Manitoba_Rancher
Well-known member
rancher said:
Are you sure Rancher? Seems to me theres always an ole bull moose on here goes by the name of OT- "he's usually cranky.... could be mad moose disease....."... :wink:
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Eating Wild Deer Can Cause Chronic Wasting Disease (CWD)
- Thread starter PORKER
- Start date
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Are you sure Rancher? Seems to me theres always an ole bull moose on here goes by the name of OT- "he's usually cranky.... could be mad moose disease....."... :wink:
Kathy
Well-known member
The theory of infection, sounds alot more controllable and less accountability involved, than a theory of toxic poisoning of metals, including radio-active metals.
flounder continues to ignore my question and drown us in copy and paste information.
Can't you explain in your own words, how minute changes in temperature of the rendering procedure altered the "in-activation" of prions?
Concentrated prions used for inoculation into the brain of animals were ASHED, at temperatures above 660 degrees Celcius, and the transmission experiments still worked in some of the animals. The changes in the rendering temperatures had nothing to do with
in-activating a prion.
Even when devoid of proteins, and protein fragments surrounding the metals particles (nanoscale) found accumulated in the brain stem, the metals, and carbon complexes still caused disease. The agents of transmission are metals. They bio-accumulate in the animals' bones and organs, including the brain.
flounder continues to ignore my question and drown us in copy and paste information.
Can't you explain in your own words, how minute changes in temperature of the rendering procedure altered the "in-activation" of prions?
Concentrated prions used for inoculation into the brain of animals were ASHED, at temperatures above 660 degrees Celcius, and the transmission experiments still worked in some of the animals. The changes in the rendering temperatures had nothing to do with
in-activating a prion.
Even when devoid of proteins, and protein fragments surrounding the metals particles (nanoscale) found accumulated in the brain stem, the metals, and carbon complexes still caused disease. The agents of transmission are metals. They bio-accumulate in the animals' bones and organs, including the brain.
J Comp Pathol. 1984 Apr;94(2):215-31. Related Articles, Links
Neuropathological lesions in experimental lead toxicosis of dogs.
Hamir AN, Sullivan ND, Handson PD.
Light microscopical examinations were carried out on the central and peripheral nervous systems of 9 dogs maintained on a high-fat-low-calcium diet and dosed orally with a mixture of lead chloride, lead bromide and lead sulphate. Microscopic lesions were present in 7 (78 per cent) of the lead-treated dogs. Cerebrocortical lesions comprising spongiosis, vascular hypertrophy and gliosis predominated. These lesions were bilateral, had a predilection for gyri and were located mainly in the parietal and frontal cortex. There were bilaterally symmetrical spongiform changes in the brain stem. The cerebellum had spongiform changes in the roof nuclei and in the lingula there was spongiosis of the Purkinje cell layer and vacuolation of Purkinje cells. Axonal degeneration was evident in a sciatic nerve of one dog. In a second experiment, designed to study the early ultrastructural changes in the brains of dogs with lead intoxication, 2 groups of dogs, one on a commercial balanced diet and the other fed a high-fat-low-calcium diet, were given similar amounts of lead. Cytoplasmic accumulation of lipid was found in the cerebrovascular pericytes of all dogs treated with lead but vascular changes were otherwise not obvious. Quantitative evaluation of numbers of blood vessels by light microscopy revealed an apparent increase in all dogs receiving lead. This increase in vascularity was greatest in the dogs fed the high-fat-low-calcium diet.
PMID: 6736309 [PubMed - indexed for MEDLINE]
Northern Rancher
Well-known member
Eating wild game might give me CjD and walking in the rain I might get hit by lightning-the probability is about the same so I'm not stopping doing either.
PORKER
Well-known member
How about your childern?
Kathy
Well-known member
Once again, I can't get a straight answer to my question about "inactivating" a prion. I am not speaking about risk assessments: I want flounder to explain how changes in the rendering procedures caused (causes) changes in the "in-activation" of prions - the physical changes that make it go from active - to inactive.
Concentrated prions used for inoculation into the brain of animals were ASHED, at temperatures above 660 degrees Celcius, and the transmission experiments still worked in some of the animals. The changes in the rendering temperatures had nothing to do with de-activating a prion.
But flounder says that this change in temperature caused something to happen, what????
The problem with CWD is environmental, over-population and contamination by the development of mines, minerals and oil and gas. The one zone in SE Alberta which has seen a few cases, is way overpopulated, has almost no natural habitat left (90% crop land) and has intensifying oil and gas activity like flaring, venting and spreading of drilling mud on the surface.
In soldiers afflicted with Gulf War Syndrome, doctors say they waste away faster than if you starved someone to death. Uranium ions preferrentially bond to phosphorous, I am told, this prevents the phosphorous from being utilized in the various enzymes of the body, so the person, or animal in the case of CWD, cannot digest the protein they are consuming. They are then dependent on their glucose stored in their body fats, to break-down and feed them. Once there is no more body fat stores, they waste away very quickly.
[/b]
Concentrated prions used for inoculation into the brain of animals were ASHED, at temperatures above 660 degrees Celcius, and the transmission experiments still worked in some of the animals. The changes in the rendering temperatures had nothing to do with de-activating a prion.
But flounder says that this change in temperature caused something to happen, what????
The problem with CWD is environmental, over-population and contamination by the development of mines, minerals and oil and gas. The one zone in SE Alberta which has seen a few cases, is way overpopulated, has almost no natural habitat left (90% crop land) and has intensifying oil and gas activity like flaring, venting and spreading of drilling mud on the surface.
In soldiers afflicted with Gulf War Syndrome, doctors say they waste away faster than if you starved someone to death. Uranium ions preferrentially bond to phosphorous, I am told, this prevents the phosphorous from being utilized in the various enzymes of the body, so the person, or animal in the case of CWD, cannot digest the protein they are consuming. They are then dependent on their glucose stored in their body fats, to break-down and feed them. Once there is no more body fat stores, they waste away very quickly.
[/b]
once again kathy is day dreaming ;
>>>The problem with CWD is environmental, over-population and contamination by the development of mines, minerals and oil and gas. The one zone in SE Alberta which has seen a few cases, is way overpopulated, has almost no natural habitat left (90% crop land) and has intensifying oil and gas activity like flaring, venting and spreading of drilling mud on the surface. <<<
kathy, i don't mind answering questions for you, but i refuse to play your games. i knew this was another one of your trick questions. most folks will be able to read the data and understand. i am sorry you cannot. not my problem. come back to the table when you find evidence that OPs/metals etc become infectious, and find someone else to ask your trick questions too. maybe some others found interest in the data.
i agree that metals and contamination of metals and toxins are killing us too, they just have not been proven to be infectious OR the cause of any TSE. ...TSS
>>>The problem with CWD is environmental, over-population and contamination by the development of mines, minerals and oil and gas. The one zone in SE Alberta which has seen a few cases, is way overpopulated, has almost no natural habitat left (90% crop land) and has intensifying oil and gas activity like flaring, venting and spreading of drilling mud on the surface. <<<
kathy, i don't mind answering questions for you, but i refuse to play your games. i knew this was another one of your trick questions. most folks will be able to read the data and understand. i am sorry you cannot. not my problem. come back to the table when you find evidence that OPs/metals etc become infectious, and find someone else to ask your trick questions too. maybe some others found interest in the data.
i agree that metals and contamination of metals and toxins are killing us too, they just have not been proven to be infectious OR the cause of any TSE. ...TSS
kathy pastes this ;
J Comp Pathol. 1984 Apr;94(2):215-31. Related Articles, Links
Neuropathological lesions in experimental lead toxicosis of dogs.
Hamir AN, Sullivan ND, Handson PD.
Light microscopical examinations were carried out on the central and peripheral nervous systems of 9 dogs maintained on a high-fat-low-calcium diet and dosed orally with a mixture of lead chloride, lead bromide and lead sulphate. Microscopic lesions were present in 7 (78 per cent) of the lead-treated dogs. Cerebrocortical lesions comprising spongiosis, vascular hypertrophy and gliosis predominated. These lesions were bilateral, had a predilection for gyri and were located mainly in the parietal and frontal cortex. There were bilaterally symmetrical spongiform changes in the brain stem. The cerebellum had spongiform changes in the roof nuclei and in the lingula there was spongiosis of the Purkinje cell layer and vacuolation of Purkinje cells. Axonal degeneration was evident in a sciatic nerve of one dog. In a second experiment, designed to study the early ultrastructural changes in the brains of dogs with lead intoxication, 2 groups of dogs, one on a commercial balanced diet and the other fed a high-fat-low-calcium diet, were given similar amounts of lead. Cytoplasmic accumulation of lipid was found in the cerebrovascular pericytes of all dogs treated with lead but vascular changes were otherwise not obvious. Quantitative evaluation of numbers of blood vessels by light microscopy revealed an apparent increase in all dogs receiving lead. This increase in vascularity was greatest in the dogs fed the high-fat-low-calcium diet.
PMID: 6736309 [PubMed - indexed for MEDLINE]
===================================
BUT KATHY IGNORES THE OBVIOUS WITH THE CANINE, SHE IGNORES THE TSE i.e. MAD COW AGENT;
GAH WELLS (very important statement here...TSS)
HOUND STUDY
AS implied in the Inset 25 we must not _ASSUME_ that
transmission of BSE to other species will invariably
present pathology typical of a scrapie-like disease.
snip...
http://www.bseinquiry.gov.uk/files/yb/1991/01/04004001.pdf
76 pages on hound study;
http://www.bseinquiry.gov.uk/files/sc/seac16/tab04.pdf
> I thought that in Britain dogs had contracted BSE, but perhaps not.
not so fast here;
The spongiform changes were not pathognomonic (ie.
conclusive proof) for prion disease, as they were atypical,
being largely present in white matter rather than grey matter in
the brain and spinal cord. However, Tony Scott, then head of
electron microscopy work on TSEs, had no doubt that these
SAFs were genuine and that these hounds therefore must have
had a scrapie-like disease. I reviewed all the sections
myself (original notes appended) and although the pathology
was not typical, I could not exclude the possibility that this was
a scrapie-like disorder, as white matter vacuolation is seen
in TSEs and Wallerian degeneration was also present in the
white matter of the hounds, another feature of scrapie.
38.I reviewed the literature on hound neuropathology, and
discovered that micrographs and descriptive neuropathology from
papers on 'hound ataxia' mirrored those in material from
Robert Higgins' hound survey. Dr Tony Palmer (Cambridge) had
done much of this work, and I obtained original sections
from hound ataxia cases from him. This enabled me provisionally to
conclude that Robert Higgins had in all probability detected
hound ataxia, but also that hound ataxia itself was possibly a
TSE. Gerald Wells confirmed in 'blind' examination of single
restricted microscopic fields that there was no distinction
between the white matter vacuolation present in BSE and
scrapie cases, and that occurring in hound ataxia and the hound
survey cases.
39.Hound ataxia had reportedly been occurring since the 1930's,
and a known risk factor for its development was the feeding
to hounds of downer cows, and particularly bovine offal.
Circumstantial evidence suggests that bovine offal may also be
causal in FSE, and TME in mink. Despite the inconclusive
nature of the neuropathology, it was clearly evident that this
putative canine spongiform encephalopathy merited further
investigation.
40.The inconclusive results in hounds were never confirmed,
nor was the link with hound ataxia pursued. I telephoned Robert
Higgins six years after he first sent the slides to CVL.
I was informed that despite his submitting a yearly report to the
CVO including the suggestion that the hound work be continued,
no further work had been done since 1991. This was
surprising, to say the very least.
41.The hound work could have provided valuable evidence
that a scrapie-like agent may have been present in cattle offal long
before the BSE epidemic was recognised. The MAFF hound
survey remains unpublished.
Histopathological support to various other published
MAFF experiments
42.These included neuropathological examination of material
from experiments studying the attempted transmission of BSE to
chickens and pigs (CVL 1991) and to mice (RVC 1994).
http://www.bseinquiry.gov.uk/witness/htm/stat067.htm
It was thought likely that at least some, and probably all, of the cases
in zoo animals were caused by the BSE agent. Strong support for this
hypothesis came from the findings of Bruce and others (1994)
( Bruce, M.E., Chree, A., McConnell, I., Foster, J., Pearson, G. &
Fraser, H. (1994) Transmission of bovine spongiform encephalopathy and
scrapie to mice: strain variation and species barrier. Philosophical
Transactions of the Royal Society B 343, 405-411: J/PTRSL/343/405
), who demonstrated that the pattern of variation in incubation period
and lesion profile in six strains of mice inoculated with brain
homogenates from an affected kudu and the nyala, was similar to that
seen when this panel of mouse strains was inoculated with brain from
cattle with BSE. The affected zoo bovids were all from herds that were
exposed to feeds that were likely to have contained contaminated
ruminant-derived protein and the zoo felids had been exposed, if only
occasionally in some cases, to tissues from cattle unfit for human
consumption.
snip...
http://www.bseinquiry.gov.uk/files/ws/s324.pdf
2005
DEFRA
Department for Environment,
Food & Rural Affairs
Area 307, London, SW1P 4PQ
Telephone: 0207 904 6000
Direct line: 0207 904 6287
E-mail: h.mcdonagh.defra.gsi.gov.uk
GTN:
FAX:
Mr T S Singeltary
P.O. Box 42
Bacliff
Texas
USA 77518
21 November 2001
Dear Mr Singeltary TSE IN HOUNDS
Thank you for e-mail regarding the hounds survey. I am sorry for the long delay in responding.
As you note, the hound survey remains unpublished. However the Spongiform Encephalopathy Advisory Committee (SEAC), the UK Government's independent Advisory Committee on all aspects related to BSE-like disease, gave the hound study detailed consideration at their meeting in January 1994. As a summary of this meeting published in the BSE inquiry noted, the Committee were clearly concerned about the work that had been carried out, concluding that there had clearly been problems with it, particularly the control on the histology, and that it was more or less inconclusive. However was agreed that there should be a re-evaluation of the pathological material in the study.
Later, at their meeting in June 95, The Committee re-evaluated the hound study to see if any useful results could be gained from it. The Chairman concluded that there were varying opinions within the Committee on further work. It did not suggest any further transmission studies and thought that the lack of clinical data was a major weakness.
Overall, it is clear that SEAC had major concerns about the survey as conducted. As a result it is likely that the authors felt that it would not stand up to r~eer review and hence it was never published. As noted above, and in the detailed minutes of the SEAC meeting in June 95, SEAC considered whether additional work should be performed to examine dogs for evidence of TSE infection. Although the Committee had mixed views about the merits of conducting further work, the Chairman noted that when the Southwood Committee made their recommendation to complete an assessment of possible spongiform disease in dogs, no TSEs had been identified in other species and hence dogs were perceived as a high risk population and worthy of study. However subsequent to the original recommendation, made in 1990, a number of other species had been identified with TSE ( e.g. cats) so a study in hounds was less
critical. For more details see-
http://www.bseinquiry, gov.uk/files/yb/1995/06/21005001 .pdf
As this study remains unpublished, my understanding is that the ownership of the data essentially remains with the original researchers. Thus unfortunately, I am unable to help with your request to supply information on the hound survey directly. My only suggestion is that you contact one of the researchers originally involved in the project, such as Gerald Wells. He can be contacted at the following address.
Dr Gerald Wells, Veterinary Laboratories Agency, New Haw, Addlestone, Surrey, KT 15 3NB, UK
You may also wish to be aware that since November 1994 all suspected cases of spongiform encephalopathy in animals and poultry were made notifiable. Hence since that date there has been a requirement for vets to report any suspect SE in dogs for further investigation. To date there has never been positive identification of a TSE in a dog.
I hope this is helpful
Yours sincerely 4
HUGH MCDONAGH
BSE CORRESPONDENCE SECTION
============================================
TSS
J Comp Pathol. 1984 Apr;94(2):215-31. Related Articles, Links
Neuropathological lesions in experimental lead toxicosis of dogs.
Hamir AN, Sullivan ND, Handson PD.
Light microscopical examinations were carried out on the central and peripheral nervous systems of 9 dogs maintained on a high-fat-low-calcium diet and dosed orally with a mixture of lead chloride, lead bromide and lead sulphate. Microscopic lesions were present in 7 (78 per cent) of the lead-treated dogs. Cerebrocortical lesions comprising spongiosis, vascular hypertrophy and gliosis predominated. These lesions were bilateral, had a predilection for gyri and were located mainly in the parietal and frontal cortex. There were bilaterally symmetrical spongiform changes in the brain stem. The cerebellum had spongiform changes in the roof nuclei and in the lingula there was spongiosis of the Purkinje cell layer and vacuolation of Purkinje cells. Axonal degeneration was evident in a sciatic nerve of one dog. In a second experiment, designed to study the early ultrastructural changes in the brains of dogs with lead intoxication, 2 groups of dogs, one on a commercial balanced diet and the other fed a high-fat-low-calcium diet, were given similar amounts of lead. Cytoplasmic accumulation of lipid was found in the cerebrovascular pericytes of all dogs treated with lead but vascular changes were otherwise not obvious. Quantitative evaluation of numbers of blood vessels by light microscopy revealed an apparent increase in all dogs receiving lead. This increase in vascularity was greatest in the dogs fed the high-fat-low-calcium diet.
PMID: 6736309 [PubMed - indexed for MEDLINE]
===================================
BUT KATHY IGNORES THE OBVIOUS WITH THE CANINE, SHE IGNORES THE TSE i.e. MAD COW AGENT;
GAH WELLS (very important statement here...TSS)
HOUND STUDY
AS implied in the Inset 25 we must not _ASSUME_ that
transmission of BSE to other species will invariably
present pathology typical of a scrapie-like disease.
snip...
http://www.bseinquiry.gov.uk/files/yb/1991/01/04004001.pdf
76 pages on hound study;
http://www.bseinquiry.gov.uk/files/sc/seac16/tab04.pdf
> I thought that in Britain dogs had contracted BSE, but perhaps not.
not so fast here;
The spongiform changes were not pathognomonic (ie.
conclusive proof) for prion disease, as they were atypical,
being largely present in white matter rather than grey matter in
the brain and spinal cord. However, Tony Scott, then head of
electron microscopy work on TSEs, had no doubt that these
SAFs were genuine and that these hounds therefore must have
had a scrapie-like disease. I reviewed all the sections
myself (original notes appended) and although the pathology
was not typical, I could not exclude the possibility that this was
a scrapie-like disorder, as white matter vacuolation is seen
in TSEs and Wallerian degeneration was also present in the
white matter of the hounds, another feature of scrapie.
38.I reviewed the literature on hound neuropathology, and
discovered that micrographs and descriptive neuropathology from
papers on 'hound ataxia' mirrored those in material from
Robert Higgins' hound survey. Dr Tony Palmer (Cambridge) had
done much of this work, and I obtained original sections
from hound ataxia cases from him. This enabled me provisionally to
conclude that Robert Higgins had in all probability detected
hound ataxia, but also that hound ataxia itself was possibly a
TSE. Gerald Wells confirmed in 'blind' examination of single
restricted microscopic fields that there was no distinction
between the white matter vacuolation present in BSE and
scrapie cases, and that occurring in hound ataxia and the hound
survey cases.
39.Hound ataxia had reportedly been occurring since the 1930's,
and a known risk factor for its development was the feeding
to hounds of downer cows, and particularly bovine offal.
Circumstantial evidence suggests that bovine offal may also be
causal in FSE, and TME in mink. Despite the inconclusive
nature of the neuropathology, it was clearly evident that this
putative canine spongiform encephalopathy merited further
investigation.
40.The inconclusive results in hounds were never confirmed,
nor was the link with hound ataxia pursued. I telephoned Robert
Higgins six years after he first sent the slides to CVL.
I was informed that despite his submitting a yearly report to the
CVO including the suggestion that the hound work be continued,
no further work had been done since 1991. This was
surprising, to say the very least.
41.The hound work could have provided valuable evidence
that a scrapie-like agent may have been present in cattle offal long
before the BSE epidemic was recognised. The MAFF hound
survey remains unpublished.
Histopathological support to various other published
MAFF experiments
42.These included neuropathological examination of material
from experiments studying the attempted transmission of BSE to
chickens and pigs (CVL 1991) and to mice (RVC 1994).
http://www.bseinquiry.gov.uk/witness/htm/stat067.htm
It was thought likely that at least some, and probably all, of the cases
in zoo animals were caused by the BSE agent. Strong support for this
hypothesis came from the findings of Bruce and others (1994)
( Bruce, M.E., Chree, A., McConnell, I., Foster, J., Pearson, G. &
Fraser, H. (1994) Transmission of bovine spongiform encephalopathy and
scrapie to mice: strain variation and species barrier. Philosophical
Transactions of the Royal Society B 343, 405-411: J/PTRSL/343/405
), who demonstrated that the pattern of variation in incubation period
and lesion profile in six strains of mice inoculated with brain
homogenates from an affected kudu and the nyala, was similar to that
seen when this panel of mouse strains was inoculated with brain from
cattle with BSE. The affected zoo bovids were all from herds that were
exposed to feeds that were likely to have contained contaminated
ruminant-derived protein and the zoo felids had been exposed, if only
occasionally in some cases, to tissues from cattle unfit for human
consumption.
snip...
http://www.bseinquiry.gov.uk/files/ws/s324.pdf
2005
DEFRA
Department for Environment,
Food & Rural Affairs
Area 307, London, SW1P 4PQ
Telephone: 0207 904 6000
Direct line: 0207 904 6287
E-mail: h.mcdonagh.defra.gsi.gov.uk
GTN:
FAX:
Mr T S Singeltary
P.O. Box 42
Bacliff
Texas
USA 77518
21 November 2001
Dear Mr Singeltary TSE IN HOUNDS
Thank you for e-mail regarding the hounds survey. I am sorry for the long delay in responding.
As you note, the hound survey remains unpublished. However the Spongiform Encephalopathy Advisory Committee (SEAC), the UK Government's independent Advisory Committee on all aspects related to BSE-like disease, gave the hound study detailed consideration at their meeting in January 1994. As a summary of this meeting published in the BSE inquiry noted, the Committee were clearly concerned about the work that had been carried out, concluding that there had clearly been problems with it, particularly the control on the histology, and that it was more or less inconclusive. However was agreed that there should be a re-evaluation of the pathological material in the study.
Later, at their meeting in June 95, The Committee re-evaluated the hound study to see if any useful results could be gained from it. The Chairman concluded that there were varying opinions within the Committee on further work. It did not suggest any further transmission studies and thought that the lack of clinical data was a major weakness.
Overall, it is clear that SEAC had major concerns about the survey as conducted. As a result it is likely that the authors felt that it would not stand up to r~eer review and hence it was never published. As noted above, and in the detailed minutes of the SEAC meeting in June 95, SEAC considered whether additional work should be performed to examine dogs for evidence of TSE infection. Although the Committee had mixed views about the merits of conducting further work, the Chairman noted that when the Southwood Committee made their recommendation to complete an assessment of possible spongiform disease in dogs, no TSEs had been identified in other species and hence dogs were perceived as a high risk population and worthy of study. However subsequent to the original recommendation, made in 1990, a number of other species had been identified with TSE ( e.g. cats) so a study in hounds was less
critical. For more details see-
http://www.bseinquiry, gov.uk/files/yb/1995/06/21005001 .pdf
As this study remains unpublished, my understanding is that the ownership of the data essentially remains with the original researchers. Thus unfortunately, I am unable to help with your request to supply information on the hound survey directly. My only suggestion is that you contact one of the researchers originally involved in the project, such as Gerald Wells. He can be contacted at the following address.
Dr Gerald Wells, Veterinary Laboratories Agency, New Haw, Addlestone, Surrey, KT 15 3NB, UK
You may also wish to be aware that since November 1994 all suspected cases of spongiform encephalopathy in animals and poultry were made notifiable. Hence since that date there has been a requirement for vets to report any suspect SE in dogs for further investigation. To date there has never been positive identification of a TSE in a dog.
I hope this is helpful
Yours sincerely 4
HUGH MCDONAGH
BSE CORRESPONDENCE SECTION
============================================
TSS
bse-tester
Well-known member
RKaiser wrote and mentioned something about me chasing the money- in so many words! Perhaps RK, if you knew my motives for testing you would not make such comments. I have made the promise to anyone who wishes to pick up our test that they can evaluate it with 1000 free tests in order to demonstrate that our test works. Further, I have already stated that I am not in this for the money - period! I am in it to further the research into prion disease and any profit that is derived from the testing will go directly into the development of post-graduate training for those researchers who wish to engage themselves with the study and research surrounding Prion Diseases. It is my goal to provide scholarships with all the funds gained from testing in order to provide for a steady and long term field of research into 1. CJD and all of its potential variants. 2. BSE specifically in the field of Risk Management for the Beef Industry. 3. Additional research into diseases such as Alzheimers which has long been misdiagnosed in the past. I am not going to expect to swim in money and I am certainly not trying to push our test down anybody's throat or put it on any pdestal as the Gold Standard. Time will tell and the appropriate authorities will make those decisions. But I will say that if there is any money left over from the testing and the research funding that our company is dedicated to making available, it will be used wisely to further the causes and goals that we feel suit the enhancement of research and perhaps even provde funding for field studies that will blend with the scholarships that we intend to fund. RKaiser, I am not seeking anything but the enhancement of the research. I have made my money elsewhere and this test that I own has all of the potential to be one that may well be the answer to a lot of concerns in the beef industry as well as the field of prion related medicine. Also, yes, we have spent in excess of 1.5 million pounds sterling and many many years of research up to this point to ensure that it not only works but provides the most accurate testing protocol ever seen - and it does. We are confident that once it has been validated, it will become a test that will be utilized. Again, time will tell.
rkaiser
Well-known member
So what are your motives BSE tester. Are they similar to those of Terry and Reader (the second). Did someone close to you pass away as well?
I am as compassionate as anyone on this site, but the continual challenge of dealing with people's feelings should not stop any of us from speaking out.
Do you all want to hear how, at 21 years of age, I carried my 95 pound (formerly 200 pound) father out to see the cattle for one last time before he passed away from cancer that started in his stomach?
Your story of charity is a nice read bse-tester, but do you truly want all of us to beleive that there will be no monetary benefit to the owner of a test that could conceivably be used on millions of cattle?
If you are ultimately concerned with the further research of Prion "disease" (word doesn't fit with prion in my dictionary) why not research. The only thing that your test does is bolster the conventional THEORY that prions are infectious. Go a step further. Show us how prions become misfolded. The X factor that Prusiner came up with and all of you scientific types follow simply does not cut it.
Good luck with your test BSE guy, I hope you are the one. The world will wait a long time for further research that proves that metal contamination is behind the misfolded prion and ranchers can't wait that long. We need to follow the lead of other contries that listen to their consumers and stop playing the BSEconomic game.
If you are willing to give up the muti millions that will flow to the company that is chosen to have "THE" test, good on you. If you waste that money on further research which follows the unproven theory of Prusiner ---shame on you.
I am as compassionate as anyone on this site, but the continual challenge of dealing with people's feelings should not stop any of us from speaking out.
Do you all want to hear how, at 21 years of age, I carried my 95 pound (formerly 200 pound) father out to see the cattle for one last time before he passed away from cancer that started in his stomach?
Your story of charity is a nice read bse-tester, but do you truly want all of us to beleive that there will be no monetary benefit to the owner of a test that could conceivably be used on millions of cattle?
If you are ultimately concerned with the further research of Prion "disease" (word doesn't fit with prion in my dictionary) why not research. The only thing that your test does is bolster the conventional THEORY that prions are infectious. Go a step further. Show us how prions become misfolded. The X factor that Prusiner came up with and all of you scientific types follow simply does not cut it.
Good luck with your test BSE guy, I hope you are the one. The world will wait a long time for further research that proves that metal contamination is behind the misfolded prion and ranchers can't wait that long. We need to follow the lead of other contries that listen to their consumers and stop playing the BSEconomic game.
If you are willing to give up the muti millions that will flow to the company that is chosen to have "THE" test, good on you. If you waste that money on further research which follows the unproven theory of Prusiner ---shame on you.
Northern Rancher
Well-known member
Porker of course my kids eat wild game-if I quit feeding them everything that was supposedly bad for them-they'd look like Ethiopians-the merchandising of fear is pretty much what drives the economies of the world today unfortunately.
bse-tester
Well-known member
I thought I made myself clear. I guess the idea of compassion and a desire to want to provide something is alien to you? All I want is to make this place I live in a little easier for those who need to have something to look forward to. Whether it be an early diagnosis of CJD or Alzheimers or whether it be the detection of BSE in a producers animal. I frankly am not concerned with these arguments as to whether or not metals cause BSE or if it is caused by the sudden onset of daisies growing on the back of your head. I own a test that will detect PrPsc in urine and that is it! I leave it to you guys to rant and rave over how it should be defined or described and how it enters the system or what causes it to manifest itself in humans or animals.
I am simply saying that I have made my money elsewhere and my company has this test which we intend to make available to all who can use it. The proceeds from it, that is, any and all profits, will be turned into precisely what I have previously explained. I leave it to the "others" who wish to make money and drive up the price of anything of value in order to rape and plunder society further. I have no interest in doing that. My partner and I are doing this purely as a humanitarian effort and nothing more. Of course, you are entitled to your own conclusions but I have made my position clear and hopefully you will understand why I am doing this? Of course, that is for you to decide. As for stories of ailing parents - they are sad and part of life. I applaud you for doing what you did.
I am simply saying that I have made my money elsewhere and my company has this test which we intend to make available to all who can use it. The proceeds from it, that is, any and all profits, will be turned into precisely what I have previously explained. I leave it to the "others" who wish to make money and drive up the price of anything of value in order to rape and plunder society further. I have no interest in doing that. My partner and I are doing this purely as a humanitarian effort and nothing more. Of course, you are entitled to your own conclusions but I have made my position clear and hopefully you will understand why I am doing this? Of course, that is for you to decide. As for stories of ailing parents - they are sad and part of life. I applaud you for doing what you did.
bse-tester
Well-known member
rKaiser wrote:
If you are willing to give up the muti millions that will flow to the company that is chosen to have "THE" test, good on you. If you waste that money on further research which follows the unproven theory of Prusiner ---shame on you.
If you are willing to give up the muti millions that will flow to the company that is chosen to have "THE" test, good on you. If you waste that money on further research which follows the unproven theory of Prusiner ---shame on you.
The only thing that your test does is bolster the conventional THEORY that prions are infectious. Go a step further. Show us how prions become misfolded. The X factor that Prusiner came up with and all of you scientific types follow simply does not cut it.
I see that you again attack Prusiner and link his research to mine - how do you come to that conclusion? Do you think that all prion research follows that of Prusiner? That would be foolish indeed. As for you making suggestions as to how our test works - you literally have no idea how it works and to make uninformed statements regarding that, is truly mundane. Look beyond your window and you may see that there are some people who want to do things and simply do not care about the monetary gain. As for suggesting that I would allow the research I fund to follow the "...unproven theory of Prusiner - shame on you," I would say to you that you have little or no understanding how the world of research actually works and if for one minute you feel that it would be my intention to waste money on mindlessly following the lead of some other scientist, even if he has won the Nobel Prize, then you are truly wrong.
rkaiser
Well-known member
bse-tester
I come to the conclusion about Prusiner very quickly when you continue to use the word disease when you speak of prions. You cannot say that your posts have been unbiased bse-tester.
Do you beleive that BSE is transmitted through feed as an agent?
I apologze if I keep pissing you off with talk about money. There will be a lot of it around for the first globally accepted test that claims to detect misfolded prions in animals of any age, and that is a fact.
I would like to learn more about your test bse-tester. I have said many times that I beleive testing animals for BSE to access markets is an opportunity for producers. Goodsness knows opportunities has been few and far between for producers in this BSE era.
Send me a link to your web site and let this frustrated rancher have a look.
[email protected]
I see that you again attack Prusiner and link his research to mine - how do you come to that conclusion? Do you think that all prion research follows that of Prusiner? That would be foolish indeed. As for you making suggestions as to how our test works - you literally have no idea how it works and to make uninformed statements regarding that, is truly mundane. Look beyond your window and you may see that there are some people who want to do things and simply do not care about the monetary gain. As for suggesting that I would allow the research I fund to follow the "...unproven theory of Prusiner - shame on you," I would say to you that you have little or no understanding how the world of research actually works and if for one minute you feel that it would be my intention to waste money on mindlessly following the lead of some other scientist, even if he has won the Nobel Prize, then you are truly wrong.
I come to the conclusion about Prusiner very quickly when you continue to use the word disease when you speak of prions. You cannot say that your posts have been unbiased bse-tester.
Do you beleive that BSE is transmitted through feed as an agent?
I apologze if I keep pissing you off with talk about money. There will be a lot of it around for the first globally accepted test that claims to detect misfolded prions in animals of any age, and that is a fact.
I would like to learn more about your test bse-tester. I have said many times that I beleive testing animals for BSE to access markets is an opportunity for producers. Goodsness knows opportunities has been few and far between for producers in this BSE era.
Send me a link to your web site and let this frustrated rancher have a look.
[email protected]
