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The Fiber Disease

Human Anatomy, Physiology, and Medicine. Anything human!

Moderator: BioTeam

Postby London » Sat Sep 02, 2006 1:19 am

Systemic,

It's also things that make our olfactory senses effect our brain chemicals. it has alot to do w/ pollution too. Also they feed the antibiotics to the animals we eat.

and, remember, just like I taught my kids in school, there is noise pollution> Now, have I confused you yet? sorry if so.
__________________________________

wow RANDY, thanks for sharing, I'm going to your links now!
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Postby Nadas Moksha » Sat Sep 02, 2006 7:24 pm

gnostic=gnosis=to know

"still controversial, it can be speculated that sanitation
procedures, vaccination, and widespread antibiotic use, imped-
ing host-to-host spread of vir plasmid-based pathogens, may
reduce the overall pathogenic power of microorganisms.
Due to the rapid acquisition and fixation of compensatory
mutations by bacteria, experiments to evaluate the biological
cost of the expression of novel antibiotic resistance and viru-
lence determinants are difficult to perform. Antibiotic resis-
tance and virulence can be acquired either by horizontal trans-
fer of antibiotic resistance genes (97) or by mutation (241).
The presence of new plasmids and transposons in the bacterial
genome has a relevant cost for the recipient bacteria"

a gift from Austria-

"An array sensor for detecting hydrogen gas was constructed by electrodepositing palladium nanowires on an HOPG surface and then transferring the nanowires to a cyanoacrylate film supported on a glass slide. The application of silver contacts to the ends of 10 to 100 nanowires--arrayedelectrically in parallel--produced sensors and switches that exhibited a high conductivity state in thepresence of hydrogen, and a low conductivity state in the absence of hydrogen. This paper describes amethod for incorporating these "portable" metal nanowire arrays into sensors.Nanowire Nanosensors for Highly Sensitive and Selective Detection of Biological and ChemicalSpecies"

http://www.freepatentsonline.com/6824981.html
Ultra-sensitive detection systems using alterable peptide tags - Patent 6824981


http://www.freshpatents.com/Drug-bio-af ... ntc424.php
Drug, bio-affecting and body treating compositions patents 200602

http://www.bio-computing.org/articleindex.php?year=2004
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Postby RANDY » Sun Sep 03, 2006 3:18 am

I watched many discussions about Randy Yaskal and London ecc. in your board, well to many written things about nothing...Lets stay by the main problems "Morgellons desease". watched many discussions about Randy Yaskal and London ecc. in your board, well to many written things about nothing...Lets stay by the main problems "Morgellons desease".
l

This is how someone in Germany says "Thank You" for spreading the word about his cream and testing it out..without it first being analyzed for toxins......unreal.....people never seem to amaze me at how crazy and mean they can be.

Randy

is there anyone who is sane out there?
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Postby Nadas Moksha » Sun Sep 03, 2006 9:19 am

all aggressive tactics cause consolidtion of ectoparasite/phagocyte to internalize host by mass exodus via quorum sensing untill further photonic band gap codon are needed per operon...

"Mutants unable to swim showed great delays in biofilm formation, suggesting flagellar motility (swimming) facilitates initial contact with thesurface. The main role of flagellar motility seems to be to provide force-generating movement that allows the cell to overcome repulsive forces when approaching the surface and become attached. In the absence of flagellar motility there appears to be enough kinetic energy from Brownian motion to allow some cells to eventually attach and form biofilms. The flagella themselves do not seem to serve as adhesins as paralyzed mutants that still have flagella are also defective in biofilm formation. Finally, while swimming plays an important role in attachment, chemotaxis does not seem to have a role, at least when attachment involves inert abiotic surfaces and homogeneous nutritive environments. Once contact with the surface is made, it is necessary for the bacteria to stabilize their interactions with the surface and in many instances pili play a critical role in this process ."

"Surface Colonization. Once stably associated with the surface, bacteria begin to colonize it. Colonization involves a combination of three distinct processes: growth and division of surface-associated cells, recruitment of additional planktonic cells via cell-to-cell interactions, and migration of attached cells along the surface. The concerted action of these three processes leads to the formation of stable microcolonies in the early phases of biofilm development. We showed that cell-to-cell interactions can be mediated by surface structures such type IV pili, which mediate twitching motility in P. aeruginosa . The biofilm defective phenotype of the P. aeruginosa Crc mutant described above is due to a decrease in twitching motility due to the fact that Crc controls the transcription of the pil genes, which encode the type IV pili apparatus."

"incongruent trees can provide evidence for recombination or horizontal transfer of genes (though other causes must also be considered, including systematic errors and cryptic paralogy). A second aspect of phylogenetic trees that can be quite striking is a lengthening of branches to genes when their function is changed, or constraints are relaxed. Finally, phylogenetic analyses provide a context within which to interpret other data, including gene presence and absence, or rearrangements."

- n a d a s
oohh....
alchemical redundance or the world of COSMETICS:

.....the same are disclosed in Korean Pat. No. 0405955. Besides, the perment set by combining hair shampoo, treatment agent, oxidant, rinse, cuticle modulator with the same, are illustrated in Korean Patent Laid-open No. 2002-0021141. Also, the process for washing hair by using shampoo containing ceramide; the process for providing a treatment agent containing ceramide on the hair;a method for pressing a permanent wherein a multiple system using one more substance among two soluble agents and a rinse product is adopted as a chemical suitable for the reductive reaction of keratin fiber... ..... . . . . ?
????????????????????????????????????????????????????


http://arep.med.harvard.edu/DOEGTL/GTLBOS_goal3.htm
http://stateslab.bioinformatics.med.umi ... tions.html
http://64.233.167.104/search?q=cache:AQ ... osal02.doc
http://www.rt-pcr.com/articleindex.php?year=2004
http://ausubellab.mgh.harvard.edu/cgi-bin/pa14/home.cgi
http://www.cfsan.fda.gov/~frf/forum03/abs03ct.html
http://www.bio-computing.org/showabstra ... d=15572320
http://eurekah.com/abstract.php?chapid= ... 3&catid=20
Early Molecular Events in Feather Morphogenesis: Induction and Dermal Condensation
http://www.freshpatents.com/Drug-bio-af ... ntc424.php
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Postby London » Sun Sep 03, 2006 11:51 am

8) :lol: :wink: spot-on Nadus gnostic, spot-on! :lol:

I'm telling you guys, they are using that damn lil parasitoid wasp to damage and make potent chemicles out of the transgenic plants. Don't remeber which all are the worst but do remember carrots and tobacco!! Now, check this out on tobacco.....

Tnt1, a mobile retroviral-like transposable element of tobacco isolated by plant cell genetics. (iNCASE you did'nt know, retroviruses means HIV, can you say Hello??? :shock: :shock: )

Transposable elements can be identified by their ability to induce mutant alleles at new loci. The retrotransposon family is thought to transpose through an RNA intermediate and has many similarities to vertebrate proretroviruses. In plants, retrotransposons have been described in maize, Arabidopsis and wheat, and non-viral retroposons in maize. Most of these elements, however, have been found as non-mobile integrated units. Here, we report the isolation of the first tobacco (Nicotiana tabacum) transposable element, Tnt1, which seems to be the most complete mobile retrotransposon characterized in higher plants. Tnt1 has been isolated after its transposition into the nitrate reductase (NR) structural gene of tobacco, and transposition events have been detected through in vitro selection of spontaneous NR-deficient (NR-) mutant lines in cell cultures derived from tobacco mesophyll protoplasts. Tnt1 is 5,334 nucleotides long, contains two 610-base-pair-long terminal repeats and a single open reading frame of 3,984 nucleotides. Comparison of the Tnt1 open reading frame coding potential with those of the Drosophila melanogaster copia retrotransposon, yeast Ty retrotransposon, and vertebrate proretroviruses revealed that Tnt1 is closely related to copia and carries all the functions known to be required for autonomous transposition by reverse transcription

and if that is not bad enough:

00.097. Pseudoviridae - ICTVdB Index of Viruses - 6:20amHowever, there are instances in the family Pseudoviridae and the family ... Members of the Family Pseudoviridae are different from the other two in that all ...
http://www.ncbi.nlm.nih.gov/ICTVdb/Ictv/fs_pseud.htm - 43k - Cached - Similar pages

I was not sure what Pseudovidiridae was, but I found this out:
Virus classification

The Pseudoviridae are a family of viruses, including the following genera:

Genus Pseudovirus; type species: Saccharomyces cerevisiae Ty1 virus
Genus Hemivirus; type species: Drosophila melanogaster copia virus

Well, this pseusovirus is in the watermelons!! I hate biotechnology and the US GOVERNMENT! :roll: :roll: :evil: :roll:

then our local USDAgriculture had this to say about our plants:
Technical Abstract: Retrotransposons are present in high copy number in many plant genomes and they show considerable degree of sequence heterogeneity and insertional polymorphism, both within and among species. The extremely high variability of Ty1-copia retrotransposons in several other crop genomes including pea, broad bean, Ipomoea, Vitis, Medicago and carrot warrants the current investigation. A large number of fragments that contain RnaseH-LTR regions of the Ty1-copia were amplified and cloned by following procedures developed by Pearce et al, 1999. Some modifications to the original method include hybridization of biotinylated gene-specific degenerate oligo and subsequent stringent washes of streptavidin coated paramagnetic beads after affinity separation. A PCR with nested primer from second RnaseH motif followed this capture. A study of putative transposon insertion sites and the resultant genetic variability is underway using terminal sequences of long-terminal repeats (LTR) using S-SAP (sequence-specific amplified polymorphism) in a set of watermelon genotypes. A genetic linkage map is currently available (Levy et al., 2002) for watermelon using a testcross population [Plant Accession Griffin 14113 (C. lanatus var. citroides) x New Hampshire Midget (NHM); Citrullus lanatus var. lanatus)] x U.S. Plant Introduction (PI) 386015 (C. colocynthis). As this map consists of RAPD and ISSR markers, further integration of PCR based markers based on insertional polymorphism will be useful to locate important genes.

http://www.ars.usda.gov/research/public ... 115=156648

and last but not least:

Identification of a defective transposable element in tobacco.

A putative defective transposable element has been identified in tobacco. This element has been found and characterised in two separate parts of the tobacco genome, specifically within the 3rd intron of the pollen-specific polygalacturonase gene (Npg1) and upstream of the endochitinase gene (Chn50). The element is ca. 0.4 kb in length and is bounded by conserved inverted repeats and putative target site duplications. It appears to fall into the category of non-autonomous transposable elements.

http://www.ncbi.nlm.nih.gov/entrez/quer ... med_docsum

So, SPOT ON, what in the hell does this mean?

I looked up retrovirus C and it said Murine Leukemia Virus, then I found this piece of dog doo:

Background
Cancer gene therapy will benefit from vectors that are able to replicate in tumor tissue and cause a bystander effect. Replication-competent murine leukemia virus (MLV) has been described to have potential as cancer therapeutics, however, MLV infection does not cause a cytopathic effect in the infected cell and viral replication can only be studied by immunostaining or measurement of reverse transcriptase activity.

so, is this what they will use to get away with putting it out there in the crops? Why not let those F-sticks grow their gd plants in their own lab then let them smoke it, eat it and bath in it. I will find these people.

oh lool :shock: , here's there names, TamTam., they are from Germany, can you go have a talk with them?

Katja Sliva,1 Otto Erlwein,1 Alexandra Bittner,1 and Barbara S Schnierle1,2
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Postby Skytroll » Sun Sep 03, 2006 6:37 pm

Ahhhhhhhhhh......look what's coming down the line in our disease, folks, but also look at how we get this way.

"Neurogenic inflammation in the skin

Rainer Haberberger and *Volker Niemeier Institutes for Anatomy and Cell Biology and Psychosomatic Medicine*, Justus-Liebig-University Giessen Neurogenic inflammation of the skin is induced by the activation of nociceptive nerve fibres followed by vasodilation and an increase in vascular permeability. Nociceptors belong to the group of unmyelinated (C-fibre) or myelinated (A-fibre) sensory nerve fibres that innervate different structures in the skin. These fibres originate from dorsal root ganglia (DRG) situated in the intervertebral foramina. Neurochemically distinct populations of sensory DRG neurons project to different regions of the skin. Specific receptors in the endings of those afferent nerve fibres in the skin can be activated by a huge variety of substances including transmitters, proteases, protons and cytokines. Activation of the nerve endings in the skin is followed by the generation of action potentials that are conveyed centrally to the laminae I and II of the spinal cord dorsal horn. Stimulation of the nerves also leads to the release of “proinflammatory” substances from peripheral nerve endings. The Calcitonin-gene-related peptide (CGRP) and substance P (SP) are two neuropeptides that are present in C- and A-fibre afferents and that are released upon stimulation of peripheral nerve endings. CGRP and SP induce pruritus, dilate arterioles, increase vascular permeability and activate mast cells. Capsaicin-induced depletion of sensory nerves prevents the neuropeptide release and inflammatory skin responses like the flare. Sensory nerves can be stimulated under pathological conditions by proteinases via activation of proteinase-activated receptors (PARs), by protons through interaction with acid sensing ion-channels (ASICs) or by the transmitter substance acetylcholine which is produced and released from keratinocytes and interacts with nicotinic and muscarinic receptors. Stimulation of nerve fibres is followed by release of e.g. neuropeptides that further affect many target cells in the skin including inflammatory cells like mast cells, leukocytes and neutrophils. This interplay between neuronal and non-neuronal cells in the skin is important for skin homeostasis and the imbalance in this system may be involved in skin diseases like psoriasis and atopic dermatitis.


MORE HERE: GOOD LEAD IN HERE:...........
"Dr J A Cotterill, Leeds, UK Should dermatologists create imposters?"

http://www.psychodermatology.info/ESDaP ... n-2005.htm

So,........Be Prepared folks, just wonder how the CDC plays a role in this?
NIH is probably funding it.

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Postby RANDY » Sun Sep 03, 2006 7:05 pm

To the MRF Board of Directors,

As you know I have made several requests for the 10 thousand dollars donated
by my dear sister-in-law, Mrs. Suzanne Steadman, to be transferred to OSU's
Morgellons Research. Since I have not heard any reply from any of you, I
must assume that our concerns regarding this research money is meaningless
to you.

For a non-profit organization to ignore requests from their donors is
unacceptable. Thus, I will be doing more investigation on how you have
treated other donors and how you have used their donated funds to date... as
well as how you plan to use donated funds in the future. You have left me
with no other choice.

Since you don't seem to have any intention of these funds going to research,
I must now ask...what are your intentions for these funds? I believe that
this is public information so I am anxiously awaiting publication of your
financial records.

I will be checking with others who have donated funds to see if they have
been ignored as I have.

Your failure to respond to my requests as well as your failure to produce
any financial documents or by-laws for your own board members has caused
increased concern regarding potential improprieties. At the very least, you
owe it to your donors to be accountable for the use of their money.

In case some of you don't understand the point of my persistence on this
issue.....Here's the deal:

Randy Wymore needs help in his lab in order to do this research. He needs
36 thousand dollars to be able to offer a years salary to a Masters prepared
assistant. I want to see that Randy gets this funding so that this research
can get going. We have thousands of desperate, suffering people out there
who want answers and who share my sense of urgency.

This brings me to a question which was brought up on one the conference
calls but was never answered. What IS this money being raised for if not
for research???

Since we share the same goals, I hope that someone in your organization can
address these issues and that we can move on in a positive way in our
efforts to achieve our common goals.

We are doing all we can to raise additional funding. I hope that some of
you will be able to join us at the upcoming celebration in Tahlequah, OK
October 7th and 8th in support of Randy Wymore's research and Oklahoma State
University's commitment to our cause.

Sincerely,

Cindy Casey, RN

Please forward this to your Nursing Coordinator and Clinical Director, since
you have yet to release their identity or contact information.
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Postby London » Mon Sep 04, 2006 1:25 am

spot on skytroll, Randy and Cindy! (Randy, I thought you had written it until I saw her name. ) But thanks to all for sharing!

Sky, going to read your great find now....(the link)

Now check this out:

Molecular Genetic Evidence for the Involvement of
Polygalacturonase, P2c, in the Invasion and Spread
of Aspergillus flavus in Cotton Bolls†


http://aem.asm.org/cgi/reprint/63/9/354 ... nt%20of%22
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Postby Skytroll » Mon Sep 04, 2006 2:02 am

Randy,

Glad to hear you are okay. 14 hours. That is close to torture, I'd say.

Hey, what do you mean about the cream? Is it toxic? Is this what you are saying?

Good letter there to the "MRF". Deserves an explanation from them.

Look at this:
Case 1. A 32-year-old woman was admitted to the department because of multiple round erosions and small ulcerations localized on the anterior surface of the right thigh. Four years earlier, during pregnancy, Clark III melanoma on the right thigh was diagnosed in the presented patient. The tumour was radically removed. On the examination, the skin lesions were distributed very regularly, each lesion was found in the distance of about 1 cm from other lesions, and the area of lesional skin was laterally very well demarcated from the healthy skin. As skin lesions were also considered to be a metastases of previous melanoma, a skin biopsy was done. Histologically only a toxic damage of the epidermis with stingy mixed infiltration of the dermis was seen. The diagnosis of dermatitis artefacta was put and occlusions with neutral topical agents were employed. As the lesional skin was not accessible for the patient manipulations, a rapid healing of skin lesions was noted.

"toxic damage of the epidermis with stingy mixed infiltration of the dermis"

sounds like one of my docs.

So, dermatitis artefacta, Now, just what does that mean?

So the case for pscho is being built folks.

I wonder what kind of transmitters could cause this psychodermatological damage to occur?

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Postby Skytroll » Mon Sep 04, 2006 4:01 am

Gooood Eeeevning,

Okay, so transmitters are most like nano or self-assembling metal particles that zero into our pores and set up the receptor status for incoming waves.

Another way we can get psychodermatological problems that warrent a new subspecialty in medicine, (because the dermatopathologists have hit the road, or been kicked out of the derm clinics, too costly), is by this thing called Proteases.

Interestingly enough, these folks with this new medial subspecialty called Psychodermatology are giving themselves away.

First this is created by transmitters, proteases, protons, and cytokines and then Yippee, time for a new job for Dermatologists, must be pay is low.

So, this idiotic label and now med school for it will defininetly drug us for life.

Meanwhile, still not looking at the real cause of this fiber disease.

Could it just be the transmitters and the Proteases?

Proteases:
Proteases (proteinases, peptidases, or proteolytic enzymes) are enzymes that break peptide bonds between amino acids of proteins. The process is called proteolytic cleavage, a common mechanism of activation or inactivation of enzymes, especially those involved in blood coagulation or digestion. They use a molecule of water for this and are thus classified as hydrolases........
There are currently six classes of proteases:

Serine proteases
Threonine proteases
Cysteine proteases
Aspartic acid proteases (e. g., plasmepsin)
Metalloproteases
Glutamic acid proteases
The threonine and glutamic acid proteases were not described until 1995 and 2004, respectively. The mechanism used to cleave a peptide bond involves making an amino acid residue (serine, cysteine and threonine peptidases) or a water molecule (aspartic acid, metallo- and glutamic acid peptidases) nucleophilic so that it can attack the peptide carbonyl group. One way to make a nucleophile is by a catalytic triad, where a histidine residue is used to activate serine, cysteine or threonine as a nucleophile.

[edit]
Occurrence
Proteases occur naturally in all organisms and constitute 1-5% of the gene content. These enzymes are involved in a multitude of physiological reactions from simple digestion of food proteins to highly regulated cascades (e.g., the blood clotting cascade, the complement system, apoptosis pathways, and the invertebrate prophenoloxidase activating cascade). Peptidases can break either specific peptide bonds (limited proteolysis), depending on the amino acid sequence of a protein, or break down a complete peptide to amino acids (unlimited proteolysis). The activity can be a destructive change abolishing a protein's function or digesting it to its principal components, it can be an activation of a function or it can be a signal in a signalling pathway.........

Well now, that last sentence says a lot!

Taking proteases a little further:

"Some viruses, with HIV among them, depend on proteases in their reproductive cycle."

I would think that many of these protease enzymes also cause fermenting to take place.

"Protease research
The field of protease research is enormous. Barrett and Rawlings estimated that approximately 8000 papers related to this field are published each year."
http://en.wikipedia.org/wiki/Protease

Why so many papers on just this?

Now lets take this even further:

"Protease refers to a group of enzymes whose catalytic function is to hydrolyze (breakdown) peptide bonds of proteins. They are also called proteolytic enzymes or proteinases. Proteases differ in their ability to hydrolyze various peptide bonds. Each type of protease has a specific kind of peptide bonds it breaks. Examples of proteases include: fungal protease, pepsin, trypsin, chymotrypsin, papain, bromelain, and subtilisin."
http://www.enzymeessentials.com/HTML/proteases.html

Take your pick, mix and match:
http://www.promega.com/techserv/enzymes/default.htm

Look where some Proteases are:

Melioidosis most commonly presents as an acute pulmonary infection, but it may present as an acute localized skin infection or septicemia. Chronic suppurative infections often develop with secondary abscesses in the skin, brain, lungs, myocardium, liver, spleen, bones, lymph nodes, or eyes. Melioidosis may remain latent for years. Even months of treatment with appropriate antibiotics do not necessarily eradicate the disease. Histologically, caseating granulomas as found in tuberculosis are seen. Melioidosis has been called the ‘Great Imitator’ because the disease does not show any specific clinical features except perhaps the presentation of suppurative parotitis in children. Fulminant respiratory failure, multiple pustular and necrotic skin lesions, or the radiologic appearance of tuberculosis without isolating any mycobacteria suggests the diagnosis of melioidosis. Definitive diagnosis requires culturing organisms from body fluids or blood. No carrier state exists; recovery of organisms denotes active disease.

Antibiotic treatment should be based on sensitivities. Ceftazidime has been most responsible for reducing mortality. Treatment must continue at least 30 days, but 60-150 days is recommended for pulmonary disease and 6-12 months for suppurative extrapulmonary disease. Before antibiotics, 95% of patients died. The mortality rate for septicemic disease is over 50% and 20% for localized disease despite treatment. Overall, mortality is 40%.

Cutaneous Manifestations:
Severe urticaria has been reported with pulmonary melioidosis. Flushing and cyanosis may develop during septicemia. No cutaneous lesion, however, is specific or diagnostic of melioidosis, nor is any likely to be present with acute pulmonary disease. Inhalational melioidosis could lead to any of the skin manifestations mentioned below, but only after metatstatic abscesses to the skin formed, and this would likely take months. Many patients in endemic areas present with pustules or cutaneous abscesses associated with lymphangitis, cellulitis, or regional lymphadenitis. Draining sinuses from lymph nodes or even bone may be present. Abscesses may ulcerate, and rarely, ecthyma gangrenosum-like lesions may form.

Biological Warfare considerations:
B. pseudomallei would most likely be delivered as an aerosol. However, its long incubation period would make it a less effective agent than anthrax. The lack of a vaccine and its high mortality despite treatment may increase its utility as a BW agent. Acute pneumonia could be confused with plague given the similar appearance of stained organisms.

References & Links

http://www.sanger.ac.uk/Projects/B_pseudomallei/
http://telemedicine.org/BioWar/biologic.htm (source for majority of above literature)
Acta Tropica - 74 (2000)
Melioidosis in the news

Image links

http://www.asmusa.org/test/division/c/photo/bpseud.JPG
http://www.asmusa.org/test/division/c/photo/Bpseud2.JPG
http://cgat.ukm.my/protease/


PROTEASE>>>>>>>>dProteases
Will go into the other two that cause nerurosensations on the skin that would lead to the new subspecialty: Psychodermatology.

Are we going to let this happen?
Or are we going to keep exposing these crooks more and more.

What devious ways many will go to hurt and destroy populations of people, set up the problem, mis name it, and produce a drug to cure it.

Fascinating how this works.

Skytroll



Keep going:
Proteases again:
BIOLOGICAL WARFARE AND ITS CUTANEOUS MANIFESTATIONS

Thomas W. McGovern, MD, MAJ, MC

George W. Christopher, LTC, USAF, MC




--------------------------------------------------------------------------------
The opinions and assertions contained herein are those of the authors and not to be considered as reflecting the views of the Department of the Army or the Department of Defense.

Key Words: biological warfare, cutaneous manifestations, hemorrhagic fever, mycotoxins, poxviruses, plague, melioidosis


--------------------------------------------------------------------------------


INTRODUCTION

Biological warfare agents have gained attention in recent years. They have been discussed in Congress and in the medical literature, and have been the subject of frequent commentaries.[109] The mention of ‘biological warfare’ often elicits a sense of deadly mystery, as summarized by a Russian journalist

"I have been gathering information on bacteriological weapons (BW) for several years. Out of all the means of mass destruction, this kind can be considered as the most mysterious."[112]
This article attempts to eliminate some of that mystery by discussing the history and background of biological weapons and by reviewing agents that cause cutaneous disease. While a biological attack could result in a made-made epidemic of unprecedented scale, the classical principles of clinical medicine and epidemiology would apply. Prompt diagnosis and early interventions could reduce morbidity and mortality, and mitigate the effects of a biological attack. In the aftermath of a biological attack, dermatologists could play a critical role in recognizing the differential diagnosis of an epidemic exanthem and alerting public health officials, leading to prompt medical and public health interventions, hopefully preventing wide-spread mortality.

History

‘Biological Warfare’ (BW) is defined as the ’employment of biological agents to produce casualties in man or animals or damage to plants.’[91] An early BW attack took place in the Black Sea port of Kaffa (now Feodossia, Ukraine) in 1346. Rats and their fleas carried the disease to attacking Tatar soldiers. In spite, the Tatars catapulted the bodies of victims at the defending Genoese who contracted plague and left Kaffa. The same rats afflicting the Tatars likely brought disease to the Genoese.[5]

Another attempted use of biological warfare occurred between 1754 and 1767 when the British infiltrated smallpox-infested blankets to unsuspecting American Indians during the French and Indian war. Smallpox decimated the Indians, but it is unclear if the contaminated blankets or endemic disease brought by the Europeans caused these epidemics.[92] In 1932, the Japanese began a series of horrific experiments on human beings at ‘Unit 731’ outside Harbin, Manchuria, China.[92] At least 11 Chinese cities were attacked with the agents of anthrax, cholera, shigellosis, salmonella, and plague, and at least 10,000 died during their gruesome experiments.[27]

The United States started an offensive biological warfare program at Camp Detrick (today Fort Detrick) in Frederick, Maryland in 1943.[27] Ten years later, the defensive program began. By 1969, the U.S. had weaponized the agents causing anthrax, botulism, tularemia, brucellosis, Venezuelan equine encephalitis, and Q fever.[92]


more here:
http://telemedicine.org/BioWar/biologic.htm
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Postby Nadas Moksha » Mon Sep 04, 2006 4:57 am

"YOU GOTTA FIGHT FOR YOUR REICH TO STAY YOU!
"?????????????????????????????"

"The autonomic nervous system is part of the human central nervous system (CNS). The CNS is basically made up of three sections, the functions of which closely interact. One part manages voluntary movement, the muscle system's response to various stimuli from the environment; this part is called motor nervous system. Another part processes informa­tion from the sense-organs, such as eye, nose, or sense of touch, into conscious per­ception; it is called sensory nervous system."

"The central nervous system's third section - the ANS - coordinates the internal organs' functions. It originates from the brainstem and the spinal cord and includes the nerves, which innervate the smooth muscles of the internal organs, heart and glands. The regulative cycles of the autonomic nervous system are tightly entwined with those of the other two sections, causing numerous interdependencies be­tween the individual systems. "

"structure of the nervous system"

"There are two substructures within the autonomic nervous system, the sympathetic and the parasympathetic, which originate from different areas in the brainstem and spinal cord, and also respond to different biochemical transmitter substances. They both regulate the internal organs by stimulating or inhibiting their activity in a co-ordinated fashion."

"The autonomic nervous system can virtually not be controlled consciously; hence the name. We cannot consciously manipulate our internal organs, such as altering the heart rate intentionally."

" origins and distribution of peripheral autonomic nerves"

"Function of the ANS"

"Most internal organs receive innervation from sympathetic as well as from parasympa­thetic nerves. Both portions of the ANS are active at the same time, but to a different extent. Their combined influence upon an organ is of opposing, but balancing antagonistic nature, meaning that the predominance of one system can inhibit a certain function, whereas that of the other system would stimulate the same function. Increased activity in one of the two autonomic systems inevitably causes an activity decrease in the other, but with­out ever completely disabling it. It is therefore impossible for an organ to be under maximal sympathetic and maximal parasympathetic influence at the same time, one can only dominate at the expense of the other. This is the equivalent of the interdepen­dency of the organs' so-called Yin and Yang states in Chinese medicine. "

"Exploring the signals......."


"So what is the nature of these mysterious Earth signals? Is it sound, or is it an electrical pulsing in the ear cellular tissue that mimics sound? [1] Researchers have encountered this same dilemma on a small percentage of people who experience a sensation of low rumbling or idling diesel-engine sounds in their ears in an area near Taos, New Mexico. It's called 'The Taos Hum', and it was first noticed in the early 1990's. Scientists equipped with an array of sensitive instruments have found no sound nor electromagnetic signals to explain the symptoms.

Scientists will continue to be baffled as to the nature and existence of these emissions until they change the type of instruments they use to look for the signals. The signals are not sound; nor are they true radio waves. Current mainstream physics looks to sound waves and radio waves, as they seem to be the only explanations that still fit within popular physics. But, using sensitive microphones or radio- wave-type sensors, whether magnetic or even electrostatic, means that finding the true, stealthy signals will only continue to be elusive.

Medical doctors are aware of a sudden onset of dizziness and nausea in patients when they move briskly while near very powerful magnetic fields of the modern day MRI (Magnetic Resonance Imaging) machine [7] [8]. Yet the earth signals do not have a powerful magnetic field and still they can cause the same type of effect with sudden onset of nausea and dizziness. In search of these Earth signals, scientists have used some of the most sensitive, super-cooled magnetic sensors available to detect any extremely weak magnetic field changes but, to date, they have found nothing.

Scientists are using the intense external power of magnetic fields and pulsed radio waves in the MRI machine to reach into the atom and excite it into resonance. But they are not thinking of the already existing powerful electrostatic fields within the atoms themselves. No batteries required! The atom has its charge within.

The sudden onset of dizziness, nausea, or other symptoms comes from within the atoms themselves. The signals from the Earth disrupt existing the powerful electrostatic fields of the atoms. This is the secret to understanding the mysterious signals. The signals disrupt existing strong magnetic fields or existing strong electrostatic fields. The other secret is that the strength of the field and the density of the atoms (or tissue in the human body sense) form a selective tuning to the type of Earth signal. This is why some people experience the symptoms differently, or not at all. "

"Experimental evidence of zero-point energy of vacuum has been established beyond question. Soviet direct measurement of this energy has been reported. Prigogine's Nobel Prize work confirms that in theory a highly disordered,chaotic, virtual state, zero-point energy can be cohered to crosstalk into observable quantum change and even macroscopic energy production. Several simple devices can be demonstrated to observably tap zero-point energy. Extension of the theory onto even a simplified hyperspace model indicates direct applications in certain specialized amplifiers. Consideration of multiple simultaneous observation (Everett's interpretation of quantummechanics) ties together virtual and observable states into the same time change, allowing super position of virtual state into observable state. By considering virtual state patterns to be carried by the individual photon,then superposition effects can be obtained upon a target radiated by a radar beam if each and every photon of the radar beam contains one virtual state pattern in common, added into its other (incoherent) virtual statepatterns. Sufficient superposition of the coherent pattern in the target produces real observable changes which may have significant applications. Such applications include electron current dissolution (dudding of electro-magnetic circuits), cancellation of electromagnetic fields, de-activation(dudding) of nuclear warheads by transmutation of fissionable materials, and simple production of particle beams of enormuous power density. Electron current dissolution is also effective against the nervous systems of biological targets. It thus appears that electromagnetic radiators such as radars could possibly be made into universal, all-purpose weapons effective against every major battle element. A mechanism and a theory for direct amplification of the virtual state into observable state is given. At least one known device, Moray's free-energy apparatus, successfully appliedvirtual state engineering to produce 55 kilowatts of power from a 55-pound device by tapping zero-point energy."
Pseudomonas aeruginosa

Mechanisms of Microbial Inactivation

The lethality of the light pulses is different at different wavelengths. Therefore, the full spectrum or selected wavelength may be used to treat the foods. Wavelengths known to produce undesirable products in foods are eliminated by filtering through glass or liquid filters. Light pulses induce photochemical or photothermal reactions in foods. The UV-rich light causes photochemical changes, while visual and infrared lights cause photothermal changes. UV light has been shown to inactivate pathogens and indicator organisms (Chang and others 1985). The antimicrobial effects of these wavelengths are primarily mediated through absorption by highly conjugated carbon-to-carbon double-bond systems in proteins and nucleic acids (Jay 1992).

The mode of action of the pulsed light process is attributed to unique effects of the high peak power and the broad-spectrum of the flash. A primary cellular target is nucleic acids. Inactivation occurs by several mechanisms, including chemical modifications and cleavage of the DNA. The impact of pulsed light on proteins, membranes, and other cellular material probably occurs concurrently with the nucleic acid destruction. For example, the motility of E. coli ceases immediately after exposure to pulsed light. In additional studies, loss of motility of protozoan sporozoites was observed after pulsed light treatment of oocysts. As with any lethal physical agent, it is difficult to determine the actual sequence of events due to the possible "domino effect" (PurePulse Technologies Inc. 1999).

Experience suggests that shorter wavelengths in the UV range of 200-320 nm are more efficient inactivation agents than the longer wavelengths due to their higher energy levels. Because DNA is a target molecule for these UV wavelengths, it is thought that 1 primary cause of killing microorganisms is through DNA structural changes (Farkas 1997). Conventional UV treatment primarily affects DNA by mechanisms that are reversible under certain experimental conditions. Cell repair systems are classified as either "dark enzymatic repair" or "light enzymatic repair" (PurePulse Technologies Inc. 1999). Experiments designed to test enzymatic repair of DNA using pulsed light have shown that this repair does not occur after pulsed light treatment. The magnitude of the damage caused by pulsed light may also be too massive for the repair mechanisms to be effective. It is conceivable the DNA repair system itself is inactivated as well as other enzymatic functions. In summary, the high energy and intensity of pulsed light are thought to amplify the known mechanisms of destruction of cellular components caused by individual wavelengths of light. The sum of the damage caused by the broad-spectrum light is thought to produce extensive irreversible damage to DNA, proteins, and other macromolecules.


http://www.monstein.de/paraphysics/para.htm
Monstein Freienbach

http://www.rexresearch.com/brown2/brown2.htm
Thomas Townsend Brown: Scientific Notebooks, Vol 2

http://www.defenselink.mil/releases/
DefenseLINK News: News Releases

http://fig.cox.miami.edu/~cmallery/150/ ... .virus.htm
Synthetic Biology - Man Made Viruses
Nadas Moksha
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Postby befour » Mon Sep 04, 2006 5:17 am

I thought you all needed to read this......it says that there is NO CDC task force!!!!

http://listserv.uh.edu/cgi-bin/wa?A2=in ... T=0&P=1985

befour
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