottom line. But he makes an excellent point about the concept of truth in business. I have often wondered how GRNO would have done in an atmosphere of truth.
I feel like Rain Man more each day and after 5 years, that is a lot of days.
I tried to reply here yesterday but it didn't respond. I think these boards are showing a lack of maintenance, maybe due to bad dot com times. I plan to remove whatever I have of value that is still on SI and keep it off line. You never know when it might still be valuable. I can't stand even going to RB any more. RB may think they have made it more attractive to advertisers but they sure drove me away.
In a way, I hated to dump cold water on all the happy chit chat on the GRNO SI site, but it reminded me too much of when I did the chatting years ago when I thought stuff pertained to GRNO.
Chas, I admire your persistance.