CWD surveillance in California (interesting quotes)

[Kathy]

Molecule
From Wikipedia, the free encyclopedia

In general, a molecule is the smallest particle of a pure chemical substance that still retains its composition and chemical properties. [1] In chemistry and molecular sciences, a molecule is a sufficiently stable, electrically neutral entity composed of two or more atoms.[2] The concept of monatomic molecule (single-atom, as in noble gases) is used almost exclusively in the kinetic theory of gases. [3] [4] [5] Polyatomic ions may sometimes be usefully thought of as electrically-charged molecules.

The science of molecules is called molecular chemistry or molecular physics, depending on the focus. Molecular chemistry deals with the laws governing the interaction between molecules that results in the formation and breakage of chemical bonds, while molecular physics deals with the laws governing their structure and properties. In practice, however, this distinction is vague. In molecular sciences, a molecule consists of a stable system (bound state) comprising two or more atoms. The term unstable molecule is used for very reactive species, i.e., short-lived assemblies (resonances) of electrons and nuclei, such as radicals, molecular ions, Rydberg molecules, transition states, Van der Waals complexes, or systems of colliding atoms as in Bose-Einstein condensates. A peculiar use of the term molecular is as a synonym to covalent, which arises from the fact that, unlike molecular covalent compounds, ionic compounds do not yield well-defined smallest particles that would be consistent with the definition above. No typical "smallest particle" can be defined for covalent crystals, or network solids, which are composed of repeating unit cells that extend indefinitely either in a plane (such as in graphite) or three-dimensionally (such as in diamond).

Protein deficiency can lead to symptoms such as fatigue, insulin resistance, hair loss, loss of hair pigment, loss of muscle mass, low body temperature, hormonal irregularities, as well as loss of skin elasticity. Severe protein deficiency, encountered only in times of famine, is fatal, due to the lack of material for the body to facilitate as energy

Reader this is indeed an interesting article you have posted. The fact that it states you "must know the enemy" really should be taken far more seriously than it has been.

Few people have analysed the prion protein - in both its healthy and mal-formed state. This analysis, or "characterization" of the PrPC and PrPSc proteins has been best demonstrated by Dr. David Brown of Bath University in the UK. Not only has he shown that the healthy prions PrPC binds many copper ions; but that the mal-formed prion PrPSc has had some, if not all, of these copper ions replaced by manganese.

The brain of CJD victims has a 50% decrease in copper, and an 10 fold increase in manganese. Quote from:
J. Neurochem 2001 Sep;78(6):1400-8.

Aberrant metal binding by prion protein in human prion disease.

"Human prion diseases are characterized by the conversion of the normal prion protein (PrP(C)) into a pathogenic isomer (PrP(Sc)). Distinct PrP(Sc) conformers are associated with different subtypes of prion diseases. PrP(C) binds copper and has antioxidation activity. Changes in metal-ion occupancy can lead to significant decline of the antioxidation activity and changes in conformation of the protein. We studied the trace element status of brains from patients with sporadic Creutzfeldt-Jakob disease (sCJD). We found a decrease of up to 50% of copper and an increase in manganese of approximately 10-fold in the brain tissues from sCJD subjects. We have also studied the metal occupancy of PrP in sCJD patients. We observed striking elevation of manganese and, to a lesser extent, of zinc accompanied by significant reduction of copper bound to purified PrP in all sCJD variants, determined by the PrP genotype and PrP(Sc) type, combined. Both zinc and manganese were undetectable in PrP(C) preparations from controls. Copper and manganese changes were pronounced in sCJD subjects homozygous for methionine at codon 129 and carrying PrP(Sc) type-1. Anti-oxidation activity of purified PrP was dramatically reduced by up to 85% in the sCJD variants, and correlated with increased in oxidative stress markers in sCJD brains. These results suggest that altered metal-ion occupancy of PrP plays a pivotal role in the pathogenesis of prion diseases. Since the metal changes differed in each sCJD variants, they may contribute to the diversity of PrP(Sc) and disease phenotype in sCJD. Finally, this study also presented two potential approaches in the diagnosis of CJD; the significant increase in brain manganese makes it potentially detectable by MRI, and the binding of manganese by PrP in sCJD might represent a novel diagnostic marker."

Dr. JS Becker et al., have identified over 20 brain proteins (tested for 176) containing naturally occurring radioactive uranium.
Anal Chem 2005 Sep 15;77(18):5851-60.

Determination of phosphorus-, copper-, and zinc-containing human brain proteins by LA-ICPMS and MALDI-FTICR-MS.

Their paper is very important as these doctors have developed a method of analyzing brain material for the various metals and elements, such as phosphorous, copper, sulfur, etc.

Within the context of this paper, the brain sections of patients with Alzheimer's disease were examined. "Protein spots with an increased 235U/238U isotope ratio were detected by LA-ICPMS in gels, for example, of Alzheimer-diseased brain samples doped with 235U-enriched uranium after 2D gel electrophoresis.24 This result demonstrates that certain proteins are able to accumulate uranium."

I have asked Dr. Becker if they have ever analysed the brains of cattle with BSE, deer with CWD, or patients with vCJD. The response was no.

I contacted the National Prions Center at Case Western and informed them of Dr. Becker's accomplishments, amoung others; and, their response was to say that Dr. Becker could apply to them for brain material to test.

This I find unacceptable, as when informed of such enlightening information regarding Alzheimer mal-formed proteins and new technology developed by this German group, I would have thought that the National Prion Institution would have requested of Dr. Becker that they analyse these TSE tissues.

Once again, if you don't look for it - you'll never find it!

This tells me that the National Prion Institute is not interested in finding the answers to disease. They must be just reactive to research requests, they must also be pro-active in having relevant experiments performed as new technology allows.

Dr. Glenn Tellings, of Kentucky University, (mentioned in the posted article re: prions in muscle/CWD) was the one to state at the Prion Symposium in Calgary, Alberta February 2/06 that:

"They have not "characterized" the prions which they use in their injection transmission experiments, and..... that it would be some time before they did so."

Once again, I must express my disbelief in such flawed-manipulative research. It is one thing to not do the tests, and quite another to TOTALLY IGNORE the existing research performed on the subject.

 

[Kathy]

I failed to mention why I brought into light the quote about 'protein deficiency",

You see, soldiers suffering from Gulf War Syndrome (caused by exposure and contamination of their bodies by depleted uranium), are said to "waste away faster than if you starved them to death".

This is because the damage done to their systems by the uranium results in the disabling of their digestive enzymes. Without these enzymes, their bodies cannot digest the protein-based foods they are eating. When their own body stores of fat are exhausted, they then 'waste away' faster than if starved them to death.

In fact, they have starved to death; just like the deer and cattle afflicted (contaminated) with uranium ions in their bodies (CWD and BSE).

Analysis of these animals bones (or {sadly} bones of deceased soldiers') would prove that uranium is prevalent in their bodies.

This metal contamination is why feeding bone meal to cattle was so distructive. And, why stopping the feeding of MBM helped to reduce BSE.

In fact, cow bones (heated to 500 degrees Celcius +) to remove proteins, can be used to sequester uranium and strontium, and heavy metals from contaminated soils and water. This is called "COW-BONE APATITE".

 

[Kathy]

Reader, are you so hopelessly bent on making me look like a bad person, that you don't want to find answers to these diseases.

I am working with a representative of GWS soldiers who unfortunately gets to see these same conditions up close. No I haven't seen it up close, myself, but in the animal world, there is nobody there to care for these creatures like in the human world.

I care deeply for your losses and the loses of others, or I wouldn't be communicating on here about this issue. The evidence I post is not "prattle".

Humans can care for their sick. Because we assist the ill and dying, they often last longer than the animals (deer/elk/cattle) which are not given aid. We are members of the mammilian family, after all. Our biological systems operate similarly.

All of the horrid conditions which you describe (and appear to be blaming me for) are happening to the soldiers suffering from Gulf War Syndrome.

It is a shame that you would rather attack my comments, then take the time to find out about other "potentially" related illnesses.

I will not stop posting these medical facts and findings. If you are upset by them, don't read my posts.

 

[Kathy]

Please show me the studies which demonstrate that CWD wasting is caused by a different mechanism than CJD or vCJD wasting.

Your comments are superficial. I have done alot of work here, and you want people to think I am generalizing. You comment about me like you know me, and you don't. We don't even know your name.

You refuse to look at these connections. Why?

At least I am working on this every day, reading new papers etc. and observing all that I can.

Scientists on the 'infectious' road refuse to acknowledge the large body of work done by scientists examining the metal connection, the loss of anti-oxidant defence mechanisms and exposure methods (of metal contamination like inhalation) they are the ones who are superficial.

If you want to call me this, you are calling all the doctors working on this area of research superficial as well.

You don't want people to find out what causes these diseases. If you did you, would be asking questions to all the researchers unveiling the metal imbalances in the brains of people with neurological diseases.

Your stuck on the "infectious" route, with flimsy evidence to support it.

I am sorry if that bothers you, but show me a study that has analyzed the PrPSc prion for the various components making it. What are the levels of phosphorous, sulfides, carbon, metals? Maybe you should read the Becker paper and some of Brown's papers.

The researchers on the infectious route, refuse to do this testing, at least openly. However, it won't stop others (especially those from outside the USA) from doing it.

 

[flounder]

reader2nd wrote to kathy;


> You prattle on but you need to educate yourself about what TSEs do more and hold forth less.


that will never happen reader, kathy has radiation poisoning. i bet she glows in the dark :roll:



kathy writes;


> Reader, are you so hopelessly bent on making me look like a bad person, that you don't want to find

> answers to these diseases.


you do a good enough job on making yourself look bad kathy, you don't need readers help or mine :lol:

and as far as finding answers to the disease, you will never find them kathy unless you take those nuclear blinders off you wear and start looking and accepting the PROVEN transmission studies. there you will find answers.


> The evidence I post is not "prattle".

if prattle is junk science, i will have to agree with reader2nd


> All of the horrid conditions which you describe (and appear to be blaming me for) are happening to the

> soldiers suffering from Gulf War Syndrome.


oh my God, now kathy is insinuating that gulf war syndrome is a TSE......gimme a break? you've got to be kidding me? the only gulf war vet that is tied to a TSE that is documented was fed a meal of 'sheep brains' over there. james alford has had cjd for over a year. now, whether it was a coincidence of him getting cjd and being so young, or was it the first of a biological war fare by insurgents by feeding him infected sheep brains with scrapie??? i dont know. some say the incubation from the time he consumbed the brains to onset of cjd symptoms was too soon. BUT, considering he was eating sheep brain ??? you cant ignore it. but for you to insinuate that GWS is a TSE/CJD, just shows how ignorant you are kathy. you insult the dead and the famlies of the dead. you do not know what you are talking about. ...


> I will not stop posting these medical facts and findings.


you have posted NO medical facts and findings that shows you nuclear particals and or OPs and metals
(you cant seem to make your mind up about that) have any relation what so ever to the cause of any TSE.
there are none out there. ...


TSS

 

[bse-tester]

Reader 2 wrote:

Quoted:

"Only in final stages of BSE do you find it abundantly in the brain," Safar says. "In mad cow, the brain is often the very last organ affected."

So, by the time an animal starts drooling, stumbling, losing hair, acting slow and stupid from this disease, it's an emphatically infected critter. There's no part of it anyone should want to eat.

As you know Reader2, this is something I have long been stating. Ron

 

[Mike]

Immune system and peripheral nerves in propagation of prions to CNS
Adriano Aguzzi, Frank L Heppner, Mathias Heikenwalder, Marco Prinz, Kirsten Mertz, Harald Seeger and Markus Glatzel

Institute of Neuropathology, Universitätsspital Zürich, Switzerland

Prions are not only unique in the way they replicate. Also the sequence of events triggered by peripheral prion infection, generically termed 'peripheral pathogenesis', sets prions aside from all other known pathogens. Whereas most bacteria, parasites, and viruses trigger innate and adaptive immune responses, the mammalian immune system appears to be remarkably oblivious to prions. Transmissible spongiform encephalopathies (TSEs) do not go along with inflammatory infiltrates, and antibodies to the prion protein are not typically raised during the course of the disease. On the other hand, there is conspicuous involvement of lymphoid organs, which accumulate sizeable concentrations of the infectious agent early during disease. Moreover, various states of immune deficiency can abolish peripheral pathogenesis and prevent 'take' of infection when prions are administered to peripheral sites. Here, we critically re-visit the current evidence for an involvement of the immune system in prion diseases, and will attempt to trace the elaborate mechanisms by which prions, upon entry into the body from peripheral sites, reach the brain.

 

[bse-tester]

Prions take a long time to manifest in the brain in sufficient numbers to affect how the brain functions. The entire issue of how it happens is known and the actual cutting off of the flow of electrons from the faring side to the receptor side is able to be compared to a fuse link. On one side of the fuse in the firing side, or the output of the electrical impulse that is designed to activate the receptor. This receptor may well be the one that allows us to move an arm or scratch that itch or rember that wonderful time in Paris. The fuse link is the path on which the now energized impulse travels on its way to the recptor. The prion attaches itself to the link set between the firing side and the receptor side. After a while, there are enough prions there to disrupt and impede the impulse. The receptor side then has literally no signal going to it and there for the arm doesn't move, the itch continues to itch and those memories of Paris simply fade away. They are still there, but like a file in a corrupted hard-drive, they are inaccessible due to the pathway being corrupted or destroyed.

I know this is a long-winded description but it is one that is known to science and it does tend to simplify the entire idea of how the prion manifests and causes its damamge in the brain.

In humans, animals - cattle and deer - the symptoms are typically the same. The onset of prion disease is incidious and deathly slow. For deer and elk in the wild, their suffering may well be ended by predators or harsh winters.