The Fiber Disease

Human Anatomy, Physiology, and Medicine. Anything human!

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Post by Serenity » Fri Jan 05, 2007 10:49 am

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Post by Serenity » Fri Jan 05, 2007 10:53 am

I like this BAE Case study the best ... ptsens.htm

Advanced Technology Centre
Case studies
Using fibre sensors to create smart structures and enable structural usage monitoring

Structural monitoring has been an important factor for operators of fast jet aircraft fleets for some years. Airframe fatigue management relies on recording and predicting the usage of the aircraft. Strain gauges distributed on a structure will give the most direct and accurate indication of fatigue consumption. This approach does, however, rely on reliable strain measurements in a sufficient number of locations. Optical fibre sensors, especially the Bragg grating strain sensors, offer significant advantages over electrical, resistive foil strain gauges which are currently the state of the art for structural monitoring purposes.
Jetstream aircraft

The Optics and Laser Technology department of the ATC has developed and evaluated strain gauge systems using optical fibres. Initial laboratory validation proceeded to deployment onto large-scale structures. Initially a maritime application in the form of a 35 m composite yacht mast with embedded Bragg grating sensors was demonstrated. This was a convenient platform on which to tackle some of the key installation and system issues. Having gained confidence, the work then progressed to the more demanding aerospace environment, only this time using surface mounted sensor configurations.

Fibre optic sensors were embedded into a carbon fibre, ocean going yacht mast. A complete structural monitoring systems was developed and underwent sea trials aboard a luxury yacht equipped with a 35-metre mast rig. Following the successful maritime demonstration a similar system was fitted to a BAE Systems Jetstream test aircraft and underwent a series of test flights from the Air Systems Warton aerodrome.

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Post by Serenity » Fri Jan 05, 2007 10:57 am

You can't make this stuff up. Where are the regulations concerning nanotechnology? Where is the protection of the average citizen?

Are there any quantuum physicists here?

I have to day is set to begin.

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King Cobra
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Post by RANDY » Fri Jan 05, 2007 11:14 am

Oh dear my intuition is having a holiday.....if anyone elses is..PM me.

It is almost funny!

During the End Times, Good will battle Evil. Where do you stand?

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Post by tamtam » Fri Jan 05, 2007 3:13 pm

Alternative formulation:

Rhinosporidosis LIKE

("rhinosporidosis" understood as caused by infection with microcystis)

Causative Agent of Rhinosporidiosis
File Format: PDF/Adobe Acrobat
We have isolated a prokaryotic cyanobacterium, a Microcystis ... regulation and molecular aspects of muscle, liver, pancreas, connective tissue ... - Similar pages

A proposal for the unification of five species of the cyanobacterial genus Microcystis Kutzing ex Lemmermann 1907 under the Rules of the Bacteriological Code
S Otsuka, S Suda, S Shibata, H Oyaizu, S Matsumoto and MM Watanabe ?Department of Applied Biological Chemistry, Graduate School of Agricultural and Life Sciences, The University of Tokyo, Yayoi, Bunkyo-ku, Tokyo 113-8657, Japan

Genomic DNA homologies were examined from six Microcystis (cyanobacteria) strains, including five different species, Microcystis aeruginosa, Microcystis ichthyoblabe, Microcystis novacekii, Microcystis viridis and Microcystis wesenbergii. All DNA--DNA reassociation values between two strains of M. aeruginosa and the other four species exceeded 70%, which is considered high enough for them to be classified within the same bacterial species. It is proposed to unify these five species into M. aeruginosa under the Rules of the Bacteriological Code and NIES843(T) (=IAM M-247(T)) is proposed as the type strain. Two other species, Microcystis flos-aquae and Microcystis pseudofilamentosa, should be regarded as morphological variations of this unified M. aeruginosa. The current taxonomy of cyanobacteria depends too much upon morphological characteristics and must be reviewed by means of bacteriological methods as well as traditional botanical methods. ... t/51/3/873

The authors of the sections on the cyanobacteria in Bergey's Manual admit that the proposed classification is a temporary one that will undoubtedly require modification in the future. They state that many generic names used in the past (e.g. Synechococcus, Leptolyngbya, Pseudanabaena) will eventually have to be split into several new genera (Castenholz, 2001). This is especially true if molecular phylogenetic analyses based on sequence comparison of 16S rRNA and other relevant genes are used as the basis of taxonomy and nomenclature. Members of the orders Chroococcales, Pleurocapsales and Oscillatoriales do not form coherent phylogenetic lineages but instead are dispersed throughout the phylogenetic tree (Wilmotte, 1994; Wilmotte & Herdman, 2001).


Rhinosporidium, is it still a fungus?

R.A. Herr, L. Mendoza, L. Ajello
Medical College of Ohio, Department of Microbiology and Immunology, Toledo,
Ohio, USA
The etiological agent of rhinosporidiosis, Rhinosporidium seeberi, was first described
by Malbran in 1892. Since this first observation, over a century has passed and the
taxonomy of this enigmatic organism remains controversial. Previous investigators
have provisionally classified R. seeberi as a protist, phycomycete, and an ascomy-
cetous fungus. These historical attempts to establish the taxonomic position of R.
seeberi have been solely based on light and electron-microscopic observations of the
pathogen within infected host tissues. Intractability to culture, lack of an animal model
of infection, and an unknown ecological niche have all contributed to the difficulties in
classification of R. seeberi.Recently, several investigators have employed molecular
phylogenetic analysis to reveal the taxonomic affinities of R. seeberi.The first of these
studies Herr et al. (1999), found that the sequence of the 18S SSU rDNA of R. seeberi
from two Sri Lankan patients with rhinosporidiosis clustered with a recently discover-
ed group of fish parasites. This study was later corroborated independently by Frede-
ricks et al. (2000), whose 18S SSU rDNA sequence from a dog with rhinosporidiosis
proved to be identical to that of the human isolates sequenced by Herr et al. Most
recently, the 18S SSU rDNA sequence of R. seeberi from a swan with conjunctival
rhinosporidiosis was also found to be identical to those previously published. These
molecular data all placed R. seeberi within the DRIP clade (DRIP: Dermocystidium,
rosette agent, Ichthyophonus, and Psorospermium) Ragan et al. (1996). The DRIP
clade, renamed as the class Ichthyosporea, by Cavalier-Smith (1998) and more
recently as the class Mesomycetozoea by Mendoza et al. (2002) is comprised of
organisms at the most basal branch of the animal-fungal divergence. R. seeberi has
several features in common with other mesomycetozoeans: (a) it was previously
classified as a fungus or a different type of protozoan; (b) it is associated with aquatic
environments; (c) it produces spherical structures containing several daughter cells
(endospores); and (d) R. seeberi and some other mesomycetozoeans are intractable
to culture. In spite of these similarities, R. seeberi differs from the other mesomyceto-
zoeans in that it is the only member known to cause disease in mammals and birds.
Cavalier-Smith, T. 1998. A revised six-kingdom system of life. Biol. Rev. Camb.
Philos. Soc. 73: 203-266.
Fredricks, D. N. et al. 2000. Rhinosporidium seeberi: a human pathogen from a
novel group of aquatic protistan parasites. Emerg. Infect. Dis. 6:273-282.
Herr, R. A. et al. 1999. Phylogenetic analysis of Rhinosporidium seeberi's 18S
small-subunit ribosomal DNA groups this pathogen among members of the
protoctistan Mesomycetozoa clade. J. Clin. Microbiol. 37:2750-2754.
Mendoza, L., et al. 2002. The class mesomycetozoea: a heterogeneous group of
microorganisms at the animal-fungal boundary. Annu. Rev. Microbiol. 56:315-344.
Ragan, M. A., et al. 1996. A novel clade of protistan parasites near the animal-
fungal divergence. Proc. Natl. Acad. Sci. 93:11907-11912.



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Post by southcity » Fri Jan 05, 2007 3:58 pm

If this was true then Randy, have them contact either of us now, or if you would be so kind as to pm their name and contact info, so we could reach them. this is exactly the same request I made which generated the reply you sent below. and no I would rather not call as I do not wish to argue with you.

To: southcity
Posted: Sat Aug 05, 2006 11:30 pm
Subject: bs Quote message
This is not bull...but TamTam will notbe covered since they need names and backgrounds. Be real. This story will be done. So do not stand in the way of progress and help for this disease. That is a sin. The ohter reporter I have also after getting back all the responsese from the scientists will not give Tam and his video tha time of day. Ths is old news. We need to know who we are talking about. Let Tam contact the Chicaog Tribune....he is a shadow, a non-entity with a BS one wants his story.

"First they ignore you...
Then they laugh at you...
Then they fight you...
Then you win." - Mahatma Gandhi

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Post by Barz » Fri Jan 05, 2007 5:56 pm

Tam Tam,

You always say that we should unite and create a legal base.

What is so frustrating is that EVERYONE has a theory and will not back away from what they believe. This is because of the different symptoms each person has. Some swear they just have worms or flukes. Some think it is just a fungus or yeast. Others believe it is an immune system disease. What advice do you have for getting everyone in the same boat?

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Post by Serenity » Fri Jan 05, 2007 6:09 pm

Tam tam.

I see where you are going with Rhinosporidium seeberi, however, I think that this are a combination of many factors. It makes sense that the hair follicle plays a role as that is where the skin is weakest. nanoparticles, nanovirii,
can and do slip into the skin layers there. You think that this nanowhatever is producing these nanotubes?

There is also a nematode somehow connected to this either by alteration of our immune function or by God knows what else.

Carbon nanotubes carry a negative charge. When they pass through the lungs into the bloodstream they attach to RBC which carry a positive charge. changing the polarity.
A person infected en mass
would have to also have pulmonary granulomas as well as clotting issues.

I don't know....i just want to get up everyday and not have to take veterinary medicine and wonder if I am going to b a subcutaneous cell phone or quantuum computer in a few months.

Thanks for Rhinosporidium seeberi,


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Post by Serenity » Fri Jan 05, 2007 6:14 pm


I am thinking that people have different symptoms because we all have colonized different things in our respiratory tract which prior to our exposure to "whateverthisflippenthingis" were harmless. After exposure, something changes and what was once harmless becomes virulent.

btw....i am the most flexible person on earth. I am theorizing.

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Post by Serenity » Fri Jan 05, 2007 6:21 pm

Has anyone heard of anyone being treated with Amphotericin? I am just asking,...this is toxic stuff.


Post by yourmother » Fri Jan 05, 2007 7:57 pm

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Post by Serenity » Fri Jan 05, 2007 9:58 pm

Thanks Mom; that was quite a read. I am wondering what the etiology of the
patients primary disease was? What caused the aplastic anemia in the 31 y/o female and did the cardiac transplant patient have a long history of cardiac disease or was this a recent viral cardiomyopathy?

I guess I am wondering if this is a "which came first, the chicken or the egg"

It was seriously a little frightening reading it, but in reality this stuff is pretty frightening as well.

Thanks for that.


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