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A buy.
"BioServe's collaboration with DNA Print is one in a number of research efforts the company is undertaking with drug, biotechnology, and diagnostic companies. BioServe said that in the second half of 2007 it signed 211 agreements with several biotechnology and pharmaceutical companies, including Novartis, Sanofi-Aventis, and Genentech, as well as research organizations, including the Broad Institute, the National Cancer Institute, Baylor University, and Health Canada.
According to the BioServe spokesperson, the company currently works with 28 of the 30 large pharma companies with more than $3 billion in revenue or with R&D expenditure of $500 million or more. Its collaborations with pharmas have been bolstered by its acquisition of Genomics Collaborative in May 2007. Since the acquisition, BioServe has acquired 76 new customers, the company reported. "
It sounds like Bioserve is quite agressive in it's efforts to collaborate with both Pharmas and small discovery companies, and that DNAPrint's work with Bioserve hasn't stalled.
So for all of you yelling scam, well, we shall see.
Guess you should e-mail Bioserve and tell them their research with DNAPrint is a farce. Save them some time, lol.
fyi
Detailed Summary
Ovarian Cancer Biomarker Research Act of 2007 - Amends the Public Health Service Act to require the Director of the National Cancer Institute to enter into cooperative agreements with, or make grants to, public or nonprofit entities to establish and operate centers to conduct research on biomarkers for use in risk stratification for, and the early detection and screening of, ovarian cancer. Designates each center as an Ovarian Cancer Biomarker Center of Excellence.
Allows federal payments under such an agreement or grant to be used for research on: (1) the development and characterization of new biomarkers and the refinement of existing biomarkers; (2) the clinical and laboratory validation of such biomarkers; (3) the development and implementation of clinical and epidemiological research on the utilization of such biomarkers; and (4) the development and implementation of repositories for new tissue, urine, serum, and other biological specimens.
Requires the Director to: (1) make available for research banked serum and tissue specimens from clinical research regarding ovarian cancer that was funded by the Department of Health and Human Services (HHS); (2) establish an Ovarian Cancer Biomarker Clinical Trial Committee to assist the Director to design and implement national clinical trials to determine the utility of such biomarkers; and (3) establish a national data center to conduct statistical analyses of trial data.
The cooling trend is from the Greenland ice cap melting into the N. Atlantic and changing the temp flow of the Gulf stream. The Gulf stream carries warm water(about 10 degrees warmer than the Pacific)north from below the equator to Greenland, and is one of the major temperature regulators and weather makers on the planet.
This trend will last awhile, or until Greenland is melted out, but the fact is global warming is here to stay, despite human's witnessing of tiny increments of time and intercessional and temporary drops of temperature. It all just means more nasty weather. Don't have grandchildren. They will witness the nasty when it gets here.
Denying that the ice sheets and glaciers are melting is typical head-in-the-sand, I live 100 years or less poppycock. Think of how many countries,(mostly poor) rely on mountain snow melt, rivers, and ground water? The fighting will be for survival, not just oil.
Good luck all.
AMEN!!!
Old Vern...
Thanks a bunch.eom.
Looks like there's a few who didn't hear the Naysayer's lies about late proxies, insider selling, and Dutchess shorts. Oh, well, guess they'll have to learn the hard way,lol.
BTW, condolences, Johnny. I hope your decision to keep a few works out.
I think all the people who were disgusted by the turn of events are now washed out of the 10 day event window and now the true speculation on the "huge" merger is culminating. Just my very honest opinion, of course.
Fingers crossed, everybody!
I am still not totally convinced about the validity of Nanobacteria science, but it is looking like the proof is very close, and acceptance is more the issue. And if it is valid, it makes this move by both companies much better for DNAPrint than the goal of financing of 50 million.
The key to this deal is obviously Gomez, and he is obviously convinced. And will Frudakis stay with the company. I think they are into this, and not by desperation. We shall see. JMHO.
More info and video from Nano Technology:
http://www.tntg.org/
(Go to the above link and scroll down to the UTube video,"detailed roadmap to the 21st century", a must see )
http;//NanoNEWS.tv
http;/thenanotechnologygroup.org
Nanobacteria has been shown by multiple scientific researchers to be the cause of the pathological (disease-causing) calcification found in Atherosclerotic Plaque, Coronary Artery Plaque, Heart Disease, Kidney Stones, Polycystic Kidney Disease (PKD), Cataracts, Scleroderma, Psoriasis, Eczema, Lichen planus, Liver Cysts, Breast Calcification, Prostate Calcification, Dental Plaque and Periodontal Disease, Rheumatoid Arthritis, Osteoarthritis, Fibromyalgia, Spurs and have been implicated to be involved in certain cancers, blood disorders, and myelodegenerative disorders such as Multiple Sclerosis, Lou Gehrig's and Alzheimer’s Disease. This is indeed a large list of diseases, but all are involved with pathological calcification. Multiple Scientific Researchers believe that Nanobacteria are the cause of all pathological calcification in humans and mammals. Prior to the basic science discoveries made by many nanobacterial researchers, there was no valid medical or scientific explanation as to why calcification is involved in all of the above disease processes. Calcification by Nanobacterium sanguineum is the only valid explanation. When this is explained to most physicians, their general response has been “Wow, it all makes sense now!”. Nanobacteria it's pathological calcification are implicated to be either the cause or instrumental in most all degenerative disease processes.
Wish as we may, there are no known natural substances that can kill these Nanobacteria. Additionally, Nanobacterium sanguineum cannot be killed by Penicillin, Cephalosporins, Macrolides, most other antibiotics, Heat under 196F (90C) degrees, Freezing, Dehydration, Gamma Irradiation under 150 MegaRads, other Bacteria or Viruses, Alcohol, Peroxides, Garlic, Colloidal silver, IP6, MGN3, Lactoferrin, Frequency generators, Immune boosters, Colostrum, Transfer Factors, Immunoglobulins or herbals. These nanobacteria are extremeophiles and are probably the most highly resistant of all bacteria to destruction. In order to treat a nanobacterial infection, you first have to remove their protective calcium shells, and then kill them with an agent specifically effective as an anti-nanobacterial, specifically our NanobacTX.
[Karl Note: You cannot kill something which is not alive! You can, however, remove it from wherever it might be!]
In one of our Pilot Studies between NanobacLabs and Drs. Ciftcioglu & Kajander (University of Kuopio, Finland) and Nanobac Oy, Finland using the nanobacTEST Nanobacterial Antigen and Nanobacterial Antibody Test, our scientifically-designed prescription NanobacTX was shown to eradicate calcified Nanobacterium sanguineum and its calcification in patients.
NanobacTX by NanobacLabs is the only treatment scientifically shown in clinical studies to be effective in eradicating Nanobacterium sanguineum. All other modalities have failed. NanobacTX is available only by physician prescription. The nanobacTEST for Nanobacterium sanguineum Antigen and Antibodies is now available. You may call NanobacLabs TollFree at 1-877-676-2241 to find out how to get tested for nanobacterial infection.
Interview with Dr Gary Mezo (Nanobaclabs):
http://www.nanotech.biz/i.php?id=2002_01_25
Your welcome, PL1. I hope it isn't too drab. I am very curious as to the connection between these two companies and if there is really going to be a dynamic confluence of technology that drives it forward. I want to know if something "is there" to be blunt. I will look further into NBP's Dr. Gary Mezo and his "first nanobiotic" on the market,(NanobacTX). But looks like the people they have worked with(Mayo, Scripps, etc) are right on top of the cutting edge nanotechnology in calcification, so that's a good sign.
Here's an artcle you might find interesting:
Nanobiotic Lifesavers
Synthetic peptide rings can self-assemble into antibiotic nanotubes that puncture deadly bacteria.
By Jack Mason
Nanotubes that construct themselves out of peptide rings may offer an effective new weapon against antibiotic-resistant bacteria and the threat of incurable diseases.
Resembling a molecular donut, a 2.5-nanometer ring of customized amino acids sinks into the cell wall of a staphylococcus aureus bacterium, one of the antibiotic-resistant strains responsible for life-threatening hospital infections.
Millions more of these sticky, donut-shaped "cyclic peptides"-each a looped chain of amino acids-enter the bacterium's gelatinous cell wall. They chemically gravitate toward each other and assemble themselves into elongated tubes, like stacks of tiny tires embedded in the cell membrane.
Single peptide tubes then pierce the membrane. Groups of adjacent tubes work together to open even larger, gaping pores in the cell wall. Within minutes, numerous holes kill the bacterium by disrupting the electrical potential of its membrane, effectively shutting down the cell's interior machinery.
Lethal Injectors
Developed by a team led by M. Reza Ghadiri at the La Jolla-CA based Scripps Research Institute, these nanobiotic lifesavers may be able to kill even the most drug-resistant bacteria, while sparing animal cells.
The World Health Organization estimates the total cost of treating all hospital-borne antibiotic-resistant bacterial infections is around $10 billion a year.
While human trials are two to three years away, the group has tested their synthetic, self-assembling peptide nanotubes in mice, knocking out deadly infections of methicillin-resistant staphylococcus aureus. The peptides also show promise in treating a wide variety of deadly bacteria strains, including Escherichia coli, pseudomonas aeruginosa and Enterococcus faecalis. They may eventually prove effective against fungal and parasitic infections.
Ghadiri's peptide rings, composed of a novel alternating pattern of naturally occurring and synthetic amino acids, have amino acid side chains that face outward from the "donut" and react to the environment.
These "sensor" molecules can be quickly reconfigured in the lab to adjust how the peptides work. "We can produce 100,000 variants in about two weeks," Ghadiri says. That flexibility should ultimately let drug makers choose which bacteria they target, control how the peptides insert themselves into the membrane and self-assemble, and minimize the toxicity to animal cells in the infected host.
Dr. Tomas Ganz, an experimental pathologist at UCLA medical school, says the work of Ghadiri's group represents a potential new class of molecular smart weapons. However, he cautions that these substances are not yet medications. "They must be economical to produce and prove effective and nontoxic in humans," he says.
Longer Shelf Life
The speed with which they work and the peptides' novel structure should make it harder for bacteria to develop resistance, Ghadiri says, paving the way for a new class of drugs with a longer shelf life. But, he warns, "no one should ever underestimate the adaptability of bacteria."
Cyclic peptides have been investigated for years. Many natural peptides defend against microbes in animals and plants. Other drugs based on cyclic peptides, such as Bacitracin, are commonly used as topical antibiotics.
Scripps researchers first stacked cyclic peptides into nanotubes in 1992. At first, they hoped to create nanoscale "test tubes" for biochemical research. But when they noticed the tubes' membrane activity in 1994, they quickly refocused their discovery on the treatment of multidrug-resistant bacteria.
As a result, Ghadiri feels fortunate "that in a relatively short period of time our work may be leading to something useful for millions of people."
[1]
So here ya go.....
Fast forward to 2006. If you google "calcification DNA" you will see tons of scientific work in the area. This is an example from Mayo,(one of Nanobac's collaborators)
Mayo Clinic Study Explores Link between Nanoparticles and Kidney Stones
Tuesday, December 19, 2006
ROCHESTER, Minn. — Researchers at Mayo Clinic have successfully isolated nanoparticles from human kidney stones in cell cultures and have isolated proteins, RNA and DNA that appear to be associated with nanoparticles. The findings, which appear in the December issue of the Journal of Investigative Medicine, are significant because it is one step closer in solving the mystery of whether nanoparticles are viable living forms that can lead to disease — in this case, kidney stones.
Kidney stones are associated with pathologic calcification, the process in which organs and blood vessels become clogged with calcium deposits that can damage major organs like the heart and kidneys. What causes calcium deposits to build up is not entirely known. Medical scientists at Mayo Clinic are studying calcification at the molecular level in an effort to determine how this phenomenon occurs.
There is a growing body of scientific evidence that links calcification to the presence of nanosized particles, particles so small that some scientists question whether a nanoparticle can live and if so, play a viable role in the development of kidney stones.
The presence of proteins, RNA and DNA does not prove that nanoparticles are viable living forms because a genetic signature has not been identified, says the study's author John Lieske, M.D., a nephrologist with Mayo Clinic. A genetic signature would prove that nanoparticles are indeed living forms that replicate and can cause disease.
"We are looking at how kidney stones start as very small calcifications inside the kidney and then eventually grow into stones," says Dr. Lieske. "In the laboratory, we have isolated nanoparticles from kidney tissue and kidney stones, and have successfully propagated them in culture. This does not clearly confirm the role of nanoparticles in the formation of kidney stones, but it offers insight not otherwise known."
Approximately 12 percent of men and 5 percent of women will develop kidney stones by the time they reach 70 years old. Some $5 billion is spent in the United States each year to treat patients with kidney stones, but exactly how kidney stones form is not known. Scientists theorize that if nanoparticles become localized in the kidney, they can become the focus of subsequent growth into larger stones over months to years. Other factors, such as physical chemistry and protein inhibitors of crystal growth, also play a role. But what scientists don't quite understand is why, where and how they start growing, Dr. Lieske says.
The study cites evidence that indicates the unlikelihood that events linked to the calcification process are driven solely by physical chemistry, but instead are influenced by specific proteins and cellular responses. Understanding these events will provide clues to develop new therapy to treat kidney stones, the authors say.
"There are at least two novel hypotheses here in terms of how stones might actually form. One: an infectious agent. If that was the case, that would point us in the direction of using different kinds of treatments specific to an infectious agent. Two: the idea that cells drive calcification. That would suggest other alternative therapies," according to Virginia Miller, Ph.D., a specialist in vascular research at Mayo Clinic and a study author.
In addition, researchers examined how urine proteins alter the way crystals and cells interact in binding to cells — the way in which cells respond to the crystals and assume more of a bone-like morphology and drive calcification over time.
Here is a sample of a WIPO patent from 2000 by a company called Osteometer:
GENETIC PREDISPOSITION TO ABNORMAL CALCIFICATION CONDITIONS
GENETIC PREDISPOSITION This invention relates to a method for assessing predisposition to various conditions based upon polymorphisms in a bone sialoprotein gene, a matrix gla protein gene, an osteopontin gene and/or an osteoprotegerin (OPG)/osteoclastogenesis inhibitory factor (OCIF) gene.
More specifically, the invention relates to a method of assessing. an individual's predisposition to various pathological calcification conditions including osteo- porosis and atherosclerosis by screening for these polymorphisms. The method of the present invention is especially useful in determining allelic variations in the human bone sialoprotein gene, the human matrix gla protein gene, the human osteopontin gene and/or the osteoprotegerin (OPG)/osteoclastogenesis inhibitory factor (OCIF) gene thus predicting predisposition to high or low bone mineral density (BMD). The invention also relates to bone sialoprotein (BSP) genes, matrix gla protein (MGP) genes, ostepeopontin (OPN) genes and OPG/OCIF genes containing the polymorphisms and to probes and primers therefor.
Osteoporosis is today one of the most common diseases in individuals over 60 years of age. In America alone it affects an estimated 25 million people with a 5: 1 ratio of women to men. This corresponds to approximately 25-30% of people over 60 years of age. In Europe the percentage of people affected by this disease is approximately the same.
At present there is no cure for osteoporosis. However, hormone replacement therapy as well as treatment with bisphosphonates can halt or slow accelerated bone loss.
Hence, the sooner such a bone loss can be diagnosed the better the impact of treatment. It would, accordingly, be of particular advantage to be able to identify individuals predisposed to osteoporosis as early as possible. Since there is a strong genetic component associated with the development of osteoporosis (see below) the identification of genes having an impact on peak bone mass and/or the rate of bone loss would be of enormous help because individuals with genotypes predisposing to osteoporosis could be identified early in their life, leaving plenty of time for preventive. measures to be instituted.
From this point of view it is relevant to identify individuals or groups who are predisposed either to have a relatively low peak bone mass or bone mineral density or who are predisposed to a relatively fast rate of loss of bone mass or bone mineral density.
The extent of genetic contribution to bone mineral density and, hence, possibly to osteoporosis became evident more than 20 years ago from twin studies (Smith et al., 1973). Larger BMD and bone width variances were found in dizygotic than in monozygotic twins, indicating a considerable genetic influence on the regulation of bone mass (Smith et al., 1973). Another twin study reported a statistically significant effect of genetic factors on the rate of BMD change (Kelly et al., 1993). Other studies have demonstrated a strong genetic impact on the acquisition of peak bone mass (Gueguen et al., 1995; Lutz & Tesar, 1990).
Hence, the genetic component seemingly has an impact on both peak bone mass and the rate of bone loss. Genetic segregation analysis has strongly suggested that bone mass is controlled by several genes, each with modest effects (Gueguen et al., 1995).
Very little is known about the molecular mechanisms and genetics, leading to osteoporosis, even though there has been an intense search for genes influencing bone formation and bone resorption. Within the last five years polymorphisms identified in genes mainly encoding regulatory proteins have been associated with BMD: 1) A vitamin D receptor gene polymorphism identified by Morrison and co-workers (Morrison et al., 1994; W094/03633) has been subject of numerous publications.
Only abo
DNA & Calcification);
Evidence of nanobacterial-like structures in calcified human arteries and cardiac valves
Submitted 28 January 2004 ; accepted in final form 11 May 2004
Mechanisms mediating vascular calcification remain incompletely understood. Nanometer scale objects hypothesized to be a type of bacteria (nanobacteria) are associated with calcified geological specimens, human kidney stones, and psammona bodies in ovarian cancer. Experiments were designed to evaluate human vascular tissue for the presence of similar nanometer-scale objects. Calcified human aneurysms (n = 8), carotid plaques (n = 2), femoral arterial plaques (n = 2), and cardiac valves (n = 2) and noncalcified aneurysms from patients with bicuspid aortic valve disease (n = 2) were collected as surgical waste from the Heart Hospital of Austin, Austin, Texas, and Mayo Clinic, Rochester, Minnesota. Whole mounts or adjacent sections from each specimen were examined by electron microscopy, stained for calcium phosphate, or stained with a commercially available antibody (8D10). Filtered (0.2 µm) homogenates of aneurysms were cultured and costained with 8D10 antibody followed by PicoGreen to detect DNA or incubated with [3H]uridine. Staining for calcium phosphate was heterogeneously distributed within all calcified tissues. Immunological staining with 8D10 was also heterogeneously distributed in areas with and without calcium phosphate. Analysis of areas with positive immunostaining identified spheres ranging in size from 30 to 100 nm with a spectral pattern of calcium and phosphorus (high-energy dispersive spectroscopy). Nanosized particles cultured from calcified but not from noncalcified aneurysms were recognized by a DNA-specific dye and incorporated radiolabeled uridine, and, after decalcification, they appeared via electron microscopy to contain cell walls. Therefore, nanometer-scale particles similar to those described as nanobacteria isolated from geological specimens and human kidney stones can be visualized in and cultured from calcified human cardiovascular tissue.
THE DENTAL – CARDIOVASCULAR EVENT- MORTALITY LINK
Dental pulp stones are Nanobacterial, and if you or a family member have them, then you seem to be at risk for pathological calcification elsewhere. Calcified dental plaque also involves Nanobacteria. Well big deal! We’re worried about heart disease, something important; why should we care about the goings on in the mouth.
Well, some people feel that what goes on in the mouth has something to do with what goes on in the heart, as well as the tendency of some patients to not go on at all. Americans do not enjoy good periodontal health, just as they don’t enjoy good cardiovascular health. The average American has 10-17 decayed, filled, or missing teeth. Periodontitis is not uncommon, and gingivitis is our number one infection. The following study set out to establish a link between poor oral health and future cardiovascular health status.
Oral health status was evaluated in 9,760 25-74 year-old American men and women, all free of known cardiovascular disease. The number of decayed or missing teeth was recorded, along with the presence or absence of gingivitis or periodontitis.
No intervention was carried out. These individuals were followed, on average, for fourteen years. Using hospital records and patient interviews, new onset coronary disease, cardiac death, and overall mortality were noted. Follow-up was 90% complete. The investigators then looked for a relationship between dental and periodontal health at baseline, and cardiovascular and vital status fourteen years later.
Compared to persons with pristine dental health, individuals demonstrating gingivitis at baseline were 5% more likely to develop new onset coronary disease over the following 14 years. Periodontitis or the absence of teeth, presumably reflecting advanced dental/periodontal disease, was associated with a 23-25% increased risk. Individuals with gingivitis, periodontitis, or no teeth, were 23, 46, and 46% more likely to die over the follow-up period
In men, the presence of periodontitis was associated with a 72% greater risk of developing coronary disease at a young age. Gingivitis was associated with a 42% increased risk; individuals with periodontitis or no teeth were 2.1 and 2.6-fold more likely to die before their 50th birthday.
It has been proposed that the link between periodontal and cardiovascular disease is bacterial in origin. N. sanguineum is present in the mouth and is associated with Figure 4impaired dental and periodontal health. Later on we will learn that N. sanguineum is present in the coronaries, where it is associated with coronary artery calcification. So can necking break your heart?
Nanobacterium sanguineum fixes calcium and phosphorus and converts it into carbonate apatite, the form in which these minerals are found in pathologically calcified tissue. N. sanguineum can be cultured from kidney stones, calcified arteries, and polycystic kidney tissue (which involves pathological calcification), and its antigen has been detected in dental pulp stones and calcified pineal tissue. So far, it appears that wherever we find pathological calcification, we will also find N. sanguineum. So how do we get from Nanobacterium sanguineum to pathological calcification?
Many sea creatures are small and defenseless, but within their shell they enjoy protection from their natural predators. The only natural predator of N. sanguineum is the immune system of their host. Given the small size and slow growth rate of this organism, N. sanguineum vs. immune system wouldn’t seem to be a fair fight – it isn’t, the Nanobacteria always win! The immune system can engulf or surround Nanobacteria, if the immune response is aggressive enough. Even then our defense is moot, as the Nanobacteria either kill the cell that engulfed them, or they calcify inside the immune cell only to kill it later. Host generated antibodies to the Nanobacterial biofilm should bind to the individual Nanobacteria, rendering them a tasty morsel for circulating phagocytes. Rapidly dividing bacteria should hog all the available nutrients, crowding Nanobacteria out. But this does not happen, because:
a) Nanobacteria shelters itself from the immune system (calcific semi-dormant defense),
and
b) Nanobacteria can live where other bacteria cannot (extremophilic defense.
We are born with calcium in our teeth and bones. Osteoblasts and odontoblasts fix calcium and phosphorus, and then precipitate the product onto an organic matrix; this is the process of physiologic biomineralization involving apatite minerals. We are supposed to die with calcium in our bones and teeth, and nowhere else. However, as a result of “ageing” and disease states, typically disease states with an inflammatory component, we calcify our blood vessels and internal organs. Consider the following examples of this “pathological calcification”.
♦ Soft tissue calcification ♦ Gall stones ♣ Surrounding/In damaged joints ♦ Pineal gland calcification - “Brain Sand” ♣ Dysfunctional areas in the brain . Atherosclerotic arteries & veins ♣ Diseased organs Cardiac ;Scleroderma ♦ Cataracts ♣ Prostate Stones Salivary Stones; Kidney stones ♦ Damaged cardiac valves
♦ Dental pulp stones & Dental Plaque ♦ Malakoplakia
Nanobacteria trigger cellular apoptosis. At lower inoculums the targeted cells may survive, but they also won’t be able to kick out the Nanobacterial invaders. Nanobacteria can be seen within the cells, acting, as we will see, sort of like a parasite. The appearance of the intracellular Nanobacteria is a little different. Instead of goey biofilm, the Nanobacteria cell body appears to be surrounded by a “hairy coating”. This “hairy coating” is carbonate apatite (fig. 8, a Nanobacterium within polycystic kidney disease tissue). Other times, spicule like structures can be seen surrounding the cell body, where the biofilm used to be (fig. 9). These linear structures are composed of carbonate apatite, the same stuff that we find in abnormally calcified mammalian structures. This is an example of abnormal or pathological calcification. The Nanobacterium, acting like a parasite, fixes the host’s calcium and phosphorus, and then spins out this carbonate apatite webbing. I wonder why they do this?
N. sanguineum is difficult to detect, difficult to exclude, and thus difficult to keep out of biological products. N. sanguineum is present in fetal bovine sera, human and animal blood, vaccines, and diseased human tissues. N. sanguineum is thus within us and within our field of vision, but we haven’t noticed it until now. Why?
First of all, N. sanguineum is essentially too small to see. Apatite bearing Nanobacteria can be seen under microscopy using polarized light, but they don’t pick of standard stains, and are thus invisible under standard microscopy. With their small diameter, electron microscopy is absolutely required. Nanobacteria are coccoid to coccobacilar in shape, with a cell wall that varies between 20 to 200 nm in thickness. Divisional septa may occur in the central part of the cell, indicating binary fission (fig. 1), or at the end of the cell, suggesting a budding process (fig. 2, cell division by budding). Budding seems to start by formation of a capsule for a new cell, followed by transfer of cytoplasmic contents into this sheltered compartment.
N. sanguineum does not grow in standard bacteriologic media; it grows only in cell culture media, and then only under the right conditions. N. sanguineum grows only slowly, doubling once every three to six days, so patience is required. Kajander and Ciftcioglu worked long and hard to learn how to culture this organism. An American group tried to culture N. sanguineum out of kidney stones and they weren’t successful, but they didn’t follow Kajander and Ciftcioglu’s stringent protocol to isolate Nanobacteria. Another NIH funded American group, specifically after being trained by Ciftcioglu & Kajander, worked for many months trying to develop a pure Nanobacterial culture, only to find it contaminated with regular bacteria. This NIH research group ran out of grant money and was unable to restart so his particular study was unsuccessful. The Mayo Clinic Infectious Disease, Microbiology & Nephrology Departments, after being taught by Ciftcioglu & Kajander, have been intensively studying Nanobacteria for 6+ years. Mayo has repeated and validated independently all of the work done by Ciftcioglu & Kajander; publication is expected in mid-2002.
The experts are correct – a minimum diameter of 30 nanometers is necessary for cell-walled bacteria to carry out “standard” metabolic functions, that is, bacteria as we know them. N. sanguineum is, of course, unique. It gets away with being “too small” by utilizing “primordial growth strategies” and by being parasitic in its nature. It can function with fewer enzymes and structural proteins, because it can use environmental minerals to catalyze its metabolic processes and provide it with structural support. It uses nutrients in its environment to live. It only “flourishes and lives” where it finds a hospitable environment, otherwise it remains dormant in a “spore-like” calcified form. It flourishes and lives well in the nutrient-rich soup that we call blood and urine.
When times get tough, the tough get going. If you are a bacterial species, a scarce supply of nutrients constitutes tough times. Regular bacteria aren’t tough, so they have to be smart, so when times get tough, the smart bacteria slow down their growth rate. N. sanguineum seems to be the most resilient of all bacteria – part of its extremophlilic defense.
N. sanguineum generates biomass at 1/10,000th the rate of E. coli. When semi-dormant and sheltered in their calcium igloos, Nanobacteria double once every 6 days, about 1/20,000th the rate of common bacteria. When uncalcified, these Nanobacteria, now free in the circulation, assume a “normal” growth rate, doubling every three days. When under attack by whatever means, chemical or otherwise, they can replicate every day (1/3000th the rate of regular bacteria), and make large amounts of “slimy” calcific biofilm to cover themselves. Slowly growing bacteria don’t need much nutrition; they can survive where others cannot. N. sanguineum is the slowest growing bacterial species of relevance to human health; N. sanguineum can survive where other pathogens cannot.
Nanobacterium sanguineum is a unique organism: there is no other like it on earth. N. sanguineum displays a helical cell wall ultrastructure, contains unique peptides, and its RNA and DNA have an unusual appearance. N. sanguineum is the smallest cell-walled organism yet described; it is smaller than the Vaccinia virus. N. sanguineum takes up amino acids from its environment, but produces biomass at just 1/10,000 the rate of E. coli. N. sanguineum divides only once every three to six days, also 1/10,000 the rate of common bacteria. Nanobacteria is the only mineral forming bacterial species to be isolated from mammalian blood. It is also the only bacteria that can create a calcific biomass at physiologic pH and mineral concentrations. N. sanguineum is pleomorphic, but all of its forms fix calcium and phosphorus to generate a carbonate apatite coating – the same stuff present in diseased arteries and kidney stones. Nanobacteria readily bind to mammalian cells, trick the cells into internalizing them, and then trigger target cell apoptosis - including killing those cells responsible for our natural defenses like T-Lymphocytes (fig1-Nanobacteria killing a T6 Lymphocyte). N. sanguineum demonstrates unique radioresistance, related to its unique nucleic acid makeup and low division rate. 16s ribosomal RNA analysis places N. sanguineum in the alpha-2 subgroup of Proteobacteria. Nanobacteria are sturdy organisms that are resistant to nearly all commonly employed anti-bacterial and anti-septic methodologies. N. sanguineum can be cultured from animal and human blood and diseased tissues. A closer look at N. sanguineum’s biology will help us understand its causative role in human disease:
a little more...(this is all 2 yrs old)..
Pharmaceutical Drug Discovery
Nanobac's drug discovery and development efforts are focused on applying new and existing compounds that effectively inhibit, destroy or neutralize the particles. Nanobacteria or CNPs offer a unique model for studying many diseases involving soft tissue calcification or plaque. We have developed drug screening assays using this model to screen compounds using proprietary in vitro screening assays. Compounds showing efficacy can quickly move into animal models. Our business strategy is to develop, license and commercialize compounds to address the unmet needs of patients within the cardiovascular and urological disease markets. While the Company's primary focus remains cardiovascular and urological diseases, Nanobac researchers are investigating compounds for a wide range of other therapeutic areas.
Dietary Supplements
Dietary supplement products can reach the consumer market much quicker than a new pharmaceutical product. These products use ingredients such as vitamins, minerals, herbs, or amino acids that are "Generally Regarded as Safe" (GRAS). At Nanobac Life Sciences, we apply the same approach that we use to test new pharmaceutical compounds to testing dietary supplement ingredients and formulations. Ingredients and formulations that demonstrate the desired effects can be formulated into products and then validated in clinical trials. The Company markets dietary supplements through its dietary supplement marketing arm, Nanobac Sciences, LLC. Nanobac Sciences currently markets a combination Oral Supplement and EDTA rectal suppository sold under the Nanobac Supplements brand.
Diagnostics
Nanobac Oy is a wholly owned subsidiary of Nanobac Life Sciences. Nanobac Oy Diagnostics division operates out of our Nanobac Oy facility in Kuopio, Finland. Our diagnostics division markets both in vitro diagnostic products and laboratory services.
In Vitro Diagnostic Kits and Reagents
Nanobac Oy diagnostics division manufactures and markets IVD kits and reagents for the detection of Nanobacteria or calcifying nano-particles. Products include our NanoCapture(TM) and Nano-Sero(TM) ELISA assays and our Nano-Vision(TM) line of primary monoclonal antibodies and immunohistochemical reagents. These products are marketed through a network of distributors.
Nanobac Oy Clinical Laboratory Services
Nanobac Oy Clinical Laboratory provides specialized clinical laboratory testing services to clinicians, hospitals, and laboratories. We specialize in providing advanced technologies for the detection of Nanobacteria or CNPs in human samples. Nanobac Oy Clinical Laboratory is fully accredited by the Social Health Ministry of Finland.
BioAnalytical Services
Nanobacteria or CNPs expose a risk for biopharmaceuticals containing human or animal blood components or blood and animal tissue derived raw materials or production substrates.
Nanobac BioAnalytical Services works with biopharmaceutical partners to develop and apply methods for avoiding, detecting, and inactivating or eliminating Nanobacteria or CNPs from raw materials or production substrates. Our contamination control program focuses on host cell lines, animal and human derived materials, raw materials, availability of diagnostic procedures and downstream processes capable of inactivating or removing contaminants.
An excerpt;
Reputations, money and perhaps the foundations of life ride on the 16S rRNA dispute. Resolving it may determine who gets money to find the next great biological kingdom.
NANOBACTERIAL INFECTION
How relevant is the outcome for human welfare? In 2004, researchers reported finding nanobacteria in everything from heart disease to cancer and kidney stones. Medical researchers reported to the American Heart Association's Scientific Sessions 2004 that a test for nanobacteria is an accurate predictor of heart disease risk. But the work that these researchers say may already have saved lives has been ridiculed by critics who claim that such nanobes don't exist, which in turn has made funding for basic research hard to get.
Who is right? One well-respected astrobiologist observer qualified the struggle this way: "Unless we declare [the nano-organism scientists] incompetent, then the info they have gathered is rather compelling that something interesting is going on."
That's why a few intrepid investors have plopped US$7 million and counting into a Tampa biotech start-up devoted exclusively to Ciftcioglu and Kajander's discoveries about the calcifying particle. For the big pharmaceuticals companies that's pocket change, but for these entrepreneurs it's a pocketful of faith that's been keeping them on edge for years. And it's starting to show some results, as published research from NASA, Mayo and various universities indicates. Moreover, despite its relative financial insignificance, this venture may end up wagging the dog due to a long-overdue paradigm shift in, of all things, the space program.
After decades of resistance, NASA—provoked by successful upstart private projects such as the X Prize, which led to the first private foray into space—is now collaborating with fledgling companies, instead of just corporate behemoths, on intractable problems: in this case, why perfectly healthy astronauts come down with kidney and other calcifying disorders. The result: in March 2005, NASA's Johnson Space Center put the finishing touches on a tightly secured lab aimed at decoding nanobacteria found at the core of kidney stones. After some serious growing pains, the lab is finally beginning to look into what Ciftcioglu and Kajander began examining so many years ago: the genetic content of nanobacteria. Meanwhile, Ciftcioglu and others have published results showing that nanobacteria multiply five times faster in weightlessness than in Earth gravity,5 which may explain why calcification shows up so suddenly in space.
But while researchers argue over what this nanobacterium is and how it multiplies, doctors are finding that, when they treat it with a medical cocktail, their patients improve.
Nor is it unusual that doctors are succeeding before science figures out why. Antibiotics were used successfully against bacteria long before scientists deciphered DNA. Doctors stopped infecting patients by washing their hands long before they were able to identify all the viruses and bacteria that they inadvertently transported from patient to patient.
Most recently, a vaccine that prevents cervical cancer has been put on the market. It apparently works by targeting the human papilloma virus. Problem is, researchers can't show exactly how the virus causes cancer; they can only show that when it is stopped, the cancer doesn't occur. But that hasn't prevented the drug from being patented and put on the market. The history of medicine is full of such examples where patients improve with treatments whose mechanisms aren't fully understood at the start.
The idea that infection could be at the heart of chronic illness is intriguing because it has been around for more than a century but only now is regaining favour due to discoveries of, for example, a vaccine that prevents cervical cancer (as mentioned above). The resulting debates over infection in chronic disease have a novel twist because they are driven by new diagnostic technologies that give researchers the molecular accuracy required to confirm older theories about infection. On one hand, clinical results suggest antibiotics alone do not prevent the rate of heart attacks among coronary patients. On the other, discoveries that infection is responsible for most stomach ulcers and some cancers support the long-held idea that the same might be true in heart disease, if only science could find the right infection and get rid of it.
Some say that nanobacteria may be one such infection. Yet scientists' inability to fully explain the genetics of nanobacteria is being used by high-ranking medical authorities as an excuse to ignore the pathogen and its treatment. This is especially perplexing because scientists involved in the discoveries work at some of the highest level institutions in America, including NASA, Mayo Clinic, Cleveland Clinic, Washington Hospital Center and many others, and are not only respected in their field but are also award winners. Other centres of excellence internationally, such as University Hospital in Vienna, have also isolated the pathogen and observed it in diseases such as ovarian cancer.
For decades, scientists have shown that disease can be caused by contaminants that are not "alive" and cannot replicate on their own. Environmental toxins, many viruses and, most recently, particles known as prions have all been shown as players in disease processes, although they cannot self-replicate.
So it seems unusual that nanobacteria would be discounted just because no one has yet shown how they multiply. Which takes us to the question of where nanobacteria might come from.
Read this at your leisure...
Posted by: nanopatent
The Nanobacteria Link to Heart Disease and Cancer
Nanoparticles are implicated in the harmful calcification that's common to many illnesses.
A simple treatment is now reversing the symptoms, especially in heart disease, so why aren't the health authorities telling patients and doctors about it?
Extracted from Nexus Magazine, Volume 12, Number 5 (August - September 2005)
PO Box 30, Mapleton Qld 4560 Australia. editor@nexusmagazine.com
Telephone: +61 (0)7 5442 9280; Fax: +61 (0)7 5442 9381
From our web page at: www.nexusmagazine.com
by Douglas Mulhall © May–July 2005
Email: info@calcify.com
Website: http://www.calcify.com
Based on the book The Calcium Bomb
by Douglas Mulhall and Katja Hansen
(The Writers' Collective, 2005)
Millions of seriously ill patients are unaware that heart disease is being measurably reversed with an approach pioneered by researchers at the National Aeronautics and Space Administration (NASA) and in Finland, aided by Mayo Clinic and Washington Hospital Center findings. This approach is now prescribed by hundreds of doctors for thousands of patients. A similar approach has been developed with prostate disease at the renowned Cleveland Clinic in Florida. According to doctors, both approaches are practical options for those whose other medicines and surgery have failed. So why aren't other desperately ill patients whose treatments don't work being told about it?
In July 2004, the medical journal Pathophysiology published a peer-reviewed research paper with the innocuous title "Calcification in coronary artery disease can be reversed by EDTA–tetracycline long-term chemotherapy".1 In plain terms, it meant that hardening of the arteries was being reversed. Not only were rock-hard calcium deposits being reduced, but chest pains were being resolved in most patients and bad cholesterol levels were being cut beyond what other medicines had achieved. The findings were important for patients whose other drugs and surgery weren't working, i.e., the "cardiac cripples", whose numbers are in the millions and whose doctors have told them there is nothing more to be done. They were the ones who responded most favourably to the new approach.
Then, in February 2005, a paper published in the prestigious Journal of Urology by researchers from the Cleveland Clinic, one of the leading urology hospitals in America, reported "significant improvement" in chronic prostatitis—a growing problem for millions of men—again, where other approaches had failed.2
The studies, although otherwise separate, had a compelling link. They used a cocktail of well-known, inexpensive medicines that have been around for half a century but were never before used in this combination. Both reports urged more studies to confirm their conclusions, and emphasised that not every patient experienced a reversal; only a majority did. Nonetheless, the results were encouraging. Chronic diseases that had befuddled modern medicine were being reversed.
To put a human face on this, take the case reported by Dr Manjit Bajwa of McLean, Virginia, who did not participate in the clinical studies but whose experience with one patient paralleled study results. Dr Bajwa reported in a testimonial of 5 May 2005:
"Two years ago I had a patient with severe coronary artery disease with a 75–85% blockage in left coronary and two other arteries. Open heart surgery was recommended as stents could not be put in. The patient was told he would probably die within two weeks if surgery was not performed.
"He declined surgery and instead chose chelation. [Author's note: chelation in this case is an intravenous form of heavy metal removal.] After twenty-five treatments of chelation, his angina worsened [author's emphasis]. With [his] heart calcium score of 2600, I started the nanobacteria protocol. Within two to three weeks his angina abated. He was able to return to all his normal activities and exercises in two months.
"Nanobacteria protocol helped this patient measurably, when other treatments had failed. I am quite impressed with his results. With heart calcium scores of 750 or more, nothing else seems to work."
Bajwa and her patient are far from alone. In Santa Monica, California, general practitioner Dr Douglas Hopper said he recorded impressive results with a diabetic patient when he used the treatment to help her recover from congestive heart failure. Hopper then put his patient on the same treatment used in the clinical study: a regimen of tetracycline, EDTA and nutraceuticals,3 administered by the patient at home. Note that this was not intravenous chelation, which has been broadly analysed and critiqued, but, instead, a mix of oral and suppository treatments.
In Toledo, Ohio, cardiologist Dr James C. Roberts, who pioneered early patient treatment with this approach, has on his website case histories from dozens of patients who have shown remarkable improvement. In Tampa, Florida, cardiologist Dr Benedict Maniscalco, who supervised the clinical study [Pathophysiology study, referenced previous page], reports that patients who stayed on the treatment after the study was completed showed dramatic reductions in their heart disease symptoms. There are many more examples.
Normally results such as these, when reinforced by clinical studies, however preliminary, would be cause for loud celebration. If the findings had been reported by a major pharmaceuticals company, they could have easily made the front pages of medical news services because, until then, no one had reported reversing the symptoms of such diseases to such an extent. More encouraging still, because the medicines have been around for many years and their side effects are minimal and well known, the new approach is already available across the USA and used with thousands of patients. That leaves thousands more doctors with millions more patients who might benefit right now. On top of that, a blood test based on the new approach has been used to identify heart disease early in patients who show no outward symptoms.
Why, then, has the response from government authorities, medical associations and health experts been cavernous silence?
To understand this requires looking at a scourge that has been with us for millennia, and which science has been at a loss to explain until now. It is known as calcification.
CALCIFICATION
Calcification is a rock-hard mix of the most plentiful minerals in the body: calcium and phosphorus. Normally this calcium phosphate mix is essential for building bones and teeth. But as we age, and sometimes when we are still young, some of it goes haywire, stiffening arteries, roughing up skin, destroying teeth, blocking kidneys and salting cancers.
The arithmetic is frighteningly easy. Calcification doubles in the body about every three or four years. We can have it as teenagers and not notice, although it mysteriously accelerates in some athletes. Then as we age and also live longer, it becomes so endemic that most people over seventy have it.
For decades, calcification has been growing imperceptibly in tens of millions of baby boomers. Politicians and pundits are among the high-profile victims of this slow-motion explosion that is ripping apart healthcare with skyrocketing treatment costs. In December 2004, doctors diagnosed US President George W. Bush with one of the more commonly known forms: coronary artery calcification. Former President Clinton required emergency surgery because doctors missed much of his calcification when they used older tests to track it. Vice President Dick Cheney and many of his Senate colleagues are calcified. At least three sitting US women governors have had it in breast cancer as well. And they are not alone. Media types who cover politics or poke fun at it haven't escaped. Larry King and David Letterman are both calcified, as are many ageing news anchors. A much younger CBS Early Show co-host, Rene Syler, has it too.
As we learn more about it, calcification is competing to be the leading medical disorder. Although it is nowhere on the "Leading Causes of Death" list, it contributes to most diseases that kill us, including heart disease, diabetes and cancer. The numbers are staggering. For the 60 million Americans who have heart disease, most have calcification. Of the millions of women who develop breast or ovarian cancer or who have breast implants, calcification is a warning. Men with prostate disease often have it, as do kidney-stone sufferers. Athletes with stress injuries like bone spurs and tendonitis get it frequently.
Most of us don't know the pervasiveness of calcification because it has a different name in many diseases, and here are just a few: dental pulp stones, hardening of the arteries, kidney stones, pitcher's elbow, bone spurs, microcalcification in breast cancer and "brain sand".
Unsuspecting patients aren't the only ones in the dark. Many doctors are unaware of new studies that show calcification is toxic, causing acute inflammation, rapid cell division and joint destruction. Oddly, these nasty effects are well known to specialists who study calcification in arthritis, but awareness of them hasn't translated very well to the cardiovascular community, with the result that calcification is still misperceived by many as an innocent bystander instead of an inflammatory devil.
The double-think about calcification is illustrated by how it is treated in breast cancer. When microcalcification is detected in the breast with routine scans, it is a warning sign for cancer and the deposits are biopsied for malignancies. This was the case, for example, with Connecticut Governor Jody Rell in early 2005. Doctors found cancer in the calcium deposits in her breast before scans detected a tumour. This let them surgically remove it before it spread to her lymph nodes.
That typifies one perverse advantage of calcification: it helps doctors pre-empt more serious disease. In some ways, it is a canary in the mine of the body. And yet, if cancer is not found in calcium deposits, these are often declared as "benign" and patients are told there is nothing to worry about.
The same thing goes for heart disease. Coronary artery calcification is seen as an excellent predictor of the illness.
Tens of billions of dollars are spent every year on scanning technology to identify the telltale thin white lines that betray its presence. Yet most doctors see calcification in the arteries as something that comes along later once the disease takes hold, despite evidence that calcium phosphate crystals generate the same type of inflammation that, according to cardiologists, plays a big role in heart attacks.
Incredibly, with all the advanced detection techniques, there has been no way to find calcium deposits where they get started in the billions of capillaries in the human body—so, without being able to see the starting point, doctors often conclude that what they don't see isn't there. But make no mistake: calcification is there, and it is a medical disorder. It was registered in 1990 as a disorder under the International Classification of Diseases list of the World Health Organization and was adopted by WHO member states as of 1994 (see http://www.who.int/classifications/icd/en/).
When well established, calcification stares defiantly at radiologists every day from X-rays as it multiplies incessantly. There has been no proof of where it comes from, and there is no known way to prevent it or sustainably get rid of it without removing it surgically. Due to its gestation period of years before it triggers real trouble, it has just begun sucking the life out of baby boomers and their healthcare budgets.
Among its more exotic effects, it threatens space exploration when it disables astronauts with unexpected kidney calcification and it is a budget-breaker for pro-sport-team owners who lose athletes to its ravages. At the more mundane level, it complicates root canals and it disrupts the lives of otherwise healthy young people when it strikes as kidney stones. Worst of all, it infiltrates plaque in heart disease and stroke and it plugs bypasses and stents used to fix our internal plumbing.
The US National Library of Medicine holds thousands of research documents referencing calcification, and various medical journals cover it in depth. GE Healthcare, Toshiba, Philips and Siemens sell thousands of machines for detecting it.
TREATMENT A THREAT TO PHARMCO PROFITS
But with all this money being thrown at calcification, there has been virtually no success at finding the cause. So when researchers such as those at Mayo Clinic and NASA find something that seems to cause it, and clinical studies show that a new approach seems to get rid of it, you'd think that most of the medical establishment would be rapt with attention, right? Wrong.
Only a few small studies have been co-financed by the National Institutes of Health (NIH) to look into this, and neither has to do with the treatment. The only thing the Food and Drug Administration (FDA) seems to have done is to make rumblings about whether the treatment is legitimate, although the active ingredients—tetracycline and EDTA—have been FDA approved for other uses for decades. So far, no government agency has made public note of the peer-reviewed studies that many physicians say are so promising.
According to doctors familiar with the approach, here are a few reasons why the treatment has not been given the attention that it seems to merit...
• The most perturbing for patients: the treatment is relatively inexpensive and produces poor profits compared to other drugs. It is exponentially cheaper than open heart surgery. Because it does not have to be taken for life at full dose—as is the case with most other heart drugs—it does not provide the steady cash flow that other medicines do.
• Although the treatment is initially used alongside other medicines as a precaution to make sure patients don't switch prematurely and suffer problems, evidence suggests that the new approach might replace more profitable blood thinners and anti-inflammatories that are staples of the pharmaceuticals industry.
• And if the approach continues to reverse coronary artery disease, it will cut down on expensive surgical procedures that are the financial mainstay of hospitals.
That's not to say surgeons don't want to get rid of calcification. New stents that go into arteries are specially coated with time-release drugs that seem to ward off calcification. But that only happens where the stent is located, not in the other 99.999 per cent of the arteries.
Also, the EDTA–tetracycline–nutraceutical combo that has demonstrated such promise is not the only treatment shown to work. A group of drugs known as bisphosphonates, used for example to treat osteoporosis, has been shown to be effective in the lab against some calcification. But bisphosphonates can have nasty side effects, especially with the type of regular application that seems to be necessary to reverse heart disease in seriously ill patients. Due to these risks, the only present approach that seems to be safe and effective in reversing heart disease is the one that uses the EDTA–tetracycline–nutraceutical mix.
Critics claim the reason why the treatment isn't adopted more broadly has nothing to do with money but instead with science. They say researchers can't show how the treatment works.
NANOBACTERIA DISCOVERED IN OUR BLOOD
It all comes down to a sub-microscopic blood particle known as a nanobacterium, discovered in 1988 by Finnish researcher Dr Olavi Kajander at Scripps Research Institute in California.
The particle has a special habit no other blood particle has been known to possess: it forms a rock-hard calcium phosphate shell that is chemically identical to the stuff found in hardening of the arteries, prostate disease, kidney disease, periodontal disease and breast cancer. The problem is, the particle is so small that it apparently can't accommodate nucleic acid strings that, according to commonly accepted wisdom, would let it replicate on its own and be alive. So scientists are stumped over how it manages to self-replicate.
For 15 years, microbiologist Dr Neva Ciftcioglu (pronounced "shift-show-lew") has been peering with an electron microscope at this blood particle that critics say doesn't live. But according to NASA colleagues and Mayo Clinic researchers, the question of whether it lives is less important than what it does. Despite or perhaps due to its tiny size and genetic elusiveness, this speck may be the Rosetta stone for a calcified language found in most diseases on the Leading Causes of Death list.
Like her science, Ciftcioglu's life is full of unusual turns. Being a woman microbiologist from Turkey speaks volumes. Throw into that her once-fluent Finnish, a position at NASA and professorships on both sides of the Atlantic, and you've got a determined character struggling with a stubborn scientific cryptogram.
Ciftcioglu's work with nanobacteria began when her PhD scholarship took her to the University of Kuopio in Finland, where alongside her once mentor, biochemist Olavi Kajander, she developed the antibodies necessary to find the particle in the human body. A decade later, her work caught the eye of NASA chief scientist Dr David McKay and she ended up at the Johnson Space Center in Houston, gathering science awards that testify to her success.
Now Ciftcioglu and long-time collaborator Kajander, who discovered the nanoscopic artifact, stand at the eye of a growing storm. They and their colleagues are garnering praise and scorn because they claim to have evidence for why most of us are literally petrified by the time we die. More profoundly, their work may influence how new life is found on Earth and other planets.
SELF-REPLICATING NANOPARTICLES
An intense dispute has raged for years that connects how we look for infection in the body with how we look for bio-kingdoms on Earth and throughout the universe. Researchers have long sought terrestrial extremophiles that tell them what might survive on Mars, while others doubt the wisdom of looking for life on Mars at all. The mystery remains: what is the most effective way to find novel organisms?
Until recently, every life-form was found to have a particular RNA sequence that can be amplified using a technique known as Polymerase Chain Reaction (PCR). Nucleic acid sub-sequences named 16S rRNA have been universally found in life-forms. By making primers against these sub-sequences, scientists amplify the DNA that codes for the 16S rRNAs. Resulting PCR products, when sequenced, can characterise a life-form.
One high-powered group persuaded NASA with a "Don't fix it if it ain't broke" line and lobbied successfully to use the same method employed for years: get a piece of RNA and amplify it. The group—led by scientists such as Dr Gary Ruvkun at the Department of Genetics in Massachusetts General Hospital, Boston, and advised by luminaries such as Dr Norman Pace at the University of Colorado—got money from NASA to build a "PCR machine" that would automatically seek such clues in harsh environments such as those found on Mars.
Other scientists known as astrobiologists say the PCR machine approach is a waste of money because such amplification shows only part of the picture—not what nature might have done on other planets or, for that matter, in extreme Earthly environments.
However, their argument always suffered from lack of evidence—that is, until 2003 when scientists associated with the San Diego–based Diversa Corporation and advised by Professor Karl Stetter, of the University of Regensburg, Germany, published the genome of an extremophile known as Nanoarchaeum equitans, which Stetter's team had discovered in Icelandic volcanic vents.
N. equitans was special because it had the smallest known genome found so far, but it also had another intriguing trait. With Nanoarchaeae, the particular 16S rRNA sequence found in other life-forms wasn't in the place that it was expected to be and did not respond to conventional PCR tests. The 16S rRNA sequence was different in areas addressed by the PCR primers and did not amplify. Stetter noted that the so-called universal probes that work with humans, animals, plants, eukaryotes, bacteria and archaeae did not work in this organism.
How, then, was the discovery made if the organism couldn't be sequenced in that way? Stetter had found that the organism's sequence where the traditional "universal" primers are located was abnormal. This finding let him use other means to sequence the gene. In reporting their discovery in the Proceedings of the National Academy of Sciences,4 the Stetter team observed that the information-processing systems and simplicity of Nanoarchaeum's metabolism suggests "an unanticipated world of organisms to be discovered". In other words, it might be the tip of a nano-lifeberg.
Stetter's finding gave ammunition to scientists such as Neva Ciftcioglu who say they have found other extremophiles, including human nanobacteria, that cannot have their nucleic acids detected with standard PCR amplification.
One of the differences between Stetter's N. equitans and the nanobacteria found by Ciftcioglu and Kajander's team is that Nanoarchaeae need another organism to replicate, whereas at least some nanobacteria seem to replicate by themselves. Another difference is that Nanoarchaeae are slightly wider: 400 nanometres compared to 100–250 for nanobacteria. The greater size allows for what conventional wisdom says is the smallest allowable space for life-replicating ribosomes.
Which leads to the question: how do nanobacteria copy themselves? Evidence for self-replicating nanoparticles has been around for years in everything from oil wells to heart disease, but failure to sequence them using regular PCR led some to dismiss them as contamination or mistakes. However, researchers have found characteristics that make the particles hard to explain away. They replicate on their own, so are not viruses. They resist high-level radiation, which suggests they are not bacteria. They respond well to light, where non-living crystals don't. So if they aren't viruses, regular bacteria or crystals, what are they?
Some supporters of standardised 16S rRNA tests are quick to discount nanobacteria. That's not surprising. If a novel nucleic sequence holds true with other extremophiles as with N. equitans, then a machine that searches for life using standard PCR tests might miss them and be obsolete. Conscious of this, the PCR machine team has said that as part of their work, they plan to "search for the boundaries" of the 16S sequences, but what exactly that means and how they plan to overcome the problem hasn't been set out yet.
Reputations, money and perhaps the foundations of life ride on the 16S rRNA dispute. Resolving it may determine who gets money to find the next great biological kingdom.
NANOBACTERIAL INFECTION
How relevant is the outcome for human welfare? In 2004, researchers reported finding nanobacteria in everything from heart disease to cancer and kidney stones. Medical researchers reported to the American Heart Association's Scientific Sessions 2004 that a test for nanobacteria is an accurate predictor of heart disease risk. But the work that these researchers say may already have saved lives has been ridiculed by critics who claim that such nanobes don't exist, which in turn has made funding for basic research hard to get.
Who is right? One well-respected astrobiologist observer qualified the struggle this way: "Unless we declare [the nano-organism scientists] incompetent, then the info they have gathered is rather compelling that something interesting is going on."
That's why a few intrepid investors have plopped US$7 million and counting into a Tampa biotech start-up devoted exclusively to Ciftcioglu and Kajander's discoveries about the calcifying particle. For the big pharmaceuticals companies that's pocket change, but for these entrepreneurs it's a pocketful of faith that's been keeping them on edge for years. And it's starting to show some results, as published research from NASA, Mayo and various universities indicates. Moreover, despite its relative financial insignificance, this venture may end up wagging the dog due to a long-overdue paradigm shift in, of all things, the space program.
After decades of resistance, NASA—provoked by successful upstart private projects such as the X Prize, which led to the first private foray into space—is now collaborating with fledgling companies, instead of just corporate behemoths, on intractable problems: in this case, why perfectly healthy astronauts come down with kidney and other calcifying disorders. The result: in March 2005, NASA's Johnson Space Center put the finishing touches on a tightly secured lab aimed at decoding nanobacteria found at the core of kidney stones. After some serious growing pains, the lab is finally beginning to look into what Ciftcioglu and Kajander began examining so many years ago: the genetic content of nanobacteria. Meanwhile, Ciftcioglu and others have published results showing that nanobacteria multiply five times faster in weightlessness than in Earth gravity,5 which may explain why calcification shows up so suddenly in space.
But while researchers argue over what this nanobacterium is and how it multiplies, doctors are finding that, when they treat it with a medical cocktail, their patients improve.
Nor is it unusual that doctors are succeeding before science figures out why. Antibiotics were used successfully against bacteria long before scientists deciphered DNA. Doctors stopped infecting patients by washing their hands long before they were able to identify all the viruses and bacteria that they inadvertently transported from patient to patient.
Most recently, a vaccine that prevents cervical cancer has been put on the market. It apparently works by targeting the human papilloma virus. Problem is, researchers can't show exactly how the virus causes cancer; they can only show that when it is stopped, the cancer doesn't occur. But that hasn't prevented the drug from being patented and put on the market. The history of medicine is full of such examples where patients improve with treatments whose mechanisms aren't fully understood at the start.
The idea that infection could be at the heart of chronic illness is intriguing because it has been around for more than a century but only now is regaining favour due to discoveries of, for example, a vaccine that prevents cervical cancer (as mentioned above). The resulting debates over infection in chronic disease have a novel twist because they are driven by new diagnostic technologies that give researchers the molecular accuracy required to confirm older theories about infection. On one hand, clinical results suggest antibiotics alone do not prevent the rate of heart attacks among coronary patients. On the other, discoveries that infection is responsible for most stomach ulcers and some cancers support the long-held idea that the same might be true in heart disease, if only science could find the right infection and get rid of it.
Some say that nanobacteria may be one such infection. Yet scientists' inability to fully explain the genetics of nanobacteria is being used by high-ranking medical authorities as an excuse to ignore the pathogen and its treatment. This is especially perplexing because scientists involved in the discoveries work at some of the highest level institutions in America, including NASA, Mayo Clinic, Cleveland Clinic, Washington Hospital Center and many others, and are not only respected in their field but are also award winners. Other centres of excellence internationally, such as University Hospital in Vienna, have also isolated the pathogen and observed it in diseases such as ovarian cancer.
For decades, scientists have shown that disease can be caused by contaminants that are not "alive" and cannot replicate on their own. Environmental toxins, many viruses and, most recently, particles known as prions have all been shown as players in disease processes, although they cannot self-replicate.
So it seems unusual that nanobacteria would be discounted just because no one has yet shown how they multiply. Which takes us to the question of where nanobacteria might come from.
NANOBACTERIA-CONTAMINATED VACCINES
When Dr Olavi Kajander discovered nanobacteria in 1988, he was not looking for disease at all. He was looking for what was killing the cells that are used to develop vaccines. Labs everywhere have a vexing and expensive problem with these widely used cell cultures: they stop reproducing or die after a few generations and have to be thrown out.
Kajander surmised that something invisible was killing them; and when he incubated supposedly sterile samples for more than a month under special conditions, he got a milky biofilm. That biofilm contained particles that he later named nanobacteria, unaware at the time that some of their characteristics made them quite distinct from bacteria.
The serum that Kajander used to grow the nanobacteria came from the blood of cow foetuses. Serum from the UK especially was full of nanobacteria, but a much later study also concluded they were present in some cow herds in the eastern US. In other words, nanobacteria are in cows, and cow blood is used to develop many vaccines. Kajander emphasises that this should not stop people from using vaccines, because the immediate risk from diseases that the vaccines are intended to prevent is relatively higher than the calcification risk in the short term. Nonetheless, the potentially explosive implications of contaminated vaccines and cow by-products would be clear to everyone at government agencies who has examined the issue.
In that context, a series of hotly disputed discussions went back and forth between Kajander and Ciftcioglu and disease prevention agencies. And it certainly wasn't a secret because the Medical Letter on the CDC & FDA (10 June 2001) published an article entitled "Nanobacteria Are Present In Vaccines; But Any Health Risks Remain Unknown", explaining that nanobacteria had been discovered in some polio vaccines.
The minutes of a subsequent meeting of the FDA Center for Biologics Evaluation and Research (CBER) advisory committee in November 2002 reveal an extraordinary decision by the committee members: they elected not to investigate the potential contamination. According to the minutes they based their decision on a lone experiment, suggesting that what Kajander had found was a contaminant often found in lab experiments and nothing new. In other words, they maintained that Kajander had made a mistake.
But one of the glaring problems with the NIH-funded experiment performed around late 1999 or early 2000, as shown in the published paper about the results,6 is that it did not use a control sample that could have been provided by Kajander. In other words, the experiment never examined the particle that Kajander had discovered, but instead relied on growing the particle independently without knowing if it was the same one Kajander was referring to. Moreover, the experiment was never repeated after the preliminary finding. On that very slim basis, according to the CBER committee minutes, the whole issue of nanobacteria was dismissed as a potential contamination issue for the time being. Since then, papers have been published showing that nanobacteria have been grown in labs around the world and that patients began to improve when the pathogen was targeted in disease. Nonetheless, neither the FDA nor NIH has indicated much readiness to re-investigate the vaccine contamination issue or the nanobacteria treatment.
What might be the price for this delay in researching nanobacteria? Annually, millions of heart disease patients go through agony or die because drugs and surgery prescribed for them haven't worked. For this last-ditch group, the choices are simple: try something new or die.
The question that the NIH and FDA may one day face is: when such promising early evidence was being reported and so many patients had exhausted their other options, why were doctors not advised of this new possibility so that they could at least tell patients and make some informed decisions?
Researchers like Ciftcioglu and Kajander, along with cardiologists like Benedict Maniscalco plus experienced general practitioners such as Douglas Hopper, profess frustration that so many patients and their doctors are not being given the information that could help them, especially in last-ditch situations. Meanwhile, calcification continues its relentless march in millions, and the human and financial costs are mounting.
POSTSCRIPT
In May 2005, Dr Olavi Kajander delivered a sobering message to a joint meeting of the US FDA and the European Medicines Agency on viral safety when he presented new evidence to support something first published in 1997: that vaccines are contaminated with nanobacteria.
Since 1999, government agencies have done virtually nothing to investigate the claim, due largely to that NIH experiment which failed to use particles discovered by Kajander as control samples; so now that the vaccine contamination has been officially reported to authorities, the question is: what will be done?
Then on 24 June 2005, a "smoking gun" was announced about calcium deposits in heart disease. British researchers published proof in the leading medical journal Circulation Research7 that calcium phosphate crystals cause inflammation in the arteries. Inflammation is a leading cause of heart attacks, but until now most cardiologists have believed calcification to be an innocent bystander in the inflammatory process. Because of that, calcium deposits were never targeted with treatment. If true, the British discovery would force a re-evaluation of the whole medical approach, not only to inflammation but also to the foundations of heart disease, looking at calcification as a prime culprit.
About the Author:
Douglas Mulhall is a leading nanotechnology journalist who appears often on nationally syndicated talk shows in the US. As managing director of the Hamburg Environmental Institute, he co-developed methods now used by government agencies to measure environmental impacts. His book Our Molecular Future (Prometheus Books, 2002) describes how to use nanotechnology as a defence against tsunamis and other natural disaster risks. His disease prevention experience comes from pioneering water purification technologies in China and South America.
Mr Mulhall's communications background began with a Bachelor of Journalism (Hons.), progressed to (award-winning) documentary film making, then diversified into management when he co-founded the first commercial TV network in the Republic of Ukraine. He has written articles for US media such as News Day, The Futurist and The National Post as well as for publications in Germany and Brazil. He contributed to the first Financial Times (UK) book on green business opportunities and has also written and edited a range of technology training books. Douglas Mulhall sits on the advisory boards of the Center for Responsible Nanotechnology and the Acceleration Studies Foundation. He has given invited lectures to organisations such as the National Research Council, the US EPA and the Institute of Medicine.
Editor's Note:
This article is based on material in the book The Calcium Bomb: The Nanobacteria Link to Heart Disease & Cancer, by Douglas Mulhall and Katja Hansen (The Writers' Collective, 2005; see review this issue), which was selected as a Finalist for the 2004 Book of the Year Award for Health by
Not one person in three days has discussed what Nanobac actually does, especially on the subject of something that has or will affect us all, the complications of calcification and the bacteria that help this process along in our blood system and arteries.
I just had open heart surgery 3 weeks ago. I have spent all of my down time reading up on statins, chelation, calcificaton, enzymes(co-enzyme 10 to be exact), and a myriad of other factors relating to the heart and blood. I have always been the healthiest of all my friends and I am only 54.
So they are all freaked out. I want to live another 20 years, so I am reading everything I can on reducing plaque in the arteries.
If anyone was surprised by this merger, or buyout, or whatever you want to call it, I was. At first I thought it was a desperate move by our DNAP, and it was obvious Gabriel couldn't get financing.
But, knowing it would only be foolish to jump to conclusions, especially with Gomez in the mix, I read & dd'd all I could, including reading every post on their board for the last 2 years.
Let me just say this. Before you all jump to immediate conclusions, try to understand what exactly Nanoac does and what they are trying to do. And if you still own shares of Dnaprint and have decided to keep them, even out of disgust of losing so much, just shut your whining mouths, please. It does not help ANYTHING.
Good luck to you all, (and us).
Did anyone see CBS evening news w/ Katie Couric?
The last piece of the night was on DNA personalized, using 23andMe as an example of personalized DNA genotyping.
The two women were interviewed,(one of them is a Google founder's wife) and said how they hope their company will do for the personalized DNA medical world what Google has done for the internet. How's that for ambition.
Another dude said the DNA revolution is at the head of a virtual "tsunami" and is about to explode.
It will be interesting to see where Aims fall into all of this.
DNAG is ahead of all these people, IMO
Scroll down to "searchg for answers in DNA" and pick the video:
http://www.cbsnews.com/sections/eveningnews/main3420.shtml
TruTV...
I looked at the schedule and it airs again on Saturday Feb 9th @ 7:30 pm.
PL1,
Thanks for the looksee on Genebase. I'm wondering how many of these fly-by-night companies are gonna ruin the show.
Q:
Does anyone here know who the originators of Genebase,(out of Canada) are?
Altarboy,
What it all really comes down to in the end is if Ancestry will someday end up being the backbone of DNA research in all aspects and applications for cancer, drugs, and cell therapy and research.
The acqusition of Trace Genetics will prove, in my opinion, to be one of the best moves DNAPrint has made. Also, the most important milestone is yet to be realized, as the AIM patent(s)could be the "golden fleece" for DNAPrint.
All JMHO
altarboy,
You probably wouldn't see a contract of any kind in forensics until the complete spectrum of DNA to facial recognition technology is available. That means predictable facial bone structure, nose, ears, eyes, skin, etc., etc. And even then it would probably be a military, high security homeland security government contract or equivilent.
Even though there is a backlog of criminal DNA to process, it is too much money for a law enforcement agency to contract out to just get ethnic backround on a dna sample.
Very similar to what you are asking about though, is our business entity created with Beckman-Coulter. It is essentially the same thing, but even better. The 600,000 samples we will eventually run through the Ancestry platform will be available for a myriad of uses through Beckman, and the revenues will grow with time.
O.T.
Looks like the Denver station changed the content of the story at the last minute to exclude the portion where they used DNAPrint to run the DNA. Now it bypasses that and says it was a criminal database matchup. Maybe DNAPrint will be mentioned in the actual station video at newstime, but I am thinking that they took it out as it made reference to "hispanic or native american descent" in the original report. Anyone agree?:
Suspect Arrested For 1997 Murder In Boulder
By Catherine Tsai, AP Writer
BOULDER, Colo. (AP) ― Police announced Sunday the arrest of a suspect in the rape and beating death in December 1997 of University of Colorado senior Susannah Chase.
"The department is ecstatic over this," Police Chief Mark Beckner said.
Detective Chuck Heidel, who had worked the case from the start, broke the news to Chase's mother Friday. "She is extremely happy, she and her family," Heidle said.
The suspect was identified as 38-year-old Diego Olmos-Alcalde, who was being held $5 million bail on charges of first-degree murder, second-degree kidnapping and first-degree sex assault.
"As you might imagine our emotions have run the gamut since we first heard of the DNA match with Susannah's case. We are delighted that a suspect has been identified and apprehended," said a family statement.
Police had never given up on the case, talking with more than 100 people possibly involved in the death of the 23-year-old from Stamford, Conn.
In recent years, as forensic science was enchanced, detectives focused on the DNA found in seminal fluid in Chase's body.
DNA from the suspect entered into the growing national database was a match with DNA found at the scene.
He had spent time in a Wyoming prison for a kidnapping in 2000. He was released to immigration officials in July of 2007. Olmos-Alcalde, from Chile, failed to report to Wyoming parole officials and on Saturday he was arrested by Boulder and Aurora police on the parole violations.
He was served with the murder warrant Saturday.
BigLab
I would rather see them exercise their options before a restructure/spinoff. Clean slate. So would the SEC.
Alterboy,
Whatever happens, one thing I do know is it won't help anybody or anything for me to complain about things. If you own a car that you purchased cheap but was a color you hated,
what do you do? Do you drive around for years telling everyone you hate the color? Do you make an effort to change and repaint it? Or do you sell it? Which one of these options changes things for the better and discontinues the self-imposed suffering?
The complaining does no-one no-good. It only denigrates the stock you still own to other people. I myself do not care to help any supposed bankrupcy along with negative comments. But it is even easier for myself, as this company isn't going bankrupt. It's here to stay. After 7 years, no less.
David,
Let's talk a little bit about financing. If you listen to that video from August with Gabriel, it again gives a overview of what must happen in terms of sucesssion in order to proceed with a financing/spinoff plan that will be attractive to a lender, ( one that is not necessarily from this country). We need to remind ourselves of the difficulty and steps that must be taken even in the preliminary stages.
1. Gabriel is going to have to present a full plan to interested lenders that shows a total breakdown of where the company is going, with a structure that incorporates the "spinoff" but has been APPROVED by the SEC. That right there is time. We all saw the slide show with the projected earnings and cash flow that was presented in October. That will be part of the business plan laid out to lenders.
2. This is not your typical home loan or your small business
loan. It is a lot of money that is not guaranteed by the FHA or even collateralized by tangible liquidities. I.E., Gabriel will have to have serious ducks in a row to show where this company is going, and the best way to do that is to start producing revenues from the projected income sources laid out in the plan, and to have the SEC stamp of approval on the goods. If you were a lender, would you touch a spinoff w/out SEC approval?
3. This is all going to take time. But the fact that we aren't hearing much from the company is probably a good thing. Because it is standard proceedure. Once again I will state, and only as my opinion, that Gabriel et al are going about this process in a diligent and meticulous manner, and have had the shareholders along with the benefit of the company first and foremost in their sights. This will not happen in one day, or even 7 years and one day for that matter. LOL
Regards!
BigLab,
Nice post. And very true. I have been here 7 years also, but am excited to see how well this company has kept up and used this time to apply it's science. Where others have persecuted the officers of this company for non-performance, I have never lost faith in their direction and ability to accomplish in eventuality those goals that will be a standard of this segment of the biotech industry. As a matter of fact, my opinion is that they have done quite well, considering all of those obstacles inherent to this particular realm, biotech research. There are a lot of laymen out there, (and right here) who have no idea as to the difficulty of extrapolating and implementing this type of research and discovery. It is obvious that you do understand, though.
There will be people bashing their heads against the wall when the vibility here is finally proven. Even now, if you look at daily chart volume of buys and sells, there are large blocks of buys sneaking thru every day, outnumbering sells. Someone knows.
mcmartin,
I thought I heard mention that Gabriel had said there would be a "sient period of 90 days while financing was undertaken, which would mean supposedly that something was in the works. But here is a qoute from other companies:
"In order to prevent the leakage of financial information and provide fairness to stockholders, the company has instituted a silent period" commencing 21 days before year end..etc, etc
" The company has implemented a silent period which will take place 14 days prior to the first quarterly financial reports of 2007, and will engage a policy of the suspension of all corporate board meetings, manager meetings, and communication with stockholders and the news media...."
I guess it makes it easier to track down a leak in the company if somene lets insider news out or uses it to gain an advantage. Don't know if DNAP is in a silent period. You can take the non-response from "Louise" in several different ways. The last thing you want is somebody or something messing with your SEC process while awaiting approval on financing or stock/company restructure(which DNAP is doing), especially when it appears you have some rivals out there.
A positive attitude can carry you miles past any hardship. Doubting will get you nowhere. The money is already spent.
Nothing to lose here other than self-composure.
DNAP will survive and thrive.