Reversing Heart Disease with EDTA by Jeffrey Dach MD

http://www.alive.com/articles/view/19103/the_nanobacteria_revolution
The Nanobacteria Revolution  by Zoltan P. Rona, MD, MSc

Dr. Zoltan P. Rona is a graduate of McGill University Medical School (1977) and has a Master’s Degree in Biochemistry and Clinical Nutrition from the University

I have been using the nanobacteria treatment protocol in my practice for nearly a year now, mostly on people who have been advised by their specialists that they would have to live with their symptoms and no alternatives were available. Even in such severe cases, I have noticed at least a 75-percent improvement in arterial plaque (as seen on ultrasounds and CT scans) as well as in symptoms such as low energy, chest pain, and stamina.

Zoltan P. Rona, MD, MSc, has a private medical practice in Toronto.

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COM-ET  NANOBACTX

2004

1) http://www.pathophysiologyjournal.com/article/S0928-4680%2804%2900079-3/abstract
Maniscalco, B.S., Mezo, G.S. Calcification in coronary artery disease can be reversed.Intl Journal of Pathophysiology.11(2): 95-101. Pathophysiology 11 (2004) 95–101
Calcification in coronary artery disease can be reversed by
EDTA–tetracycline long-term chemotherapy
Benedict S. Maniscalco a, Karen A. Taylor b,*
a 4730 N. Habana Avenue, Suite 201, Tampa, FL 33614, USA
b PA-C 2727 W. Martin Luther King Blvd., Suite 850, Tampa, FL 33607, USA

Abstract

Atherosclerosis is a complex process with multiple mechanisms and factors contributing to its initiation and progression. Detection and quantification of coronary artery calcium (CAC) scores with electron beam tomography has been shown to correlate with obstructive and nonobstructive coronary artery disease (CAD). Pathogen-triggered calcification could play a role in CAD. Recent reports suggest that infectious blood nanobacteria (NB) emerge to be such a trigger. So far, minimal or no reversal of atherosclerosis has been claimed by therapies with iv ethylenediaminetetraacetic acid disodium salt (EDTA), antibiotics, or other regimens, and therapies for atherosclerosis remain non-curative. We have now combined EDTA with antibiotic tetracycline (comET), an in vitro proven nanobacteriocidal treatment, and tested comET therapy in patients with documented CAD. Three hypotheses were probed: (1) Are NB present in patients with CAD?; (2) Does treatment with comET affect blood NB antigen and serology?; (3) Does a comET decrease CAC scores?

One hundred patients with stable CAD and positive CAC scores were enrolled into a 4 month study of comET therapy. ComET therapy is composed of
(1) Nutraceutical Powder (Vitamin C, Vitamin B6, Niacin, Folic Acid, Selenium, EDTA, l-Arginine, l-Lysine, l-Ornithine, Bromelain, Trypsin, CoQ10, Grapeseed Extract, Hawthorn Berry, Papain) 5cm3 taken orally every evening;
(2) Tetracycline HCl 500mg taken orally every evening;
(3) EDTA 1500mg taken in a rectal suppository base every evening.
CAC scoring was repeated at 4 months and serum samples were analyzed for NB antigen and serology at baseline, 2 and 4 months. Complete blood count, metabolic panel, liver function, C-reactive protein (hs-CRP) and lipids were analyzed at baseline and 4 months.

Seventy-seven patients completed the study and all patients were positive for NB serology, antigen or both. Responders (n = 44; 57%) had significant decreases in total CAC scores (P = 0.001), the average decrease being 14%. Non-responders (n = 33; 44%) had no change or had increases in CAC scores. Angina was decreased or ablated in 16 of 19 patients (84%). Lipid profiles improved to non-atherogenic direction significantly (P = 0.001), a remarkable finding in a patient group where 86% were on continuous statin medication already before the trial. No adverse physiologic effects were seen in renal, hepatic, or hematopoetic systems.

In conclusion, CAC scores decreased during ComET therapy trial in most CAD patients inferring regression of calcified coronary artery plaque volume. The patients tolerated the therapy well and their angina and lipid profiles improved. Further treatment trials for long term therapy with matched controls are warranted.

 

UroBac

In 10 patients who underwent transrectal ultrasound after therapy prostatic stones were decreased in size or resolved in 50%.

2) http://www.ncbi.nlm.nih.gov/pubmed/15643213  available full text pdf
J Urol. 2005 Feb;173(2):474-7.
Anti-nanobacterial therapy for men with chronic prostatitis/chronic pelvic pain syndrome and prostatic stones: preliminary experience.
Shoskes DA1, Thomas KD, Gomez E.
Category III chronic prostatitis/chronic pelvic pain syndrome (CPPS) is a common debilitating condition of unclear etiology. Patients often have prostatic calcifications but a link to symptoms is controversial. Nanobacteria are implicated in stone formation in the urinary tract and, therefore, therapy to eliminate nanobacteria and the stones that they produce might have an impact on CPPS symptoms.
MATERIALS AND METHODS:A total of 16 men with recalcitrant CPPS refractory to multiple prior therapies were treated with comET (Nanobac Life Sciences, Tampa, Florida), which consists of 500 mg tetracycline, a proprietary nutraceutical and an ethylenediaminetetraacetic acid suppository daily. The National Institute of Health Chronic Prostatitis Symptom Index (NIH-CPSI), transrectal ultrasound, and blood and urine tests for nanobacterial antigen were performed at the start and conclusion of 3 months of therapy. One patient was lost to followup.
RESULTS:Mean NIH-CPSI total score +/- SD decreased from 25.7 +/- 1.6 to 13.7 +/- 2.0 (p <0.0001). Significant improvement was seen in each subscore domain. A total of 12 patients (80%) had at least 25% improvement on NIH-CPSI and 8 (53%) had at least 50% improvement. Nanobacterial antigen or antibody was found in 60% of serum and 40% of urine samples. In 10 patients who underwent transrectal ultrasound after therapy prostatic stones were decreased in size or resolved in 50%.
CONCLUSIONS:Therapy designed to eliminate nanobacteria resulted in significant improvement in the symptoms of recalcitrant CPPS in the majority of men, whether due to the treatment of stone producing nanobacteria or through some other mechanism. Prospective placebo controlled trials are warranted.

3) http://www.ncbi.nlm.nih.gov/pubmed/17140745
Med Hypotheses. 2007;68(6):1348-50. Epub 2006 Nov 30.
The risk of urolithiasis recurrence may be reduced with anti-nanobacterial therapy.  Silay MS1, Miroglu C.
Urolithiasis is a common disorder responsible for serious human suffering and economic cost to society. Approximately 13% of men and 7% of women in the United States will be diagnosed with urolithiasis at some time in their lives with a recurrence rate of more than 50% in 5 years. Even if some risk factors are defined for stone formation, none of them can fully explain the etiopathogenesis. A controversial pathogen bacteria called ‘nanobacteria’ (NB) has been associated with several diseases including stone formation in some studies. It is thought to be the nidi for the stone formation after its’ isolation from the renal stones and the occurrence of the stone after the percutaneus renal injection of NB. The clinical trials demonstrated that the eradication of NB prevented the calcifications in coronary arteries and prostate with an acceptable level by performing a novel combination therapy called ‘ComET’ which comprises a tetracycline antibiotic, nutraceutical and EDTA. Based on these findings, we hypothesize that the risk of urolithiasis recurrence may be reduced with combined anti-nanobacterial therapy. Long term prospective studies should be designed for evaluating the patients with positive NB cultures. If our hypotheses can be further supported with clinical trials it may change the approach of the medical management for urolithiasis.

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James Roberts MD

6) http://www.heartfixer.com/Nanobacterium/IndexNB.htm
Nanobacterium Sanguineum Home Page

http://www.heartfixer.com/Nanobacterium/NB%20-%20Case%20Studies.htm
Case Studies from our 1st 250  Patients James Roberts MD

Com-ET  study

77 patients with stable CADz and + CT Coronary calcium scans
• 57% responded with a decrease in calcium score (mean reduction 14%)
• Natural history is to increase by ≈ 44% per year

 

 

Role of Vitamin K in reversing CAC

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You Tube Videos

<iframe width=”420″ height=”315″ src=”//www.youtube.com/embed/PXO58edpIU8” frameborder=”0″ allowfullscreen></iframe>
First Live Video of Calcifying Nanoparticles

<iframe width=”420″ height=”315″ src=”//www.youtube.com/embed/zgNYaJPwvyQ” frameborder=”0″ allowfullscreen></iframe>
Nanobiotech Pharma Research
Gary Steven Mezo Gary Steven Mezo

<iframe width=”560″ height=”315″ src=”//www.youtube.com/embed/9W-PoQSKNfU?list=PL8D9545766A510E09” frameborder=”0″ allowfullscreen></iframe>
Uploaded on Mar 10, 2011
FOX NEWS REPORT on our research and development of NanobacTX at NanoBiotech Pharma. Nanobacteria the infectious cause of coronary artery calcification and heart disease. Heart Disease is a treatable infection. Heart Disease can be reversed and coronary artery plaque can be dissolved safely at home with NanobacTX. Learn more and get treatment at: www.nanobiotech.us or email at info@nanobiotech.us

all videos
http://www.youtube.com/user/gm2751?feature=watch

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2005 Nexus Magazine

5) http://www.bibliotecapleyades.net/salud/esp_salud27.htm
Nanobacteria link to heart disease by Douglas Mulhall
Extracted from Nexus Magazine.  Volume 12, Number 5 (August – September 2005) from NexusMagazine Website

 

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2004 New Scientist

http://www.newscientist.com/article/dn5009-nanobacteria-revelations-provoke-new-controversy.html?full=true#.UxrxdM6hbfg
Nanobacteria revelations provoke new controversy   May 2004 by Jenny Hogan

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references on the NanoBiotech Pharma Web Site:

2012

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3266001/#__ffn_sectitle
Int J Nanomedicine. 2012; 7: 339–350. Anton G Kutikhin, Elena B Brusina, and Arseniy E Yuzhalin Published online Jan 19, 2012. The role of calcifying nanoparticles  in Biology & Medicine

at the present time the theory about CNPs being mineralo-protein complexes has the better hand.

The only obstacle in establishing CNPs as living organisms is an absence of a fairly accurately sequenced genome at the present time, but it itself is not able to counter the theory that they are the smallest self-replicating life forms on Earth in favor of the theory that they are physicochemical mineralo-protein complexes.

Shoskes et al36 found that comET therapy (tetracycline + ethylenediaminetetraacetic acid [EDTA] + nutrients) for 3 months leads to at least a 25% improvement of conditions in 80% of patients with this disorder (according to the National Institute of Health Chronic Prostatitis Symptom Index) resistant to other therapeutic modalities, and in 53% of cases this parameter was higher than 50%. The size of stone decreased at least twofold in 50% of patients according to the results of a transrectal ultrasound test.

discussions about the nature of CNPs will continue until their genome can be fairly accurately sequenced. However, it is clear that CNPs play an important role in the etiopathogenesis of many diseases,

Two papers indicate comET-therapy as a possible effective method of treatment of CNP-associated diseases.36,41

 

_____________________________

 

Individual Research and Study Articles:

http://www.ncbi.nlm.nih.gov/pubmed/16196199
Puskas, L. G., L. Tiszlavicz, Zs Razga, L. Torday, T. Krenacs, J. G Papp. Detection of nanobacteria-like particles in human atherosclerotic plaques. Acta Biologica Hungarica 56 (3-4): 233-245.

 

Chang. Nanobacteria-caused mitral valve calciphylaxis in a man with diabetic renal failure.South Med J.Feb; 97 (2): 194- 198.

Maniscalco, B.S., Mezo, G.S. Calcification in coronary artery disease can be reversed.Intl Journal of Pathophysiology.11(2): 95-101.

Miller, V. M., G. Rodgers, J. A. Charlesworth, B. Kirkland, S. R. Severson, T. E. Rasmussen, M. Yagubyan, J. C. Rodgers, F. R Cockerill, III, R. L. Folk, V. Kumar, G. Farell-Baril, J. C. Lieske. MayoClinic. Evidence of nanobacterial-like structures in human calcified arteries and cardiac valves. Am J Physiol Heart Circ Physiol.287 (3): H1115-24.

5.Ciftcioglu, N., D. S. McKay, E.O. Kajander. Association between nanobacteria and periodontal disease.Circulation.108:e58-9.

6.Kajander, E O.Nanobacteria do exist and actively participate in the calcification of arterial plaque.Townsend Letter 234:80-82.

7.Sedivy, R., and W. B. Battistutti. Nanobacteria promote crystallization of psammoma bodies in ovarian cancer.APMIS III.951-4.

8.Sommer, A. P., U. Oron, A. M. Pretorius, D. S. McKay, N. Ciftcioglu, A. R. Mester, E. O. Kajander and H. T. Whelan, NASA-JSC. Light-modulated replication of nanobacteria and heart disease.J. Clin. Laser Med. Surg.21 (4): 231-235.

9.Ciftcioglu, N., M. A. Miller-Hjelle. J. T. Hjelle and E. O. Kajander.Inhibition of Nanobacteria as measured by a modified microdilution method.Antimicrob Agents Chemother.46: 2077-2086.Click here to view study

10.Kajander, E. O., K. Aho and V. Segal. Apatite biofilm forming agent: nanobacteria as a model system for biomineralization and biological standard for noa, a preliminary study.Proceedings of the 2nd International Conference on Near-Field Optical analysis. Houston, Texas.

11.Rasmussen, T. E., B. L. Kirkland, J. Charlesworth, et al.Electron microscope and immunological evidence of nanobacteria in calcified carotid arteries, aortic aneurysms and cardiac valves.J Am Coll Cardiol Abstracts Book.1009-79: 206A.

Lopez-Brea M., R. Selgas.Nanobacteria as a cause of renal diseases and vascular calcifying pathology in renal patients (endovascular lithiasis).Enferm Infec. Microbiol. Cli. (Spanish).18(10):491-492.

12.Ciftcioglu, N., V. Ciftcioglu, H. Vali, E. Turcott, E. O. Kajander. Sedimentary rocks in our mouth: dental pulp stones made by nanobacteria. Proc. SPIE.3441: 130-135.Click here to view study
Studies specific to Pathological Calcification & CNPs (aka Nanobacteria):

2.Kajander EO. Nanobacteria – propagating calcifying nanoparticles. Lett Appl Microbiol. 2006 Jun; 42(6):549-52. Click here to view study



8.Wang, X.J., Liu, W., Yang, Z.L., Wei, H., Wen, Y., Li, Y.G. 2004. The detection of nanobacteria infection in serum of healthy Chinese people. Zhonghua Liu Xing Bing Xue Za Zhi. 25(6): 494-4. Click here to view study

9.Wilk, I., G. Martirosian, K. Z. Mikrobiologii, S. A. Medycznei, Khatowice. 2004. Nanobacteria microbiological characteristic. Postepy Hig Med Dosw (online), 2004; 58: 60-64. Click here to view study

10.Aho K, Kajander EO. 2003. Detection of novel nanoorganisms .J Clin Microbiol. 41(7): 3460-3461. Click here to view study

Barr S. C., R. A. Linke, D. Janssen, C. L. Guard, M. C. Smith, C. S. Daugherty, J. M. Scarlett. 2003. Detection of biofilms formation and nanobacteria under long-term cell culture conditions in serum samples of cattle, goats, cats and dogs. Am J Vet Res. 64(2):176-182.

11.Miller-Hjelle, M. A., J. T. Hjelle, N. Ciftcioglu and E. O. Kajander. 2003. Nanobacteria: methods for growth and identification of this recently discovered calciferous agent. Rapid Analytical Microbiology. The chemistry and physics of microbial identification. Ed. . Olson. PDA, Bethesda, MD, USA. 297-312. Click here to view study

12.Miller-Hjelle, M. A., S. L. Stobbs, I. R. Poxton, J. T. Hjelle. 2003. Nanobacteria antigen and antibody titres in USA controls compared to UK controls and kidney disease patients. 13th European Congress of Clinical Microbiology & Infectious Diseases. P1663. Click here to view study

13.Sedivy, R., and W. B. Battistutti. 2003. Nanobacteria promote crystallization of psammoma bodies in ovarian cancer. APMIS III. 951-4. Click here to view study

15. Sommer, A. P., D. S. McKay, N. Ciftcioglu, U. Oron, A. R. Mester, and E. O. Kajander. 2003. Living nanovesicles-chemical and physical survival strategies of primordial biosystems. Perspectives, J. Proteome Res. 2:441-443. Click here to view study

16.Sommer, A. P., U. Oron, A. M. Pretorius, D. S. McKay, N. Ciftcioglu, A. R. Mester, E. O. Kajander and H. T. Whelan. 2003. A preliminary investigation into light-modulated replication of nanobacteria and heart disease. J. Clin. Laser Med. Surg. 21 (4): 231-235. Click here to view study

17.Ciftcioglu, N., M. A. Miller-Hjelle. J. T. Hjelle and E. O. Kajander. 2002. Inhibition of nanobacteria as measured by a modified microdilution method. Antimicrob Agents Chemother. 46: 2077-2086. Click here to view study

18.Kajander, E. O., K. Aho and V. Segal. October, 2002. Apatite biofilm forming agent: nanobacteria as a model system for biomineralization and biological standard for noa, a preliminary study. Proceedings of the 2nd International Conference on Near-Field Optical analysis: Photodynamic Therapy & Photobiology Effects. Houston, Texas. Click here to view study

Sommer A. P., H. I. Hassinen, E. O. Kajander. 2002. Light-induced replication of nanobacteria: a preliminary report. J Clin Laser Med Surg.20(5):241-244.www.ncbi.nlm.nih.gov

19.Sommer, A. P., U. Oron, E. O. Kajander and A. R. Mester. 2002. Stressed cells survive better with light. J. Proteome Res.1:475. Click here to view study

20.Breitschwerdt, E. B., Sushama, S., Cannedy, A., Hancock, S. I., Bradley. J. M. 2001. Infection with Bartonella weissii and detection of nanobacterium antigens in a North Carolina beef herd Journal of Clinical Microbiology. 879-882. Click here to view study

21.Vali, H., M. D. McKee, N. Ciftcioglu, S. K. Sears, F. L. Plows, E. Chelvet, P. Ghiasi, E. O. Kajander and R. N. Zare. 2001. Nanoforms: a new type of protein-associated mineralization. Geochim.Cosmochim. Acta. 65:63-74. Click here to view study

22.Ciftcioglu, N. and E. O. Kajander. 2000. Nanobacterial growth factors for nanobacteria Proc. SPIE. 3755: 113-119. Click here to view study

23.Kajander, E. O. and N. Ciftcioglu. 2000. Nanobacteria as extremophiles Proc. SPIE. 3755: 106-112. Click here to view study

Vainshtein M. B., E. B. Kudriashova. 2000. About nanobacteria. Mikrobiologiia (Russian). 69(2):163-174. www.ncbi.nlm.nih.gov

Abbott, A. 1999. Battle lines drawn between nanobacteria researchers. 1999. Nature. 401 (6749):105. www.ncbi.nlm.nih.gov

24.Ciftcioglu, N. 1999. Microbial presence versus pathogenicity. Pleomorphic microbes in health and disease. Proceedings of the first annual symposium held June 18-19. Edited by: Gitte S. Jensen Ph.D. Holger N.I.S. Inc.; 49-53. Click here to view study

25.Kajander, E. O., M. Bjorklund, N. Ciftcioglu. 1999. Nanobacteria and man. Enigmatic Microorganisms and Life in Extreme Environments. Eds.J. Seckbach, Kluwer (the Netherlands). 195-204. Click here to view study

26.Kajander, E. O. 1999. Nanobacteria in health and disease. Pleomorphic microbes in health and disease. Proceedings of the first annual symposium held June 18-19, 1999. Edited by: Gitte S. Jensen Ph.D. Holger N.I.S. Inc. Hudson, Quebec; 43-48. Click here to view study

27.Kajander, E. O., T. Heinonen, I. Kuronen, K. Luoto and N. Ciftcioglu. 1999. A new problem for sterile filtration; nanobacteria. In Proceedings, WorldPharm. 99, October 26-28, 1999, Philadelphia. Advanstar Communications, Cleveland, OH. Pp. 243-252. Click here to view study

28.Kajander, E. O., T. Heinonen, I. Kuronen, K. Luoto, and N. Ciftcioglu. Nanobacteria, mycoplasma and bacterial l-forms; problems for sterile filtration. 30th R3. Nordic Contamination Control Symposium.Helsinki, Finland. Click here to view study

Southam, G., R. Donald. 1999. A structural comparison of bacterial microfossils vs. nanobacteria and nanofossils. Earth-Science Reviews.48 (4): 251-264.

29.Wainwright, M. 1999. Nanobacteria and associated elementary bodies in human disease and cancer. Microbiology. 145: 2623-2624. Click here to view study

30.Bjorklund, M., N. Ciftcioglu, E. O. Kajander. 1998. Extraordinary survival of nanobacteria under extreme conditions. Proc. SPIE. 3441: 123-129. Click here to view study

31.Carson, D. A. 1998. An infectious origin of extraskeletal calcification. PNAS.95: 7846-7847. Click here to view study

32.Ciftcioglu, N., E. O. Kajander. 1998. Interaction of nanobacteria with cultured mammalian cells. Pathophysiology. 4: 259-270. Click here to view study

33.Ciftcioglu, N., M. Bjorklund, E. O. Kajander. 1998. Stone formation and calcification by nanobacteria in human body. Proc. SPIE.3441: 105-111. Click here to view study

34.Ciftcioglu, N., V. Ciftcioglu, H. Vali, E. Turcott, E. O. Kajander. 1998. Sedimentary rocks in our mouth: dental pulp stones made by nanobacteria.Proc. SPIE. 3441: 130-135. Click here to view study

35.Kajander, E. O., M. Bjorklund and N. Ciftcioglu. 1998. Suggestions from observations on nanobacteria isolated from blood. Size limits of very small microorganisms: proceedings of a workshop, steering group on astrobiology of the Ciftcioglu, N., M. Bjorklund, K. Kuorikoski, K. Click here to view study

Bergstrom and EO. Kajander. 1999. Nanobacteria: An infectious cause for kidney stone formation. Kidney International. 56:1893-1898. studies board National Research Council; Washington, D.C. October 22-23. www.ncbi.nlm.nih.gov

36.Kajander, E. O., N. Ciftcioglu, M. Bjorklund. 1998. Mineralization by nanobacteria Proc. SPIE. 3441: 86-94. Click here to view study

37.Kajander, E. O., N. Ciftcioglu. 1998. Nanobacteria: An alternative mechanism for pathogenic intra- and extracellular calcification and stone formation Proc. Natl. Acad. Sci. USA 95: 8274-8279. Click here to view study

38.Akerman, K. K., J. T. Kuikka, N. Ciftcioglu, J. Parkkinen, K. A. Bergstrom, I. Kuronen, and E. O. Kajander. 1997. Radiolabeling and in vivo distribution of nanobacteria in rabbit. Proc. SPIE. 3111: 436-442. Click here to view study

39.Ciftcioglu, N., A. Pelttari, E. O. Kajander. 1997. Extraordinary growth phases of nanobacteria isolated from mammalian blood. Proc. SPIE. 3111: 429-435. Click here to view study

40.Cifcioglu, N., I. Kuronen, K. Akerman, E. Hiltunen, J. Laukkanen, E.O. Kajander. 1997. E. F. Brown, D. Burton, P. Doherty, J. Makalanos, E. Norrby. A new potential threat in antigen and antibody products: nanobacteria. Cold spring harbor laboratory. Vaccines 97. 99-103. Click here to view study

41.Kajander, E. O., I. Kuronen; K. Akerman, A. Pelttari, N. Ciftcioglu. 1997. Nanobacteria from blood, the smallest culturable autonomously replicating agent on earth. Proc. SPIE. 3111: 420-428. Click here to view study

42.Kajander, E. O., E. Tahvanainen, I. Kuronen, N. Ciftcioglu. 1994. Comparison of staphylococci and novel bacteria-like particles from blood. Zbl. Bakt. (Suppl.) 26: 147-149. Click here to view study

43.Akerman, K. K., I. Kuronen, and E. O. Kajander. 1993. Scanning electron microscopy of nanobacteria-novel biofilm producing organisms in blood. Scanning. 15 (Suppl.) 3:90-91. Click here to view study

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2006

http://yester.ispub.com/journal/the-internet-journal-of-microbiology/volume-2-number-1/nanobacteria-atherosclerosis-and-chlamydia-like-microorganisms-living-in-human-blood-as-normal-flora-a-hypothesis.html#sthash.oq1ZakDR.dpbs
E. Kalfin: Nanobacteria, Atherosclerosis, and Chlamydia-like Microorganisms Living in Human Blood as Normal Flora: A Hypothesis. The Internet Journal of Microbiology. 2006 Volume 2 Number 1. Laboratory of Microbiology, State University Hospital of Pulmonary Diseases Sofia Bulgaria

Abstract   Our attention to recent announcements concerning Nanobacteria as causing atherosclerosis, was drawn by an article of their discoverer, prof. Olavi Kajander, in which he informed of his Nanobacteria isolation in 5% of healthy 1,000-humans’ blood. This article clearly states the question how it is possible Nanobacteria to cause atherosclerosis, if they are found in only 5% of healthy human blood, and atherosclerosis is found in 100% of the elderly.
The isolated by us Chlamydia-like microorganisms were found at 100% in donors’ blood. Our hypothesis is that normally Chlamydia-like microorganisms defend human blood from external medium microorganisms’ invasions. However, in old-aged organism, they promote atherosclerosis by attaching with their pili to the arterial walls, thus supporting the following adhesion and consequent actions of all other known (described in scientific sources) factors, causing atherosclerosis – Nanobacteria, inflammation, cholesterol, triglycerides, fibrin, calcium salts, hypertension, smoking, heredity, etc. The isolation of Chlamydia-like microorganisms at 100% in human blood explains atherosclerosis progression in 100% of getting old-humans, as well as the arguable announcements in sources, according to which other Chlamydia (Chlamydia pneumoniae) take part in atherosclerosis pathogenesis.

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Stephen SInatra MD  2002

http://www.a4t.org/Health/nanobacteria.html
Nanobacteria: Major Breakthrough in Arterial Health
By Stephen Sinatra, MD, FACC, FACN
Nanobacteria Implicated in Most All Degenerative Diseases
Major Breakthrough in Arterial Health is an excerpt from the June ’02 issue of The Sinatra Health Report,

2004

http://ajpheart.physiology.org/content/287/3/H1115
Evidence of nanobacterial-like structures in calcified human arteries and cardiac valves.  Virginia M. Miller , George Rodgers , Jon A. Charlesworth , Brenda Kirkland , Sandra R. Severson , Todd E. Rasmussen , Marineh Yagubyan , Jeri C. Rodgers , Franklin R. Cockerill III, Robert L. Folk , Ewa Rzewuska-Lech , Vivek Kumar , Gerard Farell-Baril , John C. Lieske
American Journal of Physiology – Heart and Circulatory Physiology Published 1 September 2004 Vol. 287

NanoBacteria
Book

The Calcium Bomb: The Nanobacteria Link to Heart Disease & Cancer [Hardcover]  by  Douglas Mulhall (Author), Katja Hansen (Author)

http://insightknowledge.co.uk/fulltext/?doi=INANO-IK.2011.15.22
K. Abo-EL-Sooud, M.M. Hashem and A.Q. Gab-Allaha , 2011.
Nanobacteria: An Infectious Cause for Various Human Diseases. Insight Nanotechnology, 1: 15-22

ABSTRACT:Background: Calcium phosphate is deposited in many diseases, but formation mechanisms remain tentative. Nanobacteria are newly found alone replicating particles that have been detected in mineral stones forming diseases. Nanobacteria were the first (may still be the only ones) calcium-phosphate mineral containing particles isolated from human blood. Results: The stimuli for calcium salt deposition in patients with these circumstances are unclear, but nidi (meaning that biomineralization is taking place out of chemical equilibrium) for precipitation and crystallization are needed. Several important human diseases have calcium phosphate deposition as a distinctive, e.g. atherosclerosis and cardiovascular diseases, stone formation in kidneys, polycystic kidney disease, gall-bladder, salivary, venous and gingival locations, other urological diseases, e.g. prostatitis, many cancers and various forms of autoimmune diseases. Conclusion: In this review, we discuss fully the possible etiological relationships of nanobacteria in the pathogenesis of each previous disease.

http://www.ncbi.nlm.nih.gov/pubmed/16196199
Acta Biol Hung. 2005;56(3-4):233-45.
Detection of nanobacteria-like particles in human atherosclerotic plaques.
Puskás LG1, Tiszlavicz L, Rázga Z, Torday LL, Krenács T, Papp JG.
Abstract Recent and historical evidence is consistent with the view that atherosclerosis is an infectious disease or microbial toxicosis impacted by genetics and behavior. Because small bacterial-like particles, also known as nanobacteria have been detected in kidney stones, kidney and liver cyst fluids, and can form a calcium apatite coat we posited that this agent is present in calcified human atherosclerotic plaques. Carotid and aortic atherosclerotic plaques and blood samples collected at autopsy were examined for nanobacteria-like structures by light microscopy (hematoxylin-eosin and a calcium-specific von Kossa staining), immuno-gold labeling for transmission electron microscopy (TEM) for specific nanobacterial antigens, and propagation from homogenized, filtered specimens in culture medium. Nanobacterial antigens were identified in situ by immuno-TEM in 9 of 14 plaque specimens, but none of the normal carotid or aortic tissue (5 specimens).

Nanobacteria-like particles were propagated from 26 of 42 sclerotic aorta and carotid samples and were confirmed by dot immunoblot, light microscopy and TEM. [3H]L-aspartic acid was incorporated into high molecular weight compounds of demineralized particles. PCR amplification of 16S rDNA sequences from the particles was unsuccessful by traditional protocols. Identification of nanobacteria-like particles at the lesion supports, but does not by itself prove the hypothesis that these agents contribute to the pathogenesis of atherosclerosis, especially vascular calcifications.

Free full text

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3865087/
Int J Nanomedicine. 2014; 9: 27–31.  Published online Dec 11, 2013.
Clinical implications of calcifying nanoparticles in dental diseases: a critical review.  Mohammed S Alenazy1 and Hezekiah A Mosadomi2,3

Conclusion

The cumulative literature evidence on CNPs since their initial description point more to the microbial nature of the particles rather than to physiological contamination. Genomic elucidation supports CNPs as living particles that do get involved positively in pathological calcifications in human organ diseases in dental pulp, salivary glands, kidneys, and arteries. Some investigators have looked into the possibility of using modified CNPs in the treatment of cracked and/or eroded teeth.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC127303/
Antimicrob Agents Chemother. Jul 2002; 46(7): 2077–2086.
Inhibition of Nanobacteria by Antimicrobial Drugs as Measured by a Modified Microdilution Method
N. Çíftçíoglu,1 M. A. Miller-Hjelle,2,* J. T. Hjelle,2 and E. O. Kajander1

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disputed that they are biologically alive organisms

http://www.okayama-u.ac.jp/user/kouhou/ebulletin/research_highlights/vol5/highlights_001.html
Naturally occurring nanobacteria-like particles and ectopic calcification: importance of common nanoparticle scaffolds containing oxidized acidic lipids.

These observations indicate that naturally occurring NLP composed of mineralo-oxidized lipids complexes are generated as byproducts of chronic inflammation, rather than etiological agents.

http://www.ncbi.nlm.nih.gov/pubmed/24028895
Nanomedicine. 2014 Feb;10(2):441-50. doi: 10.1016/j.nano.2013.08.010. Epub 2013 Sep 9.
Ectopic calcification: importance of common nanoparticle scaffolds containing oxidized acidic lipids.
Kumon H1, Matsuura E2, Nagaoka N3, Yamamoto T3, Uehara S4, Araki M4, Matsunami Y2, Kobayashi K2, Matsumoto A4.

The term nanobacteria, sometimes referred to as nanobacteria-like particles (NLPs), is presently recognized as a misnomer for inert calcified nanoparticles. However, misinterpretation of its propagation as a living organism still continues. Ultrastructural and elemental analyses, combining immuno-electron microscopy with an original NLP isolate (P-17) derived from urinary stones, and an IgM monoclonal antibody (CL-15) raised against P-17 have now revealed that, oxidized lipids with acidified functional groups were key elements in NLP propagation. Lamellar structures composed of acidic/oxidized lipids provided structural scaffolds for carbonate apatite crystals. During in vitro culture, lipid peroxidation induced by ?-irradiation of FBS was a major cause of accelerated NLP propagation. In pathological tissue samples from hyperlipidemic atherosclerosis-prone mice, CL-15 co-localized with fatty plaques, macrophage infiltrates and osteocalcin staining of aortic valve lesions. These observations indicate that naturally occurring NLP composed of mineralo-oxidized lipids complexes are generated as by-products rather than etiological agents of chronic inflammation.
FROM THE CLINICAL EDITOR:

The term “nanobacteria-like particles (NLPs)” is presently recognized as a misnomer for inert calcified nanoparticles as opposed to living organisms. This study convincingly demonstrates that naturally occurring NLPs composed of mineralo-oxidized lipid complexes are generated as by-products rather than etiological agents of chronic inflammation.

http://www.ncbi.nlm.nih.gov/pubmed/19198665
PLoS One. 2009;4(2):e4417. doi: 10.1371/journal.pone.0004417. Epub 2009 Feb 9.
Putative nanobacteria represent physiological remnants and culture by-products of normal calcium homeostasis.
Young JD1, Martel J, Young L, Wu CY, Young A, Young D.
Author information      1Laboratory of Nanomaterials, Chang Gung University, Gueishan, Taiwan, Republic of China.

Abstract Putative living entities called nanobacteria (NB) are unusual for their small sizes (50-500 nm), pleomorphic nature, and accumulation of hydroxyapatite (HAP), and have been implicated in numerous diseases involving extraskeletal calcification. By adding precipitating ions to cell culture medium containing serum, mineral nanoparticles are generated that are morphologically and chemically identical to the so-called NB. These nanoparticles are shown here to be formed of amorphous mineral complexes containing calcium as well as other ions like carbonate, which then rapidly acquire phosphate, forming HAP. The main constituent proteins of serum-derived NB are albumin, fetuin-A, and apolipoprotein A1, but their involvement appears circumstantial since so-called NB from different body fluids harbor other proteins. Accordingly, by passage through various culture media, the protein composition of these particles can be modulated. Immunoblotting experiments reveal that antibodies deemed specific for NB react in fact with either albumin, fetuin-A, or both, indicating that previous studies using these reagents may have detected these serum proteins from the same as well as different species, with human tissue nanoparticles presumably absorbing bovine serum antigens from the culture medium. Both fetal bovine serum and human serum, used earlier by other investigators as sources of NB, paradoxically inhibit the formation of these entities, and this inhibition is trypsin-sensitive, indicating a role for proteins in this inhibitory process. Fetuin-A, and to a lesser degree albumin, inhibit nanoparticle formation, an inhibition that is overcome with time, ending with formation of the so-called NB. Together, these data demonstrate that NB are most likely formed by calcium or apatite crystallization inhibitors that are somehow overwhelmed by excess calcium or calcium phosphate found in culture medium or in body fluids, thereby becoming seeds for calcification. The structures described earlier as NB may thus represent remnants and by-products of physiological mechanisms used for calcium homeostasis, a concept which explains the vast body of NB literature as well as explains the true origin of NB as lifeless protein-mineralo entities with questionable role in pathogenesis.

Free PMC Article

Elmer Cranton Skeptical
http://drcranton.com/nanobacteria.htm
Rest in peace nanobacteria, you were not alive after all
Nanobacteria are Not a Cause of Calcification in Arterial Plaque of Cardiovascular Disease
by Elmer M. Cranton, M.D.

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Reversing Coronary Calcification

2004

http://www.ncbi.nlm.nih.gov/pubmed/15364120
Pathophysiology. 2004 Oct;11(2):95-101.
Calcification in coronary artery disease can be reversed by EDTA-tetracycline long-term chemotherapy.  Maniscalco BS1, Taylor KA.

Pathophysiology. 2004 Oct;11(2):95-101.
Calcification in coronary artery disease can be reversed by EDTA-tetracycline long-term chemotherapy. Maniscalco BS1, Taylor KA.

Atherosclerosis is a complex process with multiple mechanisms and factors contributing to its initiation and progression. Detection and quantification of coronary artery calcium (CAC) scores with electron beam tomography has been shown to correlate with obstructive and nonobstructive coronary artery disease (CAD). Pathogen-triggered calcification could play a role in CAD. Recent reports suggest that infectious blood nanobacteria (NB) emerge to be such a trigger. So far, minimal or no reversal of atherosclerosis has been claimed by therapies with iv ethylenediaminetetraacetic acid disodium salt (EDTA), antibiotics, or other regimens, and therapies for atherosclerosis remain non-curative. We have now combined EDTA with antibiotic tetracycline (comET), an in vitro proven nanobacteriocidal treatment, and tested comET therapy in patients with documented CAD. Three hypotheses were probed: (1) Are NB present in patients with CAD?; (2) Does treatment with comET affect blood NB antigen and serology?; (3) Does a comET decrease CAC scores? One hundred patients with stable CAD and positive CAC scores were enrolled into a 4 month study of comET therapy. ComET therapy is composed of

(1) Nutraceutical Powder (Vitamin C, Vitamin B6, Niacin, Folic Acid, Selenium, EDTA, l-Arginine, l-Lysine, l-Ornithine, Bromelain, Trypsin, CoQ10, Grapeseed Extract, Hawthorn Berry, Papain) 5cm(3) taken orally every evening;

(2) Tetracycline HCl 500mg taken orally every evening;

(3) EDTA 1500mg taken in a rectal suppository base every evening. CAC scoring was repeated at 4 months and serum samples were analyzed for NB antigen and serology at baseline, 2 and 4 months. Complete blood count, metabolic panel, liver function, C-reactive protein (hs-CRP) and lipids were analyzed at baseline and 4 months. Seventy-seven patients completed the study and all patients were positive for NB serology, antigen or both.

Responders (n = 44; 57%) had significant decreases in total CAC scores (P = 0.001), the average decrease being 14%. Non-responders (n = 33; 44%) had no change or had increases in CAC scores. Angina was decreased or ablated in 16 of 19 patients (84%). Lipid profiles improved to non-atherogenic direction significantly (P = 0.001), a remarkable finding in a patient group where 86% were on continuous statin medication already before the trial. No adverse physiologic effects were seen in renal, hepatic, or hematopoetic systems. In conclusion, CAC scores decreased during ComET therapy trial in most CAD patients inferring regression of calcified coronary artery plaque volume. The patients tolerated the therapy well and their angina and lipid profiles improved. Further treatment trials for long term therapy with matched controls are warranted.

2007

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1876495/
Nanobacteria: Facts or Fancies?
PLoS Pathog, Vol. 3, No. 5. (25 May 2007),
Pasquale Urbano and Francesco Urbano

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2006

Calcification reduced by 50% by EDTA

http://www.medscimonit.com/download/index/idArt/451275
Two stage EDTA anti-calcification method for bioprosthetic heart valve materials.  Nehir Sucu, Kerem Karaca, Nejat Yilmaz, Nejat Yilmaz, Barlas Aytacoglu, Lulufer Tamer, Murat Ozeren, H. Ali Dondas, Yzzet Oguz, Oya Ogenler, Murat Dikmengil Med Sci Monit 2006;12(6):MT33-38  ID: 451275

Background: The aim of this study was to investigate the effect of two-stage EDTA treatment in diminishing calcific degeneration in bovine pericardial bioprosthetic heart valve material.
Material/Methods: Conventionally preserved pericardium specimens were divided into two groups. Group I  (controls, n=18) pieces were first fixed in phosphate-buffered solution (PBS)+0.6% glutaraldehyde at+4 degrees C for 24 hours, then stored in PBS+0.2% glutaraldehyde at room temperature for 6 days. GroupII (study group, n=18) pieces were treated with PBS containing 100 microg/ml ethylenediaminetetraaceticacid (EDTA) at +4 degrees C for 24 hours, then fixed in PBS+0.6% glutaraldehyde as was group I at +4degrees C for 24 hours. After a second exposure to PBS containing 100 microg/ml EDTA at room temperaturefor 24 hours, they were stored in PBS+0.2% glutaraldehyde at room temperature for 4 days. Pericardialpatches were inserted into the dorsal pouches of 18 juvenile male Wistar rats. After 7 weeks of implantation,all the pericardium pieces were harvested from sacrificed rats. The calcium content and biomechanicalproperties of the explanted tissues were evaluated and also examined histopathologically. Results: The difference in the calcium content of the control and study groups was statistically significant. Biomechanical and histopathologic assessment also supported these findings.

Conclusions: Application of two-stage EDTA was found to be useful in the attenuation of calcification in bioprosthetic heart valve materials with mildly increased durability. As calcification was reduced by approximately 50%, it can be considered for use with other agents as an adjuvant treatment.

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Patents  2005

1) Dissolve kidney stones with EDTA – Terry Grossman MD and Ray Kurzweil

http://www.google.com/patents/US7563460
Enteric coated oral pharmaceutical to erode kidney stones,

US 7563460 B2 Abstract A treatment protocol by which a renal stone patient is administered a chelating agent, generally once a day and preferably by mouth, during a treatment phase and is later administered the same chelating agent once a week, during a “maintenance” phase. The chelating agent is most preferably ethylene diamine tetraacetic acid (EDTA) and may be provided in a dosage form having an enteric coating and at least one external cathode and at least one external anode to create a galvanic current upon contact of the dosage form with the patient’s intestinal contents.

Feb 1, 2005    AS    Assignment
Owner name: RAY AND TERRY S HEALTH PRODUCTS, INC., ASSACHUSET
Free format text: ASSIGNMENT OF ASSIGNORS INTEREST;ASSIGNORS:GROSSMAN, TERRY;KURZWEIL, RAYMOND

Original Nanobac Patent  2004

https://www.google.com/patents/US20060083727?dq=coronary+calcium+score+EDTA&hl=en&sa=X&ei=AUUkU-HzCtS-2wWj14Aw&ved=0CEIQ6AEwAg
Methods and compositions for the treatment of diseases characterized by calcification and/or plaque formation,  US 20060083727 A1
Abstract
The invention provides methods and compositions that include a nutraceutical supplement, antibiotic, and metal chelating agent that is administered to a patient to treat or prevent pathological calcification and or plaque formation as associated with Nanobacteria Calcifying Nano-Particles and/or diseases caused there-from, The method includes the administration of a therapeutically effective nutraceutical supplement, tetracycline HCL, and ethylenediaminetetraacetic acid calcium di-sodium salt to a patient in order to prevent and treat calcific disease.
Publication date    Apr 20, 2006
Filing date    Jul 15, 2005
Priority date    Jul 15, 2004
Also published as    US20070048296
Inventors    E. Kajander, K. Aho, Neva Ciftcioglu, H.B. Millican, B. Maniscalco.  Original Assignee    Nanobac Pharmaceuticals, Inc.

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oral chelation Gary Gordon

http://www.gordonresearch.com/inner.cfm?itemCategory=46987&siteId=502&priorId=0

Home / Oral Chelation / Hoax or Protector
Oral Chelation – Hoax or Heart Protector?
This article is from Dr. Robert J. Rowen’s SECOND OPINION newsletter

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2010  Ciftçioğlu

2010
http://www.ncbi.nlm.nih.gov/pubmed/20094006
Pediatr Res. 2010 May;67(5):490-9. doi: 10.1203/PDR.0b013e3181d476ce.
Pathological calcification and replicating calcifying-nanoparticles: general approach and correlation.
Ciftçioğlu N1, McKay DS.
Calcification, a phenomenon often regarded by pathologists little more than evidence of cell death, is becoming recognized to be important in the dynamics of a variety of diseases from which millions of beings suffer in all ages. In calcification, all that is needed for crystal formation to start is nidi (nuclei) and an environment of available dissolved components at or near saturation concentrations, along with the absence of inhibitors for crystal formation. Calcifying nanoparticles (CNP) are the first calcium phosphate mineral containing particles isolated from human blood and were detected in numerous pathologic calcification related diseases. Controversy and critical role of CNP as nidi and triggering factor in human pathologic calcification are discussed.

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NASA

http://www.ncbi.nlm.nih.gov/pubmed/15555875
Int J Antimicrob Agents. 2004 Dec;24(6):548-9.  full text available
Keeping nanobacterial infections at bay during space travel.
Sommer AP1, Wickramasinghe NC.
Author information
Abstract
In January 2004, President George W. Bush unveiled plans to send astronauts to the Moon in 2015 and shortly thereafter to Mars. With the prospect of manned exploration of the planets drawing ever closer, the new discipline of Space Medicine is destined to come to the fore. Moreover, investigations of how human beings function under space conditions could provide important new insights into fundamental questions of human physiology and disease. We draw attention here to one such instance of a disease process that can be provoked by extended periods of exposure to low gravity.

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Nanobac company documents

 

1) http://www.sec.gov/Archives/edgar/data/925894/000114420406013205/v039344_10ksb.htm
Nanobac Pharmaceuticals, Incorporated  Form 10-KSB
For the Year Ended December 31, 2005
4730 North Habana Avenue, Suite 205, Tampa, Florida 33614

2) http://globaldocuments.morningstar.com/documentlibrary/document/09b3e1e26ed966bb.msdoc/original
For the Quarter Period Ended  March 31, 2006

3) http://yahoo.brand.edgar-online.com/EFX_dll/EDGARpro.dll?FetchFilingHtmlSection1?SectionID=7949992-1205-4457&SessionID=4vwP6j8AoLFeUm7
FORM 15 CERTIFICATION AND NOTICE OF TERMINATION OF REGISTRATION
NANOBAC PHARMACEUTICALS,   INCORPORATED
Date: May 20, 2011

2007

4) http://www.siliconinvestor.com/readmsgs.aspx?subjectid=56642&msgnum=85&batchsize=10&batchtype=Previous

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