i have a few files stored about harash narang and his urine test and the history thereof, and thought some might be interested...tss
BSE Prion Solutions Inc
BioTech Global
This is a company based in the UK that is using technology developed largely by Harash Narang with the group at the Institute of Pathology, Case Western Reserve University 2085 Adelbert Rd, cleveland Ohio.
This is using the urinary extraction of PrPc from the patients (or cattle). The method involves the extraction of the PrPc onto resins at a specific ionic level present in the urine.
They are expecting to carry out work with BSE Prion Solutions Inc. in Canada.
http://www.priondata.org/data/A_codiagBC.html
ProMetic Life Sciences Inc
www.prometic.com
ProMetic Life Sciences Inc.
Pierre Laurin, President and CEO
6100 Royalmount Ave., Montreal,
Quebec H4P 2R2, Canada
Tel.: 514-496-2115
Fax: 514-496-2079
Employees: 50-100
Financial Affairs: Revenues (2000)C$2.2M Net Profit C$5.24M R & D Expenses C$3.8M
July 3, 2001 From a press release
ProMetic Life Sciences (TSE: PLI) has signed a Memorandum of Understanding (MOU) with the American Red Cross (ARC) to form a new company (this is called PRDT). In accordance with the MOU, the final agreements are scheduled to be completed by September 30, 2001. Once established, the new venture is expected to utilize ProMetic's platform technology and the ARC's expertise in Transmissible Spongiform Encephalopathy (TSE) research and pathogen clearance in blood products.
Under the terms of the MOU ProMetic and the ARC will contribute intellectual property and other know-how to develop diagnostic and removal systems to control the possible transmission of TSEs from human blood and blood products. The scope of the agreement between the American Red Cross and ProMetic also includes the removal of viruses.
Dr Dealler's opinion
The exact technique that they are considering using is not clear. The main thing that may be involved is the use of phosphotungstic acid attached to a carrier. It is known that PTA precipitates prions, and it is considered that PTA, when carried and with the blood flowing past, would cause the prions to be taken from the blood. There are a number of potential problems with this in that PTA also removes other things and the charged compounds that also interact with the prions do the same. I think that if it is intended to use this for a diagnostic process, it may be necessary to lyse white cells first and then to use an extremely sensitive technique to indicate the prions. At the moment the problem is really with the background noise when indicating the prions and not the extraction of the prions from the blood per se. I suspect they may well be involved with Prusiner's system that has been patented (United States Patent Application 6,221,614). Its abstract:
"Devices such as flow through columns, substrates such as spherical polymer beads, and methods
of using such to remove prions from any liquid sample are disclosed. A surface of a substrate is
coated with a prion complexing agent, such as a salt of phosphotungstic acid. Blood or plasma
passing through a column containing beads coated with prion complexing agent are rendered
prion free."
You may also wish to note that Dr Harash Narang's method is fully patented and appears to do a very similar thing.
Also, you may be interested to know that Seprion from Microsens(also a powerful ligand to prions) is also patented
The announcement in 2003 of the successful experiments in the USA using their PRDT's ligands was good but the large amounts of money that American Red Cross has put into it must mean they are expecting to get a lot out and there are several compettitors.
--------------------------------------------------------------------------------
http://www.priondata.org/data/A_codiagPQ.html
The BSE Inquiry / Statement No 113
Dr Harash Narang (scheduled to give evidence 13th July 1998)
snip...
c) Urine Test
1.11 Mice inoculation studies have revealed that CJD blood has 1,000 units of
infectivity per ml. I have developed a simple method to concentrate the agent
from CJD patients' urine and I have by EM demonstrated the presence of both
NVF and SAF similar to those seen in brain samples of CJD victims. I have used
this CJD urine test on a number of live subjects who have subsequently died and
7
were confirmed to have had CJD by the Surveillance Unit in Edinburgh (For
example Victims 12, 14, 15, 16,19 and 23). Shortly after I was asked by the
parents of victim 12 to carry out a urine test on victim 12 the victim's relatives
were contacted by Dr Duke of MRC in October 1995. Dr Duke told the relatives
that the test had not been approved and suggested to the relatives that they could
take a legal action against me for ethical reasons which he would support. They
did not agree with this suggestion and I duly carried out the test. I used the urine
test on Victim 16 (see below). His parents approached me after they had been
told repeatedly by doctors that he was too young to be suffering from CJD and
that his symptoms were not those of CJD. In January 1996 the urine test
confirmed that he had CJD. Following this his mother insisted upon the post
mortem which her doctors were advising was not necessary because they were
unlikely to learn anything. Five weeks after Victim 16's death the post mortem
confirmed CJD. In the light of this experience it must be expected that other
young individuals who have died of CJD have not been subject to a post mortem
and are therefore not included in the definite, probable or possible statistics. After
I carried out the first urine test in 1995 on Victim 12 I was told by Dr Will of the
Surveillance Unit that more urine specimens from CJD victims would be made
available to me. Eventually in 1997 MRC funded a project in Leeds University to
verify the urine test.
However many of the urine specimens which we have been receiving from the
Surveillance Unit are either not fresh or have been sub-optimal in other ways (in
two cases the tubes have been empty). In one instance a specimen letter was
dated the 21st July 1997 although a handwritten note in the letter stated that the
specimen was collected on 29th July 1997 at 17.30 hours. The post office stamp
was 23rd July. The letter was delivered on the 25th July.
9
to detect CJD in humans. The science involved in this technique is well
understood. This method is more user friendly and is also cheaper. Hundreds of
specimens can be tested within one working day and this process would be very
useful for the purpose of testing blood donors. Since March 1997 I have been
funded by MRC to carry out work using EM techniques. Initially they told me at
a meeting with MAFF that they would also purchase western blotting equipment
to develop the urine test. However, they are now very reluctant to allow me to
develop western blotting at the same time. Mr Ken Bell agreed to purchase
western blotting equipment when my request for funding to MRC, MAFF and
Department of Health was not progressed. The only way to understand these
problems is to visit the laboratory.
1.13 Had any of these various tests been funded or supported in any way by
Government bodies it would have been possible to set up a slaughter house test
for diagnosing subclinical BSE in cattle that had not yet shown the symptoms of
the disease, but which were entering the national diet. In this way the disease
could have been eradicated as I explained on many occasions at the time (see paras
2.12, 2.13, 2.30, 2.31, 2.35 and 2.40). The whole culling policy, which in my
view is fundamentally flawed, would also have been avoided. Far from assisting
and furthering my researches, however, my employers and other bodies have
consistently interfered with and hindered my researches to the extent that such
progress as has in fact occurred has been solely due to the generosity of a private
businessman, Mr Ken Bell. I will deal in my chronology with the obstacles which
have been put in the way of my researches.
1.14 Details of my researches and papers are set out at paragraph 1.14 and in my book
" The Link". (ISBN-O-9530764-0-7).
P.S. Harash sent me a copy of his book the Link and it is very interesting, worth reading;
snip...
Organophosphates
1.19 There is a theory that the widespread use of organophosphates might have been
responsible for BSE. This theory could have easily been tested in laboratory
12
animals by exposing some animals to different concentrations of organophosphates
at different intervals and then injecting some with BSE but not others and then
comparing these animals with animals (both BSE infected and not BSE infected)
which have not been exposed to organophosphates.
1.20 BSE cases have appeared on some organic farms where the animals have not been
fed with MBM including the farm owned by Jeff Nichols. This led to the belief
that organophosphates might be responsible for BSE. However, I have discussed
this phenomenon with three organic farmers and I visited several organic farms
during 1994. I established that the cows on the farm had been exposed to and had
eaten poultry manure, which is widely used on organic farms. I have personally
witnessed cows eating poultry manure from a heap of manure waiting to be spread
on an organic farm. It is also an established practice to add bird droppings into
some cattle feed. Since MAFF allowed poultry to be fed on meat and bone meal
until 1996, the poultry droppings would contain large amounts of the undigested
agent.
snip...full text 56 pages;
http://www.bseinquiry.gov.uk/files/ws/s113.pdf
9. I took part in a world in Action interview which was not actually used given the plethora
of material they had to incorporate into a 30 minutes programme. During discussions
with them, the name of Harash Narang came up. I had previously seen an article in the
Liverpool Daily post alleging that this man had been removed from his research into a
live test for BSE. I had many conversations and meetings with Narang as we discussed
the possibility of testing our herd. He told that it was illegal to hold samples of urine,
brain or whatever from a bovine suspected of BSE, that his test was not recognised and
that he had no access to facilities in this country. I wrote to the Minister of Agriculture 9th
January 96 asking had he any objection to me taking random samples of urine for testing
by Harash Harang for BSE. The very people, who have the power to authorise validation
of such a test, wrote back to me telling me, that his test was invalidated!
10. I had a conversation with a Dairy Farmer who compared the situation with contagious
abortion some 15 years previous. He said to me that in some herds Brucellosis was a
serious problem and a private laboratory had developed a live test for that disease. The
Ministry of Agriculture had refused to adopt the test so, one by one, individual farmers
had their herds tested privately. In the absence of any disposal scheme they dumped their
reactors on the open market. The outcome of this was that the farms which purchased
these infected cows, had flare-ups of contagious abortion. The situation became so
serious that the Ministry of Agriculture were forced to adopt the test. Assuming this is
accurate, History would appear to be repeating itself! I was not bothered whose test for
BSE got off the ground as long as one did. There has been endless publicity about the
appalling treatment of this Encophalopathy Specialist. If this man's test does not work or
is unreliable, it would not be very difficult for other Encephalopathy specialists who
know what they are talking about, to demonstrate that fact! In the meantime I trust his
work for the Medical Research Council on new variant CJD is bearing fruit.
11. During my discussions with Harash Narang further food for thought was provided. Up till
1994 we had received annual consignments of Turkey Manor from our neighbours farm.
This material was acceptable to Organic Standards from a welfare point of view as the
deep litter Turkeys where housed at low density – their eggs were for hatching. Harash
Narang's opinion is that if infective agent goes into a Turkey through the feed, that agent
will be absorbed or excreted by the Turkey or both and that the breakdown of the agent
would be slow. There had been occasions when our cattle had been exposed to the
manure heat in the field due to failure of the Electric fence. I have personally witnessed
an animal actually eating the manure for whatever reason! Clearly we were well away
from best practice at that Juncture. This left me with the questions did our BSE come
from the animal manure and not from original animal purchase, also would there be
Organo-phosphate residues in those manure? I wrote to the producer of the Turkey
Manure asking him just that but he chosen to ignore my letter. How complex it is to
unravel the mysteries and how simple it would be just to follow well financed best
practice. I am in no doubt that Organic Livestock producers should be able to maintain
fertility without accessing manure from other holdings. Just by good practice and
maintaining legumes in the sward. I'm afraid nobody likes (what appear to be) a bargain,
more than a farmer and free manure falls into that category. We stopped accessing that
manure in 1994 and had spread the last by 1996.
12. Currently most of my farmer neighbours are allowing the paper industry to spread 100
tonnes of paper waste per acre, on their land, despite the concoction of residues from the
print process, despite the high levels of Cancer and Asthma in the print industry - despite
records of tainted milk. This process is being over seen by the Ministry of Agriculture.
13. Just to complicate the matter even further we have a problem sewer that runs through part
of the farm. Every year thousands of gallons of raw sewage and whatever else, come
down the brook courtesy of the Borough Council. Any attempts to address the problem
have been thwarted by the Alliance of the local environmental health plus the
environment agency plus the Ministry of Agriculture, that's to say we had a dead animal
who had been in the proximity of the brook. Having made no progress with
environmental health or the environment agency over 20 years, I spoke to the Ministry of
Agriculture Pollution Incidents dept. about this animal. They did not want me in their intray!
"No Mr. Nicholls! Don't have your animals tested, no Mr. Nicholls don't have your
brook tested, no Mr. Nicholls don't have your animals wormed if any of them are not
doing well." I can find no case for confidence in my Ministry of Agriculture.
14. During my discussions with MAFF BSE officials, it became apparent that the Ministry
did not encourage farmers to offer opinion! Due to problems with the decision making
process on our farm the levels of Phosphate reserves on tow of our fields, went below a
safe level. BSE cow no. 4 was seen stripping bark of trees whilst contained in one of
those fields. Soil and fodder analysis confirmed the problem. Had the imbalance made a
contribution to the cow's BSE? I told MAFF verbally, they did not want to know! They
said it would be "just an added stress!"
15. After case no. 1, there was the interrogation and the forms to fill in but I don't recall
questions about minerals and feeding practice beyond "Will they have received MBM?"
They were not looking for any other common denominators. My industry is well drilled
on how Spring applications of Potash can lock up Magnesium and cause Grass Staggers
but other problem combinations are less publicised/understood. Helen Fullerton of
Farming and Livestock Concern has I know, made a contribution to this Inquiry which
includes discussion about, in particular, selenium deficiency. Historically in this country
during at least the 60's, subsidy was paid for the application of lime and as long as such
applications followed best practice such expenditure of taxpayers money was to be
applauded. The practice was discontinued. I feel sure it should have been continued and
what is more, in this the age of science, comprehensive soil analysis should have been a
part of the programme.
16. The importance of live testing became more obvious by the day. As farms became
polarised into BSE farms and BSE free farms. I was left questioning how do you tell
which of the BSE free farmers are telling the truth? How many of them who operate a
relatively early cull policy, have failed to even observe symptoms. I could have tucked
our BSE cows into the Barrens at Chester Market without any bother. Although if we had
sent them to Beeston Market, Geoffrey Moss of "World in Action" fame, might have
picked them out. Our record could allegedly have been clean today!
snip...
http://www.bseinquiry.gov.uk/files/ws/s135a.pdf
DR HARASH NARANG
14. Dr Harash Narang first became known to me from reports in my local regional
newspaper, The Journal, of the work he was undertaking at Newcastle General
Hospital on behalf of the Public Health Laboratory Service. His work was reported to
be involved with the identification of CJD, loosely described as the human equivalent
to BSE. As the principal opposition spokesman on the issue I was naturally interested
and made contact with Dr Narang in March 1990. He invited me to his place of work
and demonstrated to me how he used electron microscopy to identify CJD; methods
he felt could be used for BSE identification which at that time was taking some
considerable time. If a speedier diagnostic test were available I felt amongst other
things this would permit random sampling of routine slaughtered cattle.
15. I of course was not in a position to make any judgement on the efficacy of his
proposals but he had worked with a Nobel Prizewinner, D Carleton Gajdusek, and
indeed they had published academic papers together. As such, I felt that his work was
at least worthy of further evaluation and contacted the Ministry of Agriculture
Fisheries and Food accordingly. However, I was disappointed by what I considered to
be the negative attitude of MAFF to this scientist employed by another department of
government.
16. This disappointment turned to shock and anger when I learned that he had been
suspended, and later dismissed, by the PHLS in April 1991. Fortunately, a generous
benefactor appeared in the form of Ken Bell a renowned seafood processor in the
North East of England. Mr Bell spent ten of thousands of pound sterling in support of
Dr Narang thus permitting further work to be undertaken.
17. I cannot substantiate my opinions but I have always felt that Harash Narang's work
was never given the serious consideration it deserved from the MAFF scientific
establishment, throughout his dealings with the authorities, he seemed to have one
obstacle after another placed in his way. I had particular experience in this when I
was involved in trying to obtain heads of cattle for him to try his experiments. Every
difficulty possible was put in his way. I feel that this is reflected in the BSE Inquiry
Draft Factual Account, "DFA 11," The Touch Test, which the Inquiry has published.
18. I was always impressed by Dr Narang's endeavours and his honesty. He was the first
person to draw to my attention the possibility of BSE being manifested in humans in
some form of CJD, a notion not generally accepted by the MAFF scientific
establishment. It seemed to me that they regarded Dr Narang's work to be in some
way heretical and it was as if he were to be successful in his diagnostic tests the
whole of the British beef industry would be put at threat.
http://www.bseinquiry.gov.uk/files/ws/s428.pdf
THE ROYAL SOCIETY: LIVESTOCK INFECTIONS
Submission by Dr Harash K Narang
a) My background, qualifications and scientific views
I have the following qualifications
a.
b.
c.
d.
e. MRC Path 198 1
f. FRC Path 1991
Batchelor of Science - Botany Chemistry and Zoology (Hons-Punjab University 1961)
Master of Science - Zoology, Rajasthan University 1963
Doctor of Philosophy - Zoology (Parasitology) Newcastle upon Tyne University 1969
Diploma in Electron microscopy 1973
I have devoted some 30 years of my professional career partly working in the Medical Research
Council as a research scientist, and partly in the Public Health Laboratory as a clinical
microbiologist, in particular with viral infections. I have a particular expertise with diseases
classified as Spongiform Encephalopathies (SEs) in both animals and humans. SEs includes
bovine spongiform encephalopathy (BSE), Creutzfeldt-Jakob disease (CJD) and Kuru.
I have published many research papers in scientific journals describing these diseases in depth;
their origins, transmission, pathogenesis and the nature of the infective agent (Appendix 1).
I have also presented numerous papers to national and international scientific meetings and have
published two books, referred to later in this submission.
The Government set up a BSE Inquiry at a cost of E27 million in order to learn something,
namely how not to repeat such incidents. But have we learned the right lessons fi-om the outbreak
and from the investigations? What did we learn?
snip...
http://www.royalsoc.ac.uk/inquiry/index/288.pdf
A Protease Resistant PrP Isoform Is Present In
Urine of Animals and Humans Affected with Prion
Diseases
Gideon M. Shaked, Yuval Shaked, Zehavit Kariv-Inbal, Michele Halimi, Inbal
Avraham and Ruth Gabizon
Department of Neurology, the Agnes Ginges Center for Human
Neurogenetics, Hadassah University Hospital, Jerusalem, Israel
Correspondence to:
Ruth Gabizon, Ph.D.
Department of Neurology
Hadassah University Hospital,
Jerusalem, Israel
Fax: 972.2.6429441
e-mail:
[email protected]
running title: Prion Protein in Urine.
Copyright 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
JBC
PrPSc, the only known component of the prion, is present mostly in the
brains of animals and humans affected with prion diseases. We now show
that a protease resistant PrP isoform can also be detected in the urine of
hamsters, cattle and humans suffering from TSEs. Most important, this PrP
isoform (UPrPSc) was also found in the urine of hamsters inoculated with
prions long before the appearance of clinical signs. Interestingly, i.c.
inoculation of hamsters with UPrPSc did not cause clinical signs of prion
disease even after 270 days, suggesting it differs in its pathogenic properties
from brain PrPSc. We propose that the detection of UPrPSc can be used to
diagnose humans and animals incubating prion diseases, as well as to
increase our understanding on the metabolism of PrPSc in-vivo.
Key words
Urine, prion, PrP, diagnosis
http://www.jbc.org/cgi/reprint/C100278200v1.pdf
MINIREVIEW
Lingering Doubts about Spongiform
Encephalopathy and Creutzfeldt-Jakob Disease
HARASH K. NARANG1
Ken Bell International, Newcastle Upon Tyne NE2 3DH, United Kingdom
Bovine spongiform encephalopathy (BSE) is an infectious disease
and has been transmitted orally to many other animals,
including humans. There is clear evidence of maternal transmission,
although disagreement on the source of the BSE agent
remains. The current theories link the origin of BSE to common
scrapie in sheep. Twenty different strains of the scrapie
agent have been isolated from sheep. A search of the literature
indicates two distinct clinical syndromes in sheep, both of
which have been called scrapie. I have designated these Type I
(the common type), which exhibits itchiness and lose their
wool, and Type II, which exhibits trembling and ataxia. Sheep
inoculated with BSE develop Type II scrapie and they exhibit
trembling. When cattle or mink are injected with the Type I
strain, only a few will develop a clinical disease. By contrast,
no clinical disease has so far been shown in cattle or mink
by feeding them with Type I-infected sheep brains. However,
either by injecting or feeding with the BSE strain, 100% of
calves and mink develop the clinical disease. Evidence suggests
that Type II is the cause of BSE. Identical clinical signs
of Type II trembling are found in kuru and many of the recent
cases of Creutzfeldt-Jakob disease. The BSE agent has caused
spongiform encephalopathies (SEs) in domestic cats, tigers,
and in some species of ruminants in zoos. The nature of the
BSE agent remains unchanged when passaged through a
range of species, irrespective of their genetic make up, demonstrating
that variations in the host PrP gene are not a major
factor in the susceptibility to the BSE agent. Since more than 85
zoo animals of many species have been diagnosed with SEs,
from these studies it seems reasonable to conclude that the
BSE agent can infect almost all mammalian species, including
humans. For eradication of BSE and to reduce the risk of infection
to humans, the development of a vaccine against BSE is
suggested. Such a possibility should be fully explored.
http://www.ebmonline.org/cgi/reprint/226/7/640.pdf
MINIREVIEW
A Critical Review of Atypical Cerebellum-Type Creutzfeldt-Jakob Disease: Its Relationship to ``New Variant'' CJD and Bovine Spongiform Encephalopathy
Harash K. Narang,1
Ken Bell International, Newcastle-upon-Tyne NE2 3DH,United Kingdom
Abstract
Shortly after the appearance of bovine spongiform encephalopathy (BSE), Creutzfeldt-Jakob disease (CJD) was identified in young patients with nonclassical presentation such as difficulty in balancing and ataxia. The classical CJD in older patients starts with dementia. To distinguish between the two types, CJD in young persons has been termed ``new variant'' (nvCJD). The distinguishing features of classical CJD include initial presentation with dementia, confluent spongiform changes are very unusual in the cerebellum, and PrP plaques are rarely observed. For nvCJD, initially, difficulty with balancing and ataxia occurs, confluent spongiform changes are seen in the cerebellum, and a large number of PrP plaques are seen. The Icelandic observation of sheep scrapie revealed a predominantly ataxic form of scrapie, termed Type II, rather than the itchy form termed Type I. Both types have been known to exist in Europe. Since the clinical signs of Type II scrapie in sheep with trembling and ataxia are similar to those seen in BSE and nvCJD, this suggests that Type II is the cause of BSE and nvCJD. Over 8 years, from 1989 to 1996, I examined the clinical histories of 33 CJD cases aged between the ages of 18 and 84. Six under the age of 40 and 15 over the age of 40 had leading clinical features such as difficulty in balancing and ataxia similar to those seen in the young cases classified as ``nvCJD.'' Brains were examined from the six of 15 cases over the age of 40, which revealed similar pathology to that seen in young patients classified as ``nvCJD.'' These findings suggest that all age groups are susceptible to the strain of the agent derived from BSE cattle.
snip...
In Conclusion
Since the first appearance of BSE, CJD has been identified in young patients. However, based on the three main distinguishing features described above and on a literature review, it has been revealed that patients of all age groups have died of CJD, but have not been recorded as such; older patients have been disqualified by age. The term ``new variant'' (nvCJD) was introduced because it was thought to be a new strain. However, realizing that the disease pre-existed, the term ``variant'' CJD (vCJD) has recently been introduced. A study of Icelandic sheep scrapie and review of the European scientific literature has demonstrated the existence of two strains of scrapie in sheep: Type I, ``itchy'' and Type II, the ataxic ``trembly'' type. Cases of the ataxic-cerebellar form of CJD were described 20 to 30 years before BSE appeared. These clinical signs, trembling and ataxia, are similar in BSE, vCJD, kuru, and in sheep inoculated with brain tissues from cows. Since the clinical signs of Type II scrapie in sheep with trembling and ataxia are similar to those seen in BSE and nvCJD, this suggests that Type II is the cause of BSE and vCJD. Many ``atypical'' cases, with all the unusual leading clinical features such as difficulty in balancing and ataxia, have been reported in patients. Because PrP immunostaining techniques were unavailable in the past, these patients' brains should be re-examined for PrP plaques, along with CJD patients who have received a blood transfusion. The pattern and distribution of PrP plaques should be used as a guide to determine the strain and source of infection and confirm that the name nvCJD is misleading.
http://www.ebmonline.org/cgi/reprint/226/7/629.pdf
MINIREVIEW
A Critical Review of the Nature of the
Spongiform Encephalopathy Agent:
Protein Theory Versus Virus Theory1
HARASH NARANG2
Ken Bell International, Newcastle Upon Tyne NE2 3DH, United Kingdom
http://www.ebmonline.org/cgi/reprint/227/1/4.pdf
Subject:
[BLOODCJD] Hadassah team identifies something already identified, but ''covered up'' for
years $$$ NARANG GETS BURNED...
Date:
Mon, 02 Jul 2001 17:29:48 -0700
From:
"Terry S. Singeltary Sr."
Reply-To:
[email protected]
To:
[email protected],
[email protected]
Greetings Lists Members,
who _really_ developed the Urine Test???
Hadassah team identifies 'mad cow' protein in urine
http://www.hadassah.org.il/news/MadCowEarltDetectJP020701.htm
NO, it was NARANG $$$
they really stuck it to old Narang,
time and time again...
damn shame $$$$$$$$$$$$$$$$$$$$$$$$
TSS
http://www.vegsource.com/talk/madcow/messages/9634.html
From: TSS
Subject: BSE REPORT APRIL 2005
Date: September 6, 2005 at 8:57 am PST
for all consumers
BSE
REPORT
April 2005
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
snip.......
http://www.vegsource.com/talk/madcow/messages/1000089.html
THE LINK ;
http://www.cjdfoundation.com/Books.htm
http://www.cjdfoundation.com/contents%20Link.htm
Death on the Menu
http://www.cjdfoundation.com/contents%20death.htm
TSS
