econ wrote ;
> It is the failed U.S. policy that is the problem, not the Japanese policy.
> The Japanese just happen to know that.
:clap: :clap: :clap:
Amen there econ! and the other thing is that most cattle ranchers, feeders, packers and such, don't, did not, and or refuse to know it. it's like what the hell, we got to die from something, and the incubation time, and this stupid spontaneous combustion of a prion theory that usda et al are pushing, is just spreading the agent even further. they knew in 2000 that kuru could last 50 years or longer. that is why this administration has put TSE on the back burner, especially in funding, compared to other disease. my only other hope if this in fact is the case, is that these old farts (politicians, industry, and there lobbyiest causing these failed policies for BSE/TSE in the USA), will die a slow death, from a TSE. yep, i said it. until some high ranking people, movie stars, or such start dying from THIS disease, nothing else will be done. it's like the same old song and dance, that more people die from car wrecks, smoking, or whatever, than TSEs. well, for one thing mom drove all her life, smoked for part of it, but she died from the Heidenhain Variant of CJD, just another name for the same gd disease. just another persons name. Reagan died from Alzhiemers, just what is Alzheimers? it's so close to a TSE that many scientists are very concerned, but you will not see that mentioned anywere. or will you?
Subject: Transmissibility of mouse AApoAII amyloid fibrils: inactivation by physical and chemical methods
Date: March 22, 2006 at 6:31 am PST
The FASEB Journal Express Article doi:10.1096/fj.fj.05-4890fje
Published online March 20, 2006
Transmissibility of mouse AApoAII amyloid fibrils: inactivation by physical and chemical methods
Huanyu Zhang, Jinko Sawashita, Xiaoying Fu, Tatsumi Korenaga, Jingmin Yan, Masayuki Mori, and Keiichi Higuchi
E-mail contact:
[email protected]
AApoAII amyloid fibrils have exhibited prion-like transmissibility in mouse senile amyloidosis. We have demonstrated that AApoAII is extremely active and can induce amyloidosis following doses less than 1 pg. We tested physical and chemical methods to disrupt AApoAII fibrils in vitro as determined by thioflavin T binding and electron microscopy (EM) as well as inactivating the transmissibility of AApoAII fibrils in vivo. Complete disruption of AApoAII fibrils was achieved by treatment with formic acid, 6 M guanidine hydrochloride, and autoclaving in an alkaline solution. Injection of these disrupted AApoAII fibrils did not induce amyloidosis in mice. Disaggregation with 6 M urea, autoclaving, and alkaline solution was incomplete, and injection of these AApoAII fibrils induced mild amyloidosis. Treatment with formalin, delipidation, freeze-thaw, and RNase did not have any major effect. A distinct correlation was obtained between the amounts of amyloid fibrils and the transmissibility of amyloid fibrils, thereby indicating the essential role of fibril conformation for transmission of amyloidosis. We also studied the inactivation of AApoAII fibrils by several organic compounds in vitro and in vivo.
AApoAII amyloidosis provides a valuable system for studying factors that may prevent transmission of amyloid disease as well as potential novel therapies.
http://www.fasebj.org/cgi/content/abstract/fj.05-4890fjev1
another transmissible protein amyloidosis? what does this implicate with Alzheimer's and TSE, if anything?.........TSS
CJD1/9 0185
Ref: 1M51A
IN STRICT CONFIDENCE
Dr McGovern From: Dr A Wight
Date: 5 January 1993
Copies: Dr Metters
Dr Skinner
Dr Pickles
Dr Morris
Mr Murray
TRANSMISSION OF ALZHEIMER-TYPE PLAQUES TO PRIMATES
1. CMO will wish to be aware that a meeting was held at DH yesterday,
4 January, to discuss the above findings. It was chaired by Professor
Murray (Chairman of the MRC Co-ordinating Committee on Research in
the Spongiform Encephalopathies in Man), and attended by relevant
experts in the fields of Neurology, Neuropathology, molecular biology,
amyloid biochemistry, and the spongiform encephalopathies, and by
representatives of the MRC and AFRC.
2. Briefly, the meeting agreed that:
i) Dr Ridley et als findings of experimental induction of p amyloid
in primates were valid, interesting and a significant advance in the
understanding of neurodegeneradve disorders;
ii) there were no immediate implications for the public health, and no
further safeguards were thought to be necessary at present; and
iii) additional research was desirable, both epidemiological and at the
molecular level. Possible avenues are being followed up by DH
and the MRC, but the details will require further discussion.
93/01.05/4.1
http://www.bseinquiry.gov.uk/files/yb/1993/01/05004001.pdf
BSE101/1 0136
IN CONFIDENCE
5 NOV 1992
CMO From: Dr J S Metters DCMO 4 November 1992
TRANSMISSION OF ALZHEIMER TYPE PLAQUES TO PRIMATES
1. Thank you for showing me Diana Dunstan's letter. I am glad that MRC have
recognised the public sensitivity of these findings and intend to report
them in their
proper context. This hopefully will avoid misunderstanding and possible
distortion by
the media to portray the results as having more greater significance than
the findings
so far justify.
2. Using a highly unusual route of transmission (intra-cerebral injection)
the
researchers have demonstrated the transmission of a pathological process
from two
cases one of severe Alzheimer's disease the other of Gerstmann-Straussler
disease to
marmosets. However they have not demonstrated the transmission of either
clinical
condition as the "animals were behaving normally when killed'. As the report
emphasises the unanswered question is whether the disease condition would
have
revealed itself if the marmosets had lived longer. They are planning funher
research
to sec if the conditions, as opposed to the partial pathological process, is
transmissible.
What are the implications for public health?
3. . The route of transmission is very specific and in the natural state of
things
highly unusual. However it could be argued that the results reveal a
potential risk,
in that brain tissue from these two patients has been shown to transmit a
pathological
process. Should therefore brain tissue from such cases be regarded as
potentially
infective? Pathologists, morticians, neuro surgeons and those assisting at
neuro
surgical procedures and others coming into contact with "raw" human brain
tissue
could in theory be at risk. However, on a priori grounds given the highly
specific
route of transmission in these experiments that risk must be negligible if
the usual
precautions for handling brain tissue are observed.
92/11.4/1-1
BSE101/1 0137
4. The other dimension to consider is the public reaction. To some extent
the GSS
case demonstrates little more than the transmission of BSE to a pig by
intra-cerebral
injection. If other prion diseases can be transmitted in this way it is
little surprise that
some pathological findings observed m GSS were also transmissible to a
marmoset.
But the transmission of features of Alzheimer's pathology is a different
matter, given
the much greater frequency of this disease and raises the unanswered
question whether
some cases are the result of a transmissible prion. The only tenable public
line will
be that "more research is required" before that hypothesis could be
evaluated. The
possibility on a transmissible prion remains open. In the meantime MRC needs
carefully to consider the range and sequence of studies needed to follow
through from
the preliminary observations in these two cases. Not a particularly
comfortable
message, but until we know more about the causation of Alzheimer's disease
the total
reassurance is not practical.
JS METTERS
Room 509
Richmond House
Pager No: 081-884 3344
Callsign: DOH 832
121/YdeS
92/11.4/1.2
http://www.bseinquiry.gov.uk/files/yb/1992/11/04001001.pdf
Regarding Alzheimer's disease
(note the substantial increase on a yearly basis)
http://www.bseinquiry.gov.uk/files/yb/1988/07/08014001.pdf
snip...
The pathogenesis of these diseases was compared to Alzheimer's disease at a
molecular level...
snip...
http://www.bseinquiry.gov.uk/files/yb/1990/03/12003001.pdf
And NONE of this is relevant to BSE?
There is also the matter whether the spectrum of ''prion disease'' is wider
than that recognized at present.
http://www.bseinquiry.gov.uk/files/yb/1990/07/06005001.pdf
Human BSE
snip...
These are not relevant to any possible human hazard from BSE nor to the much
more common dementia, Alzheimers.
snip...
http://www.bseinquiry.gov.uk/files/yb/1990/07/09001001.pdf
UNTIL politicians and industry allow scientist to finally prove the link of Alzheimers and TSE, just the misdiangosed numbers will dramatically increase the amount of human TSE documented in the USA, but you will not see it, due to the lack of enhanced surveillance, and i don't mean like the june 2004 enhanced cover-up of BSE in the USA, which is exactly what it was. sporadic CJD in the USA has already trippled in the past few years or so, even with the half @ss surveillance program in place now. imagine what they would find if it was a full blown truely enhanced human TSE surveillance in all states, mandatory autopsy for all elderly demented. now that would tell us something, espeically if they use proper and most sensitive testing protocol, not like they did with the cows and that BSE testing protocol. that was a joke from the get-go.
============
From: TSS
Subject: CJD or Alzheimer's, THE PA STUDY...full text
Date: May 7, 2001 at 10:24 am PST
Diagnosis of dementia: Clinicopathologic correlations
Francois Boller, MD, PhD; Oscar L. Lopez, MD; and John Moossy, MD
Article abstract--Based on 54 demented patients consecutively autopsied at
the University of Pittsburgh, we studied the accuracy of clinicians in
predicting the pathologic diagnosis. Thirty-nine patients (72.2%) had
Alzheimer's disease, while 15 (27.7%) had other CNS diseases (four
multi-infarct dementia; three Creutzfeldt-Jakob disease; two thalamic and
subcortical gliosis; three Parkinson's disease; one progressive supranuclear
palsy; one Huntington's disease; and one unclassified). Two neurologists
independently reviewed the clinical records of each patient without
knowledge of the patient's identity or clinical or pathologic diagnoses;
each clinician reached a clinical diagnosis based on criteria derived from
those of the NINCDS/ADRDA. In 34 (63 %) cases both clinicians were correct,
in nine (17%) one was correct, and in 11 (20%) neither was correct. These
results show that in patients with a clinical diagnosis of dementia, the
etiology cannot be accurately predicted during life.
NEUROLOGY 1989;39:76-79
=======================
Evaluation of Cerebral Biopsies for the Diagnosis of Dementia
Christine M. Hulette, MD; Nancy L. Earl, Md; Barbara J. Crain, MD, Phd
· To identify those patients most likely to benefit from a cerebral biopsy
to diagnose dementia, we reviewed a series of 14 unselected biopsies
performed during a 9-year period (1980 through 1989) at Duke University
Medical Center, Durham, NC. Pathognomonic features allowed a definitive
diagnosis in seven specimens. Nondiagnostic abnormalities but not diagnostic
neuropathologic changes were seen in five additional specimens, and two
specimens were normal. Creutzfeldt-Jakob disease was the most frequent
diagnosis. One patient each was diagnosed as having Alzheimer's disease,
diffuse Lewy body disease, adult-onset Niemann-Pick disease, and anaplastic
astrocytoma. We conclude that a substantial proportion of patients
presenting clinically with atypical dementia are likely to receive a
definitive diagnosis from a cerebral biopsy. However, in those with
coexisting hemiparesis, chorea, athetosis, or lower motor neuron signs,
cerebral biopsies are less likely to be diagnostic. (Arch Neurol.
1992;49:28-31)
==========================
Occasional PrP plaques are seen in cases of Alzheimer's Disease
snip...
full text;
http://www.bseinquiry.gov.uk/files/ws/s310.pdf
2 3 Once isolated, the agent must be capable of reproducing the disease in
experimental animals. 4 The agent must be recovered from the experimental
disease produced. 3. In the case of transmissible spongiform
encephalopathies (TSEs), these postulates are not fulfilled in the following
ways: 4. Unfulfillments of Postulate 1. 4.1 Transgenic mice with a codon 102
mutation involving a leucine substitution spontaneously develop spongiform
encephalopathy with no detectable mutant prion protein (PrPsc). (Ref. Hsiao
K.K. et al. Spontaneous neurodegeneration in transgenic mice with mutant
prion protein. Science (1990) 250: 1587-1590.) (J/S/250/1587) 4.2 Spongiform
encephalopathy in zitter rats does not involved PrP. (ref. Gomi H. et al.
Prion protein (PrP) is not involved in the pathogenesis of spongiform
encephalopathy in zitter rats. Neurosci. Lett (1994) 166: 171-174.)
(J/NSC/166/171) 4.3 Many viruses and retroviruses can produced spongiform
encephalopathies without PrPsc involvement. (Ref. Wiley C.A. Gardner M. The
pathogenesis of murine retroviral infection of the central nervous system.
Brain Path (1993) 3: 123-128.) (J/BRP/3/123) 4.4 Experiments involving the
transmission of the 'BSE agent' in mice produced symptoms of TSE, but in 55%
no PrPsc could be detected. (Ref. Lasmesaz. C. et al. Transmission of the
BSE agent to mice in the absence of detectable abnormal prion protein.
Science (1997) 275: 402- 405.) (J/S/275/402) 5. Unfulfillment of Postulate 2
5.1 Occasional PrP plaques are seen in cases of Alzheimer's Disease, where
they coexist with the more usual beta amyloid plaques. (Ref. Baker H. F.
Ridley R.M. Duchen L.W. Crow T.J. Bruton C.J. Induction of beta
full text;
http://www.bse.org.uk/files/ws/s310.pdf
http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html
IN STRICT CONFIDENCE
TRANSMISSION OF ALZHEIMER-TYPE PLAQUES TO PRIMATES
http://www.bseinquiry.gov.uk/files/yb/1993/01/05004001.pdf
Subject: Re: Hello Dr. Manuelidis Date: Fri, 22 Dec 2000 17:47:09 -0500
From: laura manuelidis Reply-To:
[email protected] Organization:
Yale Medical School To: "Terry S. Singeltary Sr."
References: <
[email protected]> <
[email protected]>
<
[email protected]> <
[email protected]>
<
[email protected]> <
[email protected]>
<
[email protected]>
Dear Terry,
One of our papers (in Alzheimer's Disease Related Disord. 3:100-109, 1989)
in text cites 6 of 46 (13%) of clinical AD as CJD. There may be a later
paper from another lab showing the same higher than expected incidence but I
can't put my hands on it right now. We also have a lot of papers from 1985
on stating that there are likely many silent (non-clinical) CJD infections,
i.e. much greater than the "tip of the iceberg" of long standing end-stage
cases with clinical symptoms. Hope this helps.
best wishes for the new year laura manuelidis
"Terry S. Singeltary Sr." wrote: Hello again Dr. Manuelidis, could you
please help me locate the 2 studies that were done on CJD where it showed
that up to 13% of the people diagnosed as having Alzheimer's actually had
CJD. trying to find reference... thank you, > Terry S. Singeltary Sr.
4.5 MILLION DEMENTED ALZHEIMER'S PATIENTS, with estimated 20 million by 2050, then think of the amount of families and caretakers taking care of those victims ???
HOW CAN ONE-IN-A-MILLION BE ACCURATE WHEN CJD IS NOT REPORTABLE in many states and in some of the ones that it is reportable, they put a 50 to 55 year age limit on CJD/TSE. THIS, will only spread the agent, iCJD knows no age limit damnit. this age limit makes absolutely no sense.
AND WHEN THE ELDERLY DO NOT GET AUTOPSIED, you just don't have the correct figures then, but everything looks rosey, and this is there only goal, make everything appear rosey, so we can export those precious commodities, and possibly expose everyone around the globe to all the strains of TSE in the USA. IT"S THE AMERICAN WAY! The Japaneese have every right to ban USA beef, sheep, deer, and elk product, even those farmed raised fish, until the feed ban is adhered to, until GW et al at USDA gets there BSe together on these SRMS, and repeal the BSE MRR policy and go back to a enhanced BSE GBR risk assessment to include all animal TSE. I don't see shipping potentially TSE tainted feed to 9 states in June of 2006, I don't see this as looking rosey to me. ...TSS
Japan's Opposition: US Beef Ban Shouldn't Be Lifted
TOKYO (AP)--Japan's opposition parties Saturday blasted plans to lift a ban on U.S. beef imports, citing `mad cow' concerns.
The Japanese government agreed to lift its ban on U.S. beef Wednesday, pending thorough inspections of U.S. meat- processing facilities.
But the Democratic Party of Japan, the Japanese Communist Party, the Social Democratic Party and the People's New Party released an appeal Saturday against a resumption of the beef trade, saying the move could put Japanese consumers at risk.
"To secure food safety for our citizens, the resumption of U.S. beef imports should not go ahead at this stage," the appeal read.
Japanese consumer groups have also opposed resuming U.S. beef imports over food safety concerns.
Japan's ban, first imposed in 2003 over concerns that U.S. beef might be infected with `mad cow' disease, was lifted at the end of last year.
But in January, Japan again halted imports of U.S. beef after one shipment was found to contain prohibited parts of cows believed at risk of the disease.
`Mad cow' disease is formally known as bovine spongiform encephalopathy, or BSE. In humans, eating meat contaminated with BSE is linked to variant Creutzfeldt-Jakob Disease, a rare and deadly nerve disease.
A group of U.S. senators has proposed legislation that contains a nonbinding call for trade sanctions unless the imports are restarted by the end of the summer.
Source: Dow Jones Newswire
TSS