Nanobac Announces Mayo Clinic Researchers Audio Interview

Last update: 9:47 a.m. EDT April 8, 2008

TAMPA, FL, Apr 08, 2008 (MARKET WIRE via COMTEX) -- Nanobac Pharmaceuticals, Inc. ("Nanobac" or "the Company") announces an audio interview of scientists at Mayo Clinic that discusses calcifying nanoparticles (CNPs or NPs) in arterial and kidney stone disease. The researchers discuss CNPs both as a cause and accelerant of diseases. Please go to Nanobac's website or www.lifelines.tv and listen to Episode 7.

Nanoparticles, which are 1,000 times smaller than a bacterium, are being manufactured and incorporated into some commercial products such as cosmetics and clothing. While nanotechnology holds promise, there is little understanding of how these super small particles might affect us if they get inside our bodies.

Two researchers from the Mayo Clinic College of Medicine will tell us about their research investigating the role these particles might play in disease. John Lieske will talk about his research on the role one nanoparticle may play in the development of kidney stones. And Virginia Miller will tell us about her work on a nanoparticle that may play a role in hardening of the arteries.

Drs. Lieske and Miller will lead a symposium on this topic at the Experimental Biology Conference on Wednesday, April 8.

About Pathologic Calcific Diseases

Irregular calcium deposits are implicated in inflammatory diseases such as heart disease, prostatitis and arthritis, and stone forming diseases such as kidney and gall stones. The impact on the health care delivery system could be substantial given that billions of dollars are spent each year on treating diseases associated with CNPs. The company is well positioned to take advantage of numerous diagnostic and therapeutic opportunities in these sectors.

Nanobac Pharmaceuticals, Inc. has moved its corporate office to 3000 Bayport Drive, Suite 910 Tampa, Florida 33607. The new phone number is 813 865-1125. For more information, visit our website at: http://www.nanobac.com.

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Self-Propagating Calcifying Nanoparticles as a Unique Entity

Nanobac Announces Peer Reviewed Publication Verifying Self-Propagating Calcifying Nanoparticles as a Unique Entity

"CNPs" Hypothesized to Resemble Prions

Last update: 11:08 a.m. EDT April 8, 2008

TAMPA, FL, Apr 08, 2008 (MARKET WIRE via COMTEX) -- Nanobac Pharmaceuticals, Inc.NNBP ("Nanobac" or "the Company") announces the multicenter publication of independent research, which reports on the characterization of calcifying nanoparticles (CNPs), formerly known as "nanobacteria," as self-propagating mineral protein complexes. The study was led by a leading French microbiologist, the esteemed professor Didier Raoult (Raoult et al, PLoS Pathogens, February 2008, volume 4, issue 2).

The authors undertook a comprehensive analysis of CNPs utilizing a Nanobacterium strain provided by Nanobac's Chief Research and Science Officer Dr. Olavi Kajander. Their goal was to gain better insight into "such a propagating calcifying agent putatively endowed with pathogenic properties." To address this question, the researchers examined CNPs' propagation conditions, susceptibility to various chemical and physical treatments and their effect on cell viability. CNPs' nucleic acid and proteomic content were also analyzed.

Dr. Kajander stated: "The Raoult study confirms the presence of protein-mineral complexes, consistent with complexes published in Nanobac's Patent Applications, which characterized numerous proteins including fetuin, that the French group studied. The group also hypothesized the conformational change of the proteins being similar to those observed in prions, confirming our position. The study also confirmed that the Company's patented 8D10 antibody effectively detected CNPs as a unique pathogen."

"This work has significant diagnostic implications and supports our findings. The published paper should end discussion about whether CNPs exist, and shift the focus on what they really are and what role they play in various diseases," said Dr. Benedict Maniscalco, Co-Chairman and Chief Medical Officer of Nanobac Pharmaceuticals.

About Pathologic Calcific Diseases

Irregular calcium deposits are implicated in inflammatory diseases such as heart disease, prostatitis and arthritis, and stone forming diseases such as kidney and gall stones. The impact on the health care delivery system could be substantial given that billions of dollars are spent each year on treating diseases associated with CNPs. The company is well positioned to take advantage of numerous diagnostic and therapeutic opportunities in these sectors.

Nanobac Pharmaceuticals Inc. has moved its corporate office to 3000 Bayport Drive, Suite 910 Tampa, Florida 33607. The new phone number is 813 865-1125. For more information, visit our website at: http://www.nanobac.com.

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Polluting nanoparticles and CNPs - Questions

Study shows how ultrafine particles in air pollution may cause heart disease

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Nice post. I wonder if this finding hurts the claims of Nanobac?
The questions that come to mind are:
Does Nanobac need to prove that the CNP we are studying are alive?
Doesn't the claim you referenced seem to contradict that the plaque buildup in the arteries is primarily the CNPs which we believe are our living little creatures?
Does our IP cover the possible eradication processes if the nanoparticles are pollution based and not alive as we believe?
Many questions but you seem to be of better overall understanding than I so any answer or opinion would be appreciated. Thanks C

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It IS surprisingly similar!!

Nanoparticles from this recent study seem to cause problems. Are calcifying nanoparticles involved? They do not say the are not - perhaps they have never heard of CNPs!! It would be prudent, IMO, to get both research groups together to analyze ALL their findings and determine EXACTLY what is going on to cause this disease process.

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Air pollution may cause heart disease

By

Rachel Champeau 1/17/2008 1:00:00 PM

Patients prone to heart disease may one day be told by physicians to avoid not only fatty foods and smoking but air pollution too.

A new academic study led by UCLA researchers has revealed that the smallest particles from vehicle emissions may be the most damaging components of air pollution in triggering plaque buildup in the arteries, which can lead to heart attack and stroke. The findings appear in the Jan. 17 online edition of the journal Circulation Research.

The scientists identified a way in which pollutant particles may promote hardening of the arteries — by inactivating the protective qualities of high density lipoprotein (HDL) cholesterol, known as "good" cholesterol.

A multicampus team from UCLA, the University of Southern California, the University of California, Irvine, and Michigan State University contributed to the research, which was led by Dr. Andre Nel, UCLA's chief of nanomedicine. The study was primarily funded by the National Institute of Environmental Health Sciences and the U.S. Environmental Protection Agency (EPA).

"It appears that the smallest air pollutant particles, which are the most abundant in an urban environment, are the most toxic," said first author Dr. Jesus Araujo, assistant professor of medicine and director of environmental cardiology at the David Geffen School of Medicine at UCLA. "This is the first study that demonstrates the ability of nano-sized air pollutants to promote atherosclerosis in an animal model."

Nanoparticles are the size of a virus or molecule — less than 0.18 micrometers, or about one-thousandth the size of a human hair. The EPA currently regulates fine particles, which are the next size up, at 2.5 micrometers, but doesn't monitor particles in the nano or ultrafine range. These particles are too small to capture in a filter, so new technology must be developed to track their contribution to adverse health effects.

"We hope our findings offer insight into the impact of nano-sized air pollutant particles and help explore ways for stricter air quality regulatory guidelines," said Nel, principal investigator and a researcher at UCLA's California NanoSystems Institute.

Nel added that the consequences of air pollution on cardiovascular health may be similar to the hazards of secondhand smoke.

Pollution particles emitted by vehicles and other combustion sources contain a high concentration of organic chemicals that could be released deep into the lungs or even spill over into the systemic circulation.

The UCLA research team previously reported that diesel exhaust particles interact with artery-clogging fats in low-density lipoprotein (LDL) cholesterol to activate genes that cause the blood-vessel inflammation that can lead to heart disease.

In the current study, researchers exposed mice with high cholesterol to one of two sizes of air pollutant particles from downtown Los Angeles freeway emissions and compared them with mice that received filtered air that contained very few particles.

The study, conducted over a five-week period, required a complex exposure design that was developed by teams led by Dr. Michael Kleinman, professor of community and environmental medicine at UC Irvine, and Dr. Constantinos Sioutas, professor of civil and environmental engineering at USC.

Researchers found that mice exposed to ultrafine particles exhibited 55 percent greater atherosclerotic-plaque development than animals breathing filtered air and 25 percent greater plaque development than mice exposed to fine-sized particles.

"This suggests that ultrafine particles are the more toxic air pollutants in promoting events leading to cardiovascular disease," Araujo said.

Pollutant particles are coated in chemicals sensitive to free radicals, which cause the cell and tissue damage known as oxidation. Oxidation leads to the inflammation that causes clogged arteries. Samples from polluted air revealed that ultrafine particles have a larger concentration of these chemicals and a larger surface area where these chemicals thrive, compared with larger particles, Sioutas noted.

"Ultrafine particles may deliver a much higher effective dose of injurious components, compared with larger pollutant particles," Nel said.

Scientists also identified a key mechanism behind how these air pollutants are able to affect the atherosclerotic process. Using a test developed by Dr. Mohamad Navab, study co-author and a UCLA professor of medicine, researchers found that exposure to air pollutant particles reduced the anti-inflammatory protective properties of HDL cholesterol.

"HDL normally helps reduce the vascular inflammation that is part of the atherosclerotic process," said Dr. Jake Lusis, study co-author and a UCLA professor of cardiology, human genetics and microbiology, immunology and molecular genetics. "Surprisingly, we found that exposure to air pollutant particles, and especially the ultrafine size, significantly decreased the positive effects of HDL."

To explore if air particle exposure caused oxidative stress throughout the body — which is an early process triggering the inflammation that causes clogged arteries — researchers checked for an increase in genes that would have been activated to combat this inflammatory progression.

"We found greater levels of gene activation in mice exposed to ultrafine particles, compared to the other groups," Lusis said. "Our next step will be to develop a biomarker that could enable physicians to assess the degree of cardiovascular damage caused by air pollutants or measure the level of risk encountered by an exposed person."

Researchers added that previous studies assessing the cardiovascular impact of air pollution have taken place over longer periods of exposure time, such as five to six months. The current study demonstrated that ill effects can occur more quickly, in just five weeks.

"Further study will pinpoint critical chemical and toxic properties of ultrafine particles that may affect humans," Nel said.

The research team included investigators from the fields of nanomedicine, cardiology and genetics. Additional co-authors included Berenice Barajas, Xuping Wang, Brian J. Bennett and Ke Wei Gong of the David Geffen School of Medicine at UCLA, and Jack Harkema from the department of pathobiology and diagnostic investigation at Michigan State University.

Additional grant support was provided by the National Institute of Allergy and Infectious Diseases; the National Heart, Lung and Blood Institute; and the Robert Wood Johnson Foundation.

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Human-derived nanoparticles and vascular response to injury in rabbit carotid arteries: Proof of principle

International Journal of Nanomedicine

Human-derived nanoparticles and vascular response to injury in rabbit carotid arteries: Proof of principle

Maria A K Schwartz1, John C Lieske2, Vivek Kumar2, Gerard Farell-Baril2, Virginia M Miller1,3

1Departments of Physiology and Biomedical Engineering, Internal Medicine; 2Division of Nephrology, and 3Surgery, Mayo Clinic College of Medicine, Rochester, MN, USA

Abstract: Self-calcifying, self-replicating nanoparticles have been isolated from calcified human tissues. However, it is unclear if these nanoparticles participate in disease processes. Therefore, this study was designed to preliminarily test the hypothesis that human-derived nanoparticles are causal to arterial disease processes. One carotid artery of 3 kg male rabbits was denuded of endothelium; the contralateral artery remained unoperated as a control. Each rabbit was injected intravenously with either saline, calcified, or decalcified nanoparticles cultured from calcified human arteries or kidney stones. After 35 days, both injured and control arteries were removed for histological examination. Injured arteries from rabbits injected with saline showed minimal, eccentric intimal hyperplasia. Injured arteries from rabbits injected with calcified kidney stone- and arterial-derived nanoparticles occluded, sometimes with canalization. The calcified kidney stone-derived nanoparticles caused calcifications within the occlusion. Responses to injury in rabbits injected with decalcified kidney stone-derived nanoparticles were similar to those observed in saline-injected animals. However, decalcified arterial-derived nanoparticles produced intimal hyperplasia that varied from moderate to occlusion with canalization and calcification. This study offers the first evidence that there may be a causal relationship between human-derived nanoparticles and response to injury including calcification in arteries with damaged endothelium.

Keywords: arterial calcification, endothelial injury, intimal hyperplasia

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Association of Nanoparticle and Kidney Stone Formation

Nanobac Announces Publication of Association of Nanoparticle and Kidney Stone Formation

Results May Change Approach to Medical Management of Kidney Stones

Last update: 11:28 a.m. EST Feb. 19, 2008

TAMPA, FL, Feb 19, 2008 (MARKET WIRE via COMTEX) -- Nanobac Pharmaceuticals Inc. ("Nanobac" or "the Company") announces publication in the International Journal of Nanomedicine research that scientists from the University of California San Francisco collaborating with Nanobac scientists at NASA's Johnson Space Center have concluded demonstrating that calcium deposits in the human kidney called Randall's Plaque may in fact be Calcifying Nano Particles (CNPs, also referred to as nanobacteria) which lead to the formation of Kidney Stones.

The study, led by Marshall Stoller M.D. of UCSF and Neva Ciftcioglu, formerly Nanobac's Director of Science at NASA Johnson Space Center, found that CNPs were identified and cultured from Randall's Plaques and detected by Nanobac's proprietary diagnostics. This could represent potential new early diagnosis and treatment opportunities for patients who suffer from Kidney Stones.

Dr. Olavi Kajander, Nanobac's Chief Research and Science Officer, stated: "A strong link was found between the presence of Randall's Plaques and the detection of CNPs. These results suggest new insights into the etiology of Randall's Plaque formation, and will help us understand the pathogenesis of stone formation. Further studies on this topic may lead to new approaches on early diagnosis and novel medical therapies of kidney stone formation."

Nanobac Pharmaceuticals Inc. is headquartered in Tampa, Florida. For more information, visit our website at: http://www.nanobac.com .

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Article - International Journal of Nanomedicine
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International Journal of Nanomedicine

Issue: ON-LINE EARLY
Pages: 0-0

Association between Randall’s plaque and calcifying nanoparticles

Neva Çiftçioglu1, Kaveh Vejdani2, Olivia Lee2, Grace Mathew1, Katja M Aho3, E Olavi Kajander4, David S McKay5, Jeffrey A Jones5, Marshall L Stoller2

1Nanobac Pharmaceuticals, Johnson Space Center, Houston, TX, USA; 2Department of Urology, University of California at San Francisco, San Francisco, CA, USA; 3University of Kuopio, Department of Biosciences/Biochemistry, Kuopio/Finland; 4Nanobac Pharmaceuticals, Tampa, FL, USA; 5National Aeronautics and Space Administration, Lyndon B. Johnson Space Center, Houston, TX, USA

Objectives: Randall initially described calcified subepithelial papillary plaques, which he hypothesized as nidi for urinary calculi. The discovery of calcifying nanoparticles (CNP), also referred to as nanobacteria, in calcified soft tissues has raised another hypothesis about their possible involvement in urinary stone formation. This research is the first attempt to investigate the potential association of these two hypotheses.

Methods: We collected renal papilla and blood samples from 17 human patients who had undergone laparoscopic nephrectomy. Immunohistochemical staining (IHS) was applied using monoclonal antibody (mAb) against CNP. Homogenized papillary tissues and serum samples were cultured for CNP. Scanning electron microscopy (SEM) and energy dispersive X-ray spectroscopy (EDS) were performed on papillary samples. Serum samples were tested for CNP antigen and antibody with enzyme-linked immunosorbent assay (ELISA).

Results: Randall’s plaques (RP) were visible on gross inspection in 11 out of 17 samples. IHS was positive for CNP antigen in 8 of the visually positive samples, but in only 1 of the remaining samples. SEM revealed spherical apatite-formations in 14 samples confirmed by EDS analysis. In cultures, all serum samples and 13 tissue homogenates grew CNP. In ELISA, 14 samples were positive for CNP-antigen and 11 samples were positive for CNP-antibody.

Conclusion: There was evidence of a link between detection of CNP and presence of RP. Although causality was not demonstrated, these results suggest that further studies with negative control samples should be made to explore the etiology of RP formation, thus leading to a better understanding of the pathogenesis of stone formation.

Keywords: calcifying nanoparticles, nanobacteria, Randall’s plaque, urinary stone

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