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A few words for flounder to ponder

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kathy writes;

>>>I don't want to waste my precious time convincing you about the harmful affects of OPs. Why don't you just get off your high horse and accept some facts, that OPs chelate copper, causing imbalances in enzymes and other bodily functions.<<<

then don't waste our time with unsubstantiated claims that OPs cause TSEs.
it's simply not so. science has proven this. PLUS, don't change my words, i never said that OPs do not cause harmful effects. they just are not the cause of TSEs...TSS
 
Twist and turn the words terry,

I didn't say that OPs caused prion disease, but that they contributed greatly to the UK experience, by making the animals highly susceptible to BSE. Chelating copper, thereby making preventing its utilization by the metalloglycoprotein produced by nerve cells.
 
TimH, smart people see the benefit of having a live animal test for TSE's and they do not get scared! Besides, that is something else you have to figure out. Yes, you do need to tell me what the "IT" is all about? So please, pray tell.
 
bse-tester said:
TimH, smart people see the benefit of having a live animal test for TSE's and they do not get scared! Besides, that is something else you have to figure out. Yes, you do need to tell me what the "IT" is all about? So please, pray tell.
Click to expand...

I didn't comment on the potential value of a live BSE test. I merely asked if you were having any luck trying to create demand for YOUR test. :roll: So......Any luck????

I "NEED" to tell you what "IT" is all about?????? :???:

WRONG-O, M'Lord.

If you explain exactly what you meant with your "rest of the children" comment, I will tell you what "IT" is(quid pro quo).... not because you say I "need" to , Governor. :lol:
 
I was greatly saddened to read some of the wildly irrelevant and impertinent comments that have been posted about my research data and hypotheses on the origins of TSE.

I feel that my critics need to do their homework first, before launching into their tirade of speculative and misguided comments about the authenticity of my first hand research into TSEs. Since most of the critics are professing to hail from an academic background, then they should study the true basis of my work, by educating themselves with my peer reviewed published papers ( chartered on the pubmed and other databases ). They will see that my hypotheses are based upon a raft of real life analytical observations which I have amassed from the numerous field excursions that i have undertaken in the main TSE cluster zones around the world . They are also based upon a cross linking of many other research works in the field of TSE science - these studies being duly referenced in my publications.

I therefore am at a loss to understand how my work can be outcast as 'suspicious' , when i have devoted twenty years of my life to an extremely intensive and thorough hands on investigation into the origins of TSEs I am insulted by such comments. Whatever information is cited in my writings ( whether nerve agent dumping in the UK seas , hand clap tests for clinical BSE , etc ), I have always utilised a valid reference in support of my statements .

And then another commentator goes on to say that " we all agree that rogue metals play a role in the cause of TSEs, but Purdey's ideas are simply.................."

What a short memory this commentator has. If they had studied the scientific literature in the proper way, they would be aware that it was my own original paper - published in Medical Hypotheses 2000 which presented my novel analytical data from Iceland , colorado, slovakia ( recieved at the Elsevier editorial office - 1st April 1998 ) and was the first paper to propose that a rogue metal replacement of the copper / zinc domains on native prion protein was responsible for the origins of TSEs. Shouldn't I therefore get some recognition for this groundbreaking observation ????

The fact that other researchers have subsequently plagiarised my data and hypotheses does not destroy the hard historical reality of my intellectual copyright, my original research investigations and publications ( internationally broadcast on a BBC world film for god's sake ) .

In this respect, I feel that it is totally unfair that my work is being subjected to this misappropriated assault on your pages .

Others go on to say that i am ever changing my theories, as and when they are refuted by the establishment.

Please describe the work by the establishment that has successfully refuted my position ? The only study that I was aware of involved the exposure of recombinant prion protein to the DFP type of organo phosphate , and this trial was totally irrelevant to the testing of my hypothesis on the following grounds ;

Firstly , because the toxicological properties of the DFP molecule are totally different to the toxicological properties of phosmet - the OP insecticide used upon UK farms during the relevant period , and secondly, because the recombinant prion protein does not contain a glycolipid anchor - the actual region of the prion protein amino acid chain which represents a target for OP induced phosphorylation and protein misfolding . So the whole experiment was worthless.

Likwise several other attempts to refute my work have employeed equally irrelevant research protocols .

Since new research discoveries are arising on a virtuaL weekly basis in the area of TSE research, my own environmental theory on TSE cause needs to be open to change in order to remain viable. Like any other theory, it has to be capable of accomadating these advancements. This is the healthy evolution of a scientific theory at work . I therefore feel unfairly criticised on grounds that my theory has evolved ( eg; changed ) over the years .

What is so wrong with that - for god's sake ? Wouldn't we all be better off if the establishment's theory had remained open to change over the years . In this respect, progress would be made towards resolving many of the missing links in the aetiology of these diseases.

Others have expanded their criticism of my work , by erroneously stating that I have moved from pesticides, to heavy metals , to sonic waves , etc, as a cause of BSE . But these people are wholly ignorant of my work. They have failed to get the most basic gist of what i am actually saying.

Clearly a straight forward metal or pesticide toxicity does not provide an adequate explanation for the cause of these unique TSE diseases - since mammalian exposure to the various metals, and to some extent , the pesticides, has obviously gone on for years prior to the emergence of TSEs . To suggest that my research has not recognised this basic factor is completely inaccurate and unfair . Its insulting of my intelligence .

However, I have advanced upon this basic tenet, after collecting further analytical data of the levels of magnetic susceptibility , radioactivity, piezoelectic capacity of the soils, hard tissues etc, in the TSE cluster and TSE-free areas. So whilst the same specific elements ( eg; phosphorous , manganese , barium, etc ) remain the central nucleating agents in the aetiology of these diseases, it is the piezoelectric capacity of the specific crystalline metal-protein conglomerates which are subsequently formed within the contaminated tissues that represent the pathogenic driving force within these diseases - eg; representing the heat resistant, transmissible , pathogenic capacity that interweaves with the other environmental prerequisties into a unified , viable hypothesis which fits all of the well recognised idiosyncratic properties that define the causal agent in TSEs.

Furthermore, my work is not a case of the egg before the chicken - I have never started off with a theory, and then tried to force subsequent observations to fit the picture as some are suggesting. I have allowed my first hand environmental observations in the cluster environments to gradually assemble the right theory that would seem to fit all of the facts . There are bound to be cul de sacs, and false leads, but the theory has kept on evolving. Nobody is going to fit the nail on the head ; particularly if they are operating without the benefits of government or corporate backed funding , like myself .

I would strongly recommend to those critics who profess to hail from a scholarly background, that they should actually begin to make the effort to read my academic publications in the first instance, rather than relying upon the misguided hearsay.

I also feel that your readers should be aware of the personal and financial hardship that entrepreneurial researchers such as myself have had to endure for the 'crime' of launching fresh observations and ideas into the public arena - particularly if those findings should threaten the reputations or vested interests of the status quo scientists in any way.

Whilst many reputable scientific establishments are currently making a small fortune out of the fruits of my own pioneering work, my own life has ironically degenerated into a state of total collapse. All I ask is for abit of basic human respect , and not for the accolades of acidity that are sent my way nearly everyday. Thank you Kathy, for being the only intelligent and open minded contributor to ranchers.com

Yours ,

Mark Purdey
 
Kathy writes;

> didn't say that OPs caused prion disease, but that they contributed greatly
> to the UK experience,

could your please reference this materials...........

thank you,
terry
 
TimH, We are working hard to get our test validated, along with a simultaneous validation for CJD. It will take time to do so as the typical validation will take approximately two years to complete (due to the vast amount of validation data that must be collected for reveiw.) Once we are finished with that level of the project, we will then move to the next stage which will be the marketing of the test kit. Not before! I leave it to those who would try to sell their untried and non-validated tests to attempt to market them without that being done! As for the other words, let us move on!
 
For some informative reading, go to the BSE Inquiry testimony of Dr. Sarah Myhill of the UK.

http://72.14.203.104/search? q=cache:CTQJHNKYdkoJ:www.bseinquiry.gov.uk/files/ws/s506.pdf+Whatley+prions+organophosphates+&hl=en

As Mark has pointed out, in his posting above, when Dr. Stephen Whatley tested an organophospate on cell cultures, he showed up-regulation of PrPC, which was dose dependent. However, the type of OP he was given to test, was not the exact same chemical formula as Phosmet. Amazingly, the manufacturers could not come forth with a sample of the questioned warblecide.

Here is the abstract for the Whatley paper:

Neuroreport. 1998 May 11;9(7):1391-5
Phosmet induces up-regulation of surface levels of the cellular prion protein.

Gordon I, Abdulla EM, Campbell IC, Whatley SA.

Department of Neuroscience, Institute of Psychiatry, London, UK.

Chronic (2 day) exposure of human neuroblastoma cells to the organophosphate pesticide phosmet induced a marked concentration-dependent increase in the levels of PrP present on the cell surface as assessed by biotin labelling and immunoprecipitation. Levels of both phospholipase C (PIPLC)-releasable and non-releasable forms of PrP were increased on the plasma membrane. These increases appear to be due to post-transcriptional mechanisms, since PrP mRNA levels as assessed by Northern blotting were unaffected by phosmet treatment. These data raise the possibility that phosmet exposure could increase the susceptibility to the prion agent by altering the levels of accessible PrP.

PMID: 9631435 [PubMed - indexed for MEDLINE]

Biochim Biophys Acta. 2005 Sep 15;1736(2):87-93.
Neuropathy target esterase and phospholipid deacylation.

Glynn P.

MRC Toxicology Unit, University of Leicester, Leicester LE1 9HN, UK. [email protected]

Certain organophosphates react with the active site serine residue of neuropathy target esterase (NTE) and cause axonal degeneration and paralysis. Cloning of NTE revealed the presence of homologues in eukaryotes from yeast to man and that the protein has both a catalytic and a regulatory domain. The latter contains sequences similar to the regulatory subunit of protein kinase A, suggesting that NTE may bind cyclic AMP. NTE is tethered via an amino-terminal transmembrane segment to the cytoplasmic face of the endoplasmic reticulum. Unlike wild-type yeast, mutants lacking NTE activity cannot deacylate CDP-choline pathway-synthesized phosphatidylcholine (PtdCho) to glycerophosphocholine (GroPCho) and fatty acids. In cultured mammalian cells, GroPCho levels rise and fall, respectively, in response to experimental over-expression, and inhibition, of NTE. A complex of PtdCho and Sec14p, a yeast phospholipid-binding protein, both inhibits the rate-limiting step in PtdCho synthesis and enhances deacylation of PtdCho by NTE. While yeast can maintain PtdCho homeostasis in the absence of NTE, certain post-mitotic metazoan cells may not be able to, and some NTE-null animals have deleterious phenotypes. NTE is not required for cell division in the early mammalian embryo or in larval and pupal forms of Drosophila, but is essential for placenta formation and survival of neurons in the adult. In vertebrates, the relative importance of NTE and calcium-independent phospholipase A2 for homeostatic PtdCho deacylation in particular cell types, possible interactions of NTE with Sec14p homologues and cyclic AMP, and whether deranged phospholipid metabolism underlies organophosphate-induced neuropathy are areas which require further investigation.

PMID: 16137924 [PubMed - in process]

Biochemistry. 2005 Aug 23;44(33):11005-13
Protonation of the binuclear metal center within the active site of phosphotriesterase.

Samples CR, Howard T, Raushel FM, DeRose VJ.

Department of Chemistry, P.O. Box 30012, Texas A&M University, College Station, Texas 77842-3012, USA.

Phosphotriesterase (PTE) is a binuclear metalloenzyme that catalyzes the hydrolysis of organophosphates, including pesticides and chemical warfare agents, at rates approaching the diffusion controlled limit. The catalytic mechanism of this enzyme features a bridging solvent molecule that is proposed to initiate nucleophilic attack at the phosphorus center of the substrate. X-band EPR spectroscopy is utilized to investigate the active site of Mn/Mn-substituted PTE. Simulation of the dominant EPR spectrum from the coupled binuclear center of Mn/Mn-PTE requires slightly rhombic zero-field splitting parameters. Assuming that the signal arises from the S = 2 manifold, an exchange coupling constant of J = -2.7 +/- 0.2 cm(-)(1) (H(ex) = -2JS(1) x S(2)) is calculated. A kinetic pK(a) of 7.1 +/- 0.1 associated with loss in activity at low pH indicates that a protonation event is responsible for inhibition of catalysis. Analysis of changes in the EPR spectrum as a function of pH provides a pK(a) of 7.3 +/- 0.1 that is assigned as the protonation of the hydroxyl bridge. From the comparison of kinetic and spectral pK(a) values, it is concluded that the loss of catalytic activity at acidic pH results from the protonation of the hydroxide that bridges the binuclear metal center.

PMID: 16101284 [PubMed - in process]


In the testimony of Dr. Dealler, also to the BSE Inquiry, he made it very clear that all testing and research regarding BSE was to be approved by the CVL which is controlled by MAFF (ministry of agriculture foods and fisheries). Dr. Dealler also commented on how Dr. Narang (while working for MAFF) was doing some "unapproved" testing and when MAFF found out he was asked to leave. Perhaps bse-tester knows more about this matter?
 
Greetings Ranchers et al,


something of interest to some, is that Harash Narang has been working at the NIH recently, even though some in the US do not believe in his hypothesis for TSEs. strange. his book 'THE LINK' was very interesting. ...

From: TSS ()
Subject: BSE REPORT APRIL 2005
Date: September 6, 2005 at 8:57 am PST

for all consumers

BSE

REPORT

April 2005

Featuring:

. Science news

. General news

. Official figures

>

BSE monthly report is compiled during the week following the month of

the report. Material is collected from news reports, science abstracts and

government sources, and is presented in good faith. However, Which?

cannot guarantee the accuracy of the information and does not necessarily

hold any of the opinions reported here.

Readers are welcome to send correspondence to the editor at

[email protected] or by post to BSE monthly report, Policy

Department, Which?, 2 Marylebone Road, London NW1 4DF.

Science news ...



snip...



Cellular prions detectable in urine

A research team in Cleveland, USA, led by Dr Harash Narang, has demonstrated

that normal cellular prions can be detected in human urine. The method "can

easily and reliably" detect PrPC in apparently healthy individuals using less than 1

ml of urine.4 The amount of urinary PrPC is estimated to be in the range of several

micrograms/litre. Dr Narang previously attempted to undertake research in

Newcastle, UK, on the detection of BSE in urine, but research funding was

withdrawn in the late 1990s in a move that caused some controversy at the time.5

Mouse prion infection is seen in spleen before brain

An investigation of prion infection in mice by Japanese researchers has shown that

the accumulation of the abnormal form of prion protein (PrPSc) in spleens occured

far in advance of its accumulation in brains, whether the infection was initially

administered through feeding, through injection into the abdomen (peritoneum) or

injection directly into the brain.6 Using Western blotting with anti-prion protein

antibodies, accumulation of PrPSc was first detected in the spleen on the 70th day

after inoculation directly into the brain, and detected in the brain on the 116th day.

Inoculation through the other routes took much longer to show the presence of

PrPSc in either the spleen or brain (see table) but the spleen showed an

accumulation of PrPSC at least 130 days in advance of it being detected in the

brain. These results indicate that PrPSc increases rapidly in the spleen compared

with the brain in a manner independent of the inoculation route. ...



snip...



http://www.which.net/campaigns/food/safety/bse_reports/bserep0405.pdf





Dear Terry,
One note to your comment. The study you mentioned (see attached) was INITIATED and performed in my lab at xxxxxxxxxxxxxxx in collaboration with Harash. This study has no relationship to any of the Harash's hypothesis on TSE.
Sincerely,

xxxxxxxxxxxxxxxxxxxxxx





TSS
 
Knowing Harash Narang personally and as well as I do, it has to be made very clear to all that Harash Narang did not at any time lead a team at the National Prion Surveillance Centre in Cleveland, Ohio. He was there as a guest of the the Dept. of Pathology and was at all times under the authority of Dr. Gambetti and the Associate Director of Pathology, Dr. Shu G. Chen. His (Narang) protocol, within which he demonstrated that he could detect PrPsc in 1ml of urine, was fundamentally correct, however, it did not work until Dr. Chen adjusted it slightly and then went further and developed the correct antibody that caused the protocol to work correctly. As a matter of fact, the entire project at Cleveland was contracted and funded by Mr. Ken Bell, of Ken Bell International in Newcastle. To that end, Dr. Chen actually travelled to Newcastle to sign the contracts with Mr. Ken Bell in which it was clearly stated that the Pathology Lab at Cleveland was under contract with Biotec Global to conduct the "proving" of the BSE/CJD Urine Test Kit. (I have copies of that contract) It was Mr. Ken Bell, the CEO of Biotec Global which is also the sole owner of the World-wide Patent for the Urine Test Kit developed by Harash Narang and quite literally paid for by Mr. Bell, who has funded just about everything that Harash Narang has done within the last 12 years or so to the tune of over 1.2 Million Pounds Sterling. Narang actually had the wording of the "Paper" (ebmonline) changed to show that the funding provided by Mr. Ken Bell was to be shown as a "Gift," instead of actual payment for the testing of the hypothesis. He even went so far as to demand that all credit went to him and that was simply not possible in light of the efforts of Dr. Chen and others there in Cleveland. To avoid any problems, he was granted 1st authorship on the Paper.

The funding of Narang, by Mr. Ken Bell of Newcastle for a period of a little over 12 years, has since come to a halt, due, in part, to Harash Narang not being completely forthright with Mr. Ken Bell as to what he has been doing with the funds and what his activities have been for the past two years or so. As a result of negotiations with Mr. Ken Bell directly and in person, I have been awarded the exclusive rights to the "BSE/CJD Urine Test Kit" for all of the America's and Canada and also for all of Europe and subsequent to this, Harash Narang has quite literally fell of the face of the earth. Ken Bell is under the impression that Narang has returned to India. He (Narang) left Cleveland on rather bad terms and I have been officially advised by the Pathology Dept. there that he will not be invited back under any circumstances at all. It is unfortunate, but he made his own bed with respect to how he is not perceived by others in the field. The fact is that when he did work for MAFF, he did go against their grain and was subsequently fired for doing things he was specifically told not to do. He made a fuss about it and made numerous accusations about how he was being treated but the facts are the facts.

I have been in discussion with Dr. Dealler and Dr. Collinge with respect to the Urine Test and we here in Canada have high hopes that we can enlist the cooperation and assistance of such people to engage their skills in the validation of the test sometime in the near future. As for Dr. Harash Narang, I am able to state catagorically that he will not be involved.

Harash Narang is a brilliant researcher but has problems working with others. I know this first-hand. Narang has indeed written a book "The Link," a copy of which I own. Incidentally, I am the North American representative of Biotec Global (UK) should anyone wish to know more.
 
Thanks for that interesting story Ron. I guess scientists have to play politics as well as anyone else in business. Prusiner sure has.
 
Mike, it is a sad affair that one has to take a stand once in a while to protect his or her integrity when others abuse friendships and professional ties. Unfortunately, it happens and we deal with it and move on. The lingering bad taste is the unfortunate side-affect that stains the landscape and that is often the part that tends to do the most damage. The person that I feel for most of all in this is Ken Bell. He took Narang under his wing, paid for practically everything he asked for, heck, Narang even spent many a Christmas at Ken Bell's home and was considered part of the family. Mr. Bell has Parkinson's Disease [fairly intense] and doesn't need to be supporting one who would only abuse the right and then go left without so much as a thankyou or explanation of any kind. Ce la vie Mike.
 
THANK YOU BSE TESTER for your reply and update on Harash Narang.
very interesting and sad. good luck with your research in Canada. ...

kindest regards,
terrry/tss
 

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