• If you are having problems logging in please use the Contact Us in the lower right hand corner of the forum page for assistance.

Gummer family friend Elizabeth Smith 23 dies of human form o

flounder

Well-known member
Joined
Sep 3, 2005
Messages
2,631
Location
TEXAS
October 11, 2007

Gummer family friend dies of human form of 'mad cow' disease

in 1990 John Gummer encouraged his four-year-old daughter, Cordelia, to eat a burger to show that beef was safe

Times Online and agencies
A family friend of John Gummer, the former Agriculture Minister who in 1990 tried to show that beef was safe by encouraging his 4-year-old child to eat a hamburger in front of the cameras, has died from the human form of "mad cow" disease.

Elizabeth Smith, 23, a student from St Margaret South Elmham, Suffolk, died from variant Creutzfeldt-Jakob disease (vCJD) on October 4, three years after becoming ill.

Her father, Roger Smith, a retired vicar, said today that his own daughter had rarely eaten burgers as a child and had enjoyed a normal, healthy diet.

"I think her [Elizabeth's] average consumption of burgers was probably about 1 per cent of the national average," Mr Smith said.

"If you live in the depths of the countryside, like Elizabeth did, there aren't burger bars everywhere so she hardly ate any.

"It may be nothing to do with beef burgers. If people knew precisely where the disease came from they would be able to stop it."

Mr Smith said Mr Gummer, who encouraged his daughter Cordelia to eat a burger in front of TV cameras in 1990 in order to demonstrate that humans were at no danger from mad cow disease, was a personal friend.

"John, not for the only time in his life, was unfairly treated by the press," Mr Smith said.

"It was a load of old cobblers. It didn't change the way I viewed meat. It changed the way I viewed the press."

Mr Smith said his daughter was first diagnosed with vCJD in 2005.

He said Miss Smith, who was reading geography at Birmingham University, needed round-the-clock care as the disease took hold.

"She first became ill in August 2004 but it wasn't diagnosed for another seven months. She was able to stay at university until March 2005," he said.


"It took so long to get diagnosed because the symptoms are so vague - it could have been various other things in the early stages. There is no blood test and no 100 per cent certain test until after death.

"Initially the symptoms can be confused with depression. Elizabeth wasn't depressed but she had numbness in her face and we thought it was MS (multiple sclerosis).

"Then she started having short-term memory loss but because her brain was young she was able to compensate, which is why she was able to carry on at university.

"However, by the time she came home she found that she had trouble swallowing and then couldn't swallow at all so for the last two-and-a-half years she was fitted with a gastro-tube.

"After that the disease was remorseless in the way that it killed her off.

"By August 2005 she was a very, very sick person. She was unable to walk for the last two years of her life and couldn't speak or smile.

"She had to be cared for 24 hours a day, seven days a week. She was more helpless for those last two years than when she was born - at least then she could move her arms and cry but by the end she couldn't even do that."

Mr Smith said his daughter began a degree course in 2002 after gaining A-Levels in biology, English, geography and chemistry at Leiston High School in Leiston, Suffolk.

His wife Molly said: "Elizabeth was clever, bright and intelligent. If she had been able to do her final exams she would have got a very good degree.

"She wanted to do primary school teaching and had a place on a post-graduate training course at Birmingham - she actually passed that interview when she was three or four months into the disease.

"She had a very active life and loved being outdoors. She was good at sports and enjoyed running, while she also liked to visit Minsmere bird reserve."

Mr Smith, vicar of Mendham and Metfield in Suffolk from 1978 until 1991, said: "We don't want to scare people because it is an extremely rare disease. Not everyone is going to die from it.

"In fact I would tell people to worry more about their driving than getting CJD."

He said his daughter's funeral would take place at the Parish Church of St John the Baptist, Metfield, tomorrow.

Mr and Mrs Smith also have a son, Andrew, 39.


http://www.timesonline.co.uk/tol/news/uk/article2639215.ece

http://www.timesonline.co.uk/tol/news/uk/article2639215.ece?token=null&offset=12


gummer and all these other political bozo's should be put in prison for what i call 'industrial and political poisoning',
with bush right along side of him for his BSE MRR policy, the legal trading of all strains of TSE globally. like i said before ;


BOTTOM LINE ;



(Adopted by the International Committee of the OIE on 23 May 2006)

11. Information published by the OIE is derived from appropriate
declarations made by the official Veterinary Services of Member Countries.
The OIE is not responsible for inaccurate publication of country disease
status based on inaccurate information or changes in epidemiological status
or other
significant events that were not promptly reported to then Central
Bureau............

http://www.oie.int/eng/Session2007/RF2006.pdf






----- Original Message -----
From: Terry S. Singeltary Sr.
To: Terry S. Singeltary Sr.
Sent: Thursday, March 29, 2007 3:44 PM
Subject: BSE; MRR; Importation of Live Bovines and Products Derived from Bovines Commodities


Sent: Sunday, January 28, 2007 9:12 PM
Subject: BSE; MRR; IMPORTATION OF LIVE BOVINES AND PRODUCTS DERIVED FROM BOVINES [Docket No. APHIS-2006-0041] RIN 0579-AC01 COMMENT SUBMISSION


----- Original Message -----
From: Terry S. Singeltary Sr.
To: Terry S. Singeltary Sr.
Sent: Thursday, March 29, 2007 3:27 PM
Subject: BSE; MRR; Importation of Live Bovines and Products Derived from Bovines Commodities





http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0703&L=sanet-mg&T=0&P=19960







Docket Title Bovine Spongiform Encephalopathy; Minimal-Risk Regions; Importation of Live Bovines and Products Derived from Bovines Commodities
Docket Type RULE
Document ID APHIS-2006-0041-0397




COMMENT FROM TERRY S. SINGELTARY SR. 1/09/2007


snip...



MY personal belief, since you ask, is that not only the Canadian border, but the
USA border, and the Mexican border should be sealed up tighter than a drum for
exporting there TSE tainted products, until a validated, 100% sensitive test is
available, and all animals for human and animal consumption are tested. all we are
doing is the exact same thing the UK did with there mad cow poisoning when they
exported it all over the globe, all the while knowing what they were doing. this BSE
MRR policy is nothing more than a legal tool to do just exactly what the UK did,
thanks to the OIE and GW, it's legal now. and they executed Saddam for
poisoning ???

go figure....


Terry S. Singeltary Sr.
P.O. Box 42
Bacliff, Texas USA 77518


see full text ;


http://www.regulations.gov/fdmspublic/ContentViewer?objectId=09000064801f3412&disposition=attachment&contentType=crtext



ATTACHMENT TO SINGELTARY COMMENT 1/09/2007


http://www.regulations.gov/fdmspublic/ContentViewer?objectId=09000064801f3413&disposition=attachment&contentType=msw8



England worried briefly about infecting other countries
27 Aug 00 confidential correspondence obtained by Terry S. Singeltary Sr.
http://www.mad-cow.org/00/aug00_last_news.html#fff



Sun, 3 Sep 2000. Unpublished Inquiry documents obtained by CJD activist Terry S. Singeltary Sr. of Bacliff, Texas



http://www.mad-cow.org/00/sep00_news.html#hhh



Other US BSE risks: the imported products picture
24 Jul 00 Trade Statistics: UK to US
Compiled by Terry S.Singeltary Sr of Bacliff, Texas

http://www.mad-cow.org/00/jul00_dont_eat_sheep.html#hhh


http://www.mad-cow.org/00/may00_news.html


http://www.mad-cow.org/00/may00_news.html#aaa


http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0612&L=sanet-mg&P=21108



Terry S. Singeltary Sr.
still disgusted in Sunny Bacliff, Texas
 
PORKER said:
I just wish that Rons BSE urine test will be avaiable SOON. I would test all my sires and cows.

I think a lot of producers would test everything just to ensure the safety of our product.Maybe then we can band together as one industry instead of all the bickering and back stabbing that is always going on.This disease is a heartless killer and I feel for family and friends that have lost a loved to it.
 
PORKER said:
I just wish that Rons BSE urine test will be avaiable SOON. I would test all my sires and cows.


I was at a meeting yesterday and had a report from a meeting that I assume it was "RON" told them his litmus type test would be ready in three months. I guess we can only hope as I always takes longer than anticipated.
 
PORKER said:
I just wish that Rons BSE urine test will be avaiable SOON. I would test all my sires and cows.

Forget it. USDA won't approve it. Hell, they won't even approve the Canadian E-Coli vaccine to give it a chance. :???:

What could THAT hurt?
 
Your Right Mike, They got interests to protect. A few Corporations have quite a few dead bodys and blood on their hands including their investors !
 
Terry when you say things like this , no one takes you seriously. Me included.

MY personal belief, since you ask, is that not only the Canadian border, but the
USA border, and the Mexican border should be sealed up tighter than a drum for
exporting there TSE tainted products, until a validated, 100% sensitive test is
available, and all animals for human and animal consumption are tested. all we are
doing is the exact same thing the UK did with there mad cow poisoning when they
exported it all over the globe, all the while knowing what they were doing. this BSE
MRR policy is nothing more than a legal tool to do just exactly what the UK did,
thanks to the OIE and GW, it's legal now. and they executed Saddam for
poisoning ???
 
Red Robin said:
Terry when you say things like this , no one takes you seriously. Me included.

MY personal belief, since you ask, is that not only the Canadian border, but the
USA border, and the Mexican border should be sealed up tighter than a drum for
exporting there TSE tainted products, until a validated, 100% sensitive test is
available, and all animals for human and animal consumption are tested. all we are
doing is the exact same thing the UK did with there mad cow poisoning when they
exported it all over the globe, all the while knowing what they were doing. this BSE
MRR policy is nothing more than a legal tool to do just exactly what the UK did,
thanks to the OIE and GW, it's legal now. and they executed Saddam for
poisoning ???


you should, it's the truth. .........


England worried briefly about infecting other countries
27 Aug 00 confidential correspondence obtained by Terry S. Singeltary Sr.
http://www.mad-cow.org/00/aug00_last_news.html#fff



Sun, 3 Sep 2000. Unpublished Inquiry documents obtained by CJD activist Terry S. Singeltary Sr. of Bacliff, Texas



http://www.mad-cow.org/00/sep00_news.html#hhh



Other US BSE risks: the imported products picture
24 Jul 00 Trade Statistics: UK to US
Compiled by Terry S.Singeltary Sr of Bacliff, Texas

http://www.mad-cow.org/00/jul00_dont_eat_sheep.html#hhh


http://www.mad-cow.org/00/may00_news.html


http://www.mad-cow.org/00/may00_news.html#aaa


http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0612&L=sanet-mg&P=21108




EXPORTATION AND IMPORTATION OF ANIMALS AND ANIMAL PRODUCTS:
BSE; MRR AND IMPORTATION OF COMMODITIES, 65758-65759 [E6-19042]






http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0701&L=sanet-mg&T=0&P=3854


http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0611&L=sanet-mg&T=0&P=3381



http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0703&L=sanet-mg&T=0&P=498


http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0702&L=sanet-mg&T=0&P=10277


http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0701&L=sanet-mg&T=0&P=9972


http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0703&L=sanet-mg&T=0&P=4492


http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0703&L=sanet-mg&T=0&P=2583


http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0703&L=sanet-mg&T=0&P=2470





BOTTOM LINE ;



(Adopted by the International Committee of the OIE on 23 May 2006)

11. Information published by the OIE is derived from appropriate
declarations made by the official Veterinary Services of Member Countries.
The OIE is not responsible for inaccurate publication of country disease
status based on inaccurate information or changes in epidemiological status
or other
significant events that were not promptly reported to then Central
Bureau............

http://www.oie.int/eng/Session2007/RF2006.pdf






----- Original Message -----
From: Terry S. Singeltary Sr.
To: Terry S. Singeltary Sr.
Sent: Thursday, March 29, 2007 3:44 PM
Subject: BSE; MRR; Importation of Live Bovines and Products Derived from Bovines Commodities


Sent: Sunday, January 28, 2007 9:12 PM
Subject: BSE; MRR; IMPORTATION OF LIVE BOVINES AND PRODUCTS DERIVED FROM BOVINES [Docket No. APHIS-2006-0041] RIN 0579-AC01 COMMENT SUBMISSION


----- Original Message -----
From: Terry S. Singeltary Sr.
To: Terry S. Singeltary Sr.
Sent: Thursday, March 29, 2007 3:27 PM
Subject: BSE; MRR; Importation of Live Bovines and Products Derived from Bovines Commodities





http://lists.ifas.ufl.edu/cgi-bin/wa.exe?A2=ind0703&L=sanet-mg&T=0&P=19960



1994 UK EXPORTS BEEF VEAL USA , MEXICO $ CANADA ONLY
other Countries list in PDF file)

USA -------- TOTALS ''8'' TONS
CANADA -- TOTALS ''29'' TONS

1995 UK EXPORT BEEF AND VEAL TO USA AND CANADA

USA ------- TOTALS ''358'' TONS

CANADA --TOTALS ''24'' TONS

BONE-IN BEEF AND VEAL

USA-------- TOTALS ''10'' TONS (i think this is part of the 358 tons
above?)

UK EXPORT OF LIKE CATTLE TO USA AND CANADA

1986 TO 1996 USA TOTAL = 1297

1986 TO 1996 CAN TOTAL = 299

http://www.bseinquiry.gov.uk/files/mb/m11f/tab10.pdf


UK EXPORT MEAT OR OFFAL OF BOVINE ANIMALS DEC 1987

CANADA -- 64,526 KG

UK EXPORT OFFALS OF BOVINE ANIMALS FRESH CHILLED
OR FROZEN OTHER THAN LIVER DEC 1987 YTD

USA -- 45,943 KG

UK EXPORT MEAT OF BOVINE ANIMAL WITH BONE IN 1988

CANADA -- 4,163 KG

PREP OR PRES MEAT OR OFFAL OF BOVINE ANIMALS CUMULATIVE
TO DEC 1988

USA -------- 28,609 KG
CANADA -- 22,044 KG

MEAT OF BOVINE ANIMALS WITH BONE IN CUMULATIVE TO ANUAL 1989

USA -------- 17,880 KG
MEXICO---- 33,444 KG

BONELESS MEAT OF BOVINE 1989

USA --------111,953 KG
CANADA---1,800 KG
MEXICO --- 1,143,387 KG

EDIBLE OFFAL OF BOVINE ANIMALS 1989

USA -------- 19,980 KG
MEXICO--- 31,244 KG

MORE........

MEAT OF BOVINE ANIMALS BONELESS 1990

USA 146,443


http://www.bseinquiry.gov.uk/files/mb/m11g/tab05.pdf




UK Exports of Live Cattle by Value 1986-96

USA 697 LIVE CATTLE

CANADA 299 LIVE CATTLE

http://www.bseinquiry.gov.uk/files/mb/m11f/tab11.pdf



UK TABLE of Exports of meal of meat and meat offal; greaves 1979 - 1995

USA 24 TONS

CANADA 83 TONS

http://www.bseinquiry.gov.uk/files/mb/m12/tab12.pdf



HOWEVER, my files show 44 tons of greaves for USA. ...TSS



Subject: Re: exports from the U.K. of it's MBM to U.S.???
From: [email protected].
Date: Tue, 8 Feb 2000 14:03:16 +0000
To: [email protected] (Receipt Notification Requested) (Non Receipt Notification Requested)

Terry Meat and bonemeal is not specifically classified for overseas trade purposes. The nearest equivalent is listed as flours and meals of meat or offals (including tankage), unfit for human consumption; greaves. UK exports of this to the US are listed below:
Country Tonnes

1980
1981 12
1982
1983
1984 10
1985 2
1986
1987
1988
1989 20
1990

Data for exports between 1975 and 1979 are not readily available. These can be obtained (at a charge) from data retailers appointed by HM Customs and Excise: BTSL (Tel: 01372 463121) or Abacus (01245 252222). Best wishes Simon Pearsall Overseas trade statistics Stats (C&F)C

====================================== END...TSS



BSE GBR RISK ASSESSMENTS, USA, CANADA, AND MEXICO




EFSA Scientific Report on the Assessment of the Geographical BSE-Risk (GBR) of the United States of America (USA)


Summary of the Scientific Report

The European Food Safety Authority and its Scientific Expert Working Group on the Assessment of the Geographical Bovine Spongiform Encephalopathy (BSE) Risk (GBR) were asked by the European Commission (EC) to provide an up-to-date scientific report on the GBR in the United States of America, i.e. the likelihood of the presence of one or more cattle being infected with BSE, pre-clinically as well as clinically, in USA. This scientific report addresses the GBR of USA as assessed in 2004 based on data covering the period 1980-2003.

The BSE agent was probably imported into USA and could have reached domestic cattle in the middle of the eighties. These cattle imported in the mid eighties could have been rendered in the late eighties and therefore led to an internal challenge in the early nineties. It is possible that imported meat and bone meal (MBM) into the USA reached domestic cattle and leads to an internal challenge in the early nineties.

A processing risk developed in the late 80s/early 90s when cattle imports from BSE risk countries were slaughtered or died and were processed (partly) into feed, together with some imports of MBM. This risk continued to exist, and grew significantly in the mid 90's when domestic cattle, infected by imported MBM, reached processing. Given the low stability of the system, the risk increased over the years with continued imports of cattle and MBM from BSE risk countries.

EFSA concludes that the current GBR level of USA is III, i.e. it is likely but not confirmed that domestic cattle are (clinically or pre-clinically) infected with the BSE-agent. As long as there are no significant changes in rendering or feeding, the stability remains extremely/very unstable. Thus, the probability of cattle to be (pre-clinically or clinically) infected with the BSE-agent persistently increases.


http://www.efsa.europa.eu/en/science/tse_assessments/gbr_assessments/573.html



http://www.efsa.europa.eu/etc/medialib/efsa/science/tse_assessments/gbr_assessments/573.Par.0004.File.dat/sr03_biohaz02_usa_report_v2_en1.pdf





EFSA Scientific Report on the Assessment of the Geographical BSE-Risk (GBR) of Canada


Summary of the Scientific Report

The European Food Safety Authority and its Scientific Expert Working Group on the Assessment of the Geographical Bovine Spongiform Encephalopathy (BSE) Risk (GBR) were asked to provide an up-to-date scientific report on the GBR in Canada, i.e. the likelihood of the presence of one or more cattle being infected with BSE, pre-clinically as well as clinically, in Canada. This scientific report addresses the GBR of Canada as assessed in 2004 based on data covering the period 1980-2003.

The BSE agent was probably imported into the country middle of the eighties and could have reached domestic cattle in the early nineties. These cattle imported in the mid eighties could have been rendered in the late eighties and therefore led to an internal challenge in the early 90s. It is possible that imported meat and bone meal (MBM) into Canada reached domestic cattle and led to an internal challenge in the early 90s.

A certain risk that BSE-infected cattle entered processing in Canada, and were at least partly rendered for feed, occurred in the early 1990s when cattle imported from UK in the mid 80s could have been slaughtered. This risk continued to exist, and grew significantly in the mid 90's when domestic cattle, infected by imported MBM, reached processing. Given the low stability of the system, the risk increased over the years with continued imports of cattle and MBM from BSE risk countries.

EFSA concludes that the current GBR level of Canada is III, i.e. it is confirmed at a lower level that domestic cattle are (clinically or pre-clinically) infected with the BSE-agent. As long as the system remains unstable, it is expected that the GBR continues to grow, even if no additional external challenges occur.



http://www.efsa.europa.eu/en/science/tse_assessments/gbr_assessments/564.html



http://www.efsa.europa.eu/etc/medialib/efsa/science/tse_assessments/gbr_assessments/564.Par.0001.File.dat/sr02_biohaz02_canada_report_v2_en1.pdf






EFSA Scientific Report on the Assessment of the Geographical BSE-Risk (GBR) of Mexico


Last updated: 8 September 2004 Publication Date: 20 August 2004

Adopted July 2004 (Question N° EFSA-Q-2003-083)


Summary of the Scientific Report

The European Food Safety Authority and its Scientific Expert Working Group on the Assessment of the Geographical Bovine Spongiform Encephalopathy (BSE) Risk (GBR) were asked by the European Commission (EC) to provide an up-to-date scientific report on the GBR in Mexico, i.e. the likelihood of the presence of one or more cattle being infected with BSE, pre-clinically as well as clinically, in Mexico. This scientific report addresses the GBR of Mexico as assessed in 2004 based on data covering the period 1980-2003.

The BSE agent was probably imported into Mexico and could have reached domestic cattle. These cattle imported could have been rendered and therefore led to an internal challenge in the mid to late 1990s. It is possible that imported meat and bone meal (MBM) into Mexico reached domestic cattle and leads to an internal challenge around 1993.

It is likely that BSE infectivity entered processing at the time of imported 'at - risk' MBM (1993) and at the time of slaughter of imported live 'at - risk' cattle (mid to late 1990s). The high level of external challenge is maintained throughout the reference period, and the system has not been made stable. Thus it is likely that BSE infectivity was recycled and propagated from approximately 1993. The risk has since grown consistently due to a maintained internal and external challenge and lack of a stable system.

EFSA concludes that the current geographical BSE risk (GBR) level is III, i.e. it is likely but not confirmed that domestic cattle are (clinically or pre-clinically) infected with the BSE-agent. The GBR is likely to increase due to continued internal and external challenge, coupled with a very unstable system.



http://www.efsa.europa.eu/etc/medialib/efsa/science/tse_assessments/gbr_assessments/565.Par.0003.File.dat/sr04_biohaz02_mexico_report_summary_en1.pdf



http://www.efsa.europa.eu/etc/medialib/efsa/science/tse_assessments/gbr_assessments/565.Par.0004.File.dat/sr04_biohaz02_mexico_report_v2_en1.pdf






truth hurts don't it. .................tss
 
"It may be nothing to do with beef burgers. If people knew precisely where the disease came from they would be able to stop it."

A very sound comment from the father of this poor girl. I bet he has had alot of time to think about this, so he hasn't made this comment lightly.

"She had a very active life and loved being outdoors. She was good at sports and enjoyed running, while she also liked to visit Minsmere bird reserve."

Elizabeth Smith was 23 years old, born in 1984.

In 1991 she would have been 7 (initial USA attacks on Iraq with DU weapons). In 2003 she would have 19 (second USA attacks on Iraq with DU weapons).
Aldermaston, UK air monitors pick up DU from Middle East War zones:
http://www.llrc.org/aldermastrept.pdf
"Over the period of the excession, the mean offsite level of uranium in air over the six weeks was 650nBq/m3 with peak levels in Reading that exceeded the Environment Agency statutory reporting level of 1000ng/m3 twice. Since the background level could be considered to be 155nBq/m3 we can say that there was an excess of uranium in air of some 500nBq/m3. If this material consisted of uranium oxide particles from the Gulf War bombing the we can first calculate the number of particles of 0.25 µm diameter in a cubic metre of air. The activity of uranium is taken to be 12.5MBq/kg. Thus the mass of 500nBq is about 4 x 10-11g. Taking the density of uranium oxide as 9.8, there are about 48,000 particles of 0.25µm diameter in one cubic metre. Using inhalation volumes from ICRP standard man (23 m3 per day; ICRP 1974) and assuming a 50% outdoor inhalation of the uranium per day, in the six weeks of elevated uranium each person would have inhaled about 23 million particles. These particles would have rapidly transferred through the lungs and into the lymphatic system where they would have access to all tissues."

Minsmere bird reserve being very close the the Sizewell Nuclear Power Stations (Unit B closer than Unit A)
Unit A opened in 1966. Closed Dec. 2006.
Unit B opened in 1995.
Minsmere Nature Reserve is also located next to former WWII Royal Air Force Base Dunwich.
Mark Purdey's paper, "
Metal microcrystal pollutants; the heat resistant, transmissible nucleating agents that initiate the pathogenesis of TSEs?
link: http://www.markpurdey.com/pdf/metal_microcrystal_tse.pdf
demonstrates the link between vCJD and many environmentally compromised regions, due to WWII military bases and where chemical weapons were dumped. In this paper, it shows two cases of vCJD at the time had occurred in the region near Minsmere Nature Reserve.
Living so close to these nuclear power plants, spending lots of time outdoors at Minsmere bird reserve, and jogging - increases exposure via inhalation of all kinds of pollutants.

All of the UK is exposed to high levels of radiation thanks to their nuclear power stations, the highly toxic reprocessing facility at Sullafield, and various weapons manufacturing facilities.

To blame this girls consumption of meat for causing her vCJD is a huge assumption, and for now, that will keep us from finding the true environmental factors causing this disease (and others).
 
Med Hypotheses. 2007 Oct 8; [Epub ahead of print] Links
Alzheimer's disease as copper deficiency.
Klevay LM.
Departments of Internal Medicine and of Pharmacology, Physiology and Therapeutics, 223 27th Avenue South, Grand Forks, ND 58201, United States.

Four classes of etiologic agents can produce toxic, hereditary, infectious and deficiency diseases. Recent research on Alzheimer's disease generally addresses pathogenesis related to the first three classes of agents with little emphasis on cause. Low copper and cytochrome oxidase in Alzheimer brain can be attributed to low copper intakes or higher than average nutritional requirements. Experiments with animals deficient in copper involving amyloid, ceruloplasmin, copper transport, cytochrome oxidase, myelination, organ analysis and oxidative defense are consonant. Decreased cognition and increased tau in cerebrospinal fluid in Alzheimer's disease also are associated with low copper status. A high requirement for copper may explain early onset of Alzheimer's disease in Down's syndrome. Copper deficiency is a plausible cause of Alzheimer's disease. This hypothesis should be tested with a lengthy trial of copper supplementation.

PMID: 17928161
 
Ah, the same old comeback from flounder.

Try reading:

"The Petkau Effect - Devastating Effect of Nuclear Radiation on
Human Health and the Environment
" by author Ralph Graeub,
with an introduction by Dr. Ernest J. Sternglass (author of
Secret Fallout and scientist that convinced USA pres. John F.
Kennedy to sign the Nonproliferation Treaty of 1963).
ISBN - 1-56858-019-3 Second revised edition September 1994

Let me quote from the foreward: (my emphasis added)

"The aim of this book is to present the range of health and ecological dangers of fission products released into the air and water. Among the most important of the recent scientific discoveries that has been successfully kept from the public is the Petkau Effect, the discovery that showed low-dose, protracted radiation exposures such as those produced by radioactive fission products, to be hundreds to thousands of times as damaging as the same dose received in a short medical X-ray.

In the past three years, new and decisive information relating to the Petkau Effect has surfaced. In both the biochemical, pharmaceutical and medical fields, the term "oxidative stress" has been introduced at long last. This condition is caused by oxygen free radicals, a highly toxic, unstable form of oxygen that attacks living cells (p. 87). These radicals already occur during the course of normal cellular life, especially in the respiratory process. They are controlled by a protective system of the body involving enzymes, vitamins and micronutrients. If the level of oxygen free radicals exceeds that which the protective system can control, the result is oxidative stress and subsequent membrane damage (Petkau's discovery, p. 86-88).

Recent highly significant epidemiological studies have demonstrated once again the supralinear dose effect curves for nuclear reactor releases and weapons. They can be explained in terms of the mechanism of the
Petkau Effect whereby peroxidation of the phospholipids in the cell membrane occurs
. It has become apparent that most diseases involve oxidative stress. In medicine parlance, we now hear the term "free-radical diseases" or "free-radical associated disease".

Research into oxidative stress and its consequences has already influenced the prescription of vitamins and micronutrients for prevention and therapy - for example in the case of cancer treatment. Besides air pollution such as nitric acid, ozone, and other agents known to produce free radicals, for instance cigarette smoke, drugs and pesticides, ionizing radiation has now also been discussed as an important factor in cell damage produced free radicals."

Disease processes are not SIMPLE. They are a result of a combination of breakdowns and exposures, in most cases.

Codex Alimentarius is being used to give pharmaceutical corporations control over natural compounds like vitamins, enzymes and micronutrients which are protective and proventative nutrients required by our "anti-oxidant" and "immune systems".

Flounder, your lack of respect for my postings, only shows your ignorance.
 
Kathy said:
Flounder, your lack of respect for my postings, only shows your ignorance.



your lack of knowledge on the cause of TSE shows your ignorance kathy, and you never answered my question. make your mink up kathy, which is it, nukes, ops', or metals? you flip flop about like some politicians i know. i would have a bit more respect for your postings if they made any sense in relations to TSE as being the cause. you have shown us nothing to date that shows this. which is nothing new. :?
 
One thing is for sure. If Kathy's theory of depleted uranium being a factor in bse is true, we should start seeing it in Iraq.
 
flounder says:
your lack of knowledge on the cause of TSE shows your ignorance kathy, and you never answered my question. make your mink up kathy, which is it, nukes, ops', or metals? you flip flop about like some politicians i know. i would have a bit more respect for your postings if they made any sense in relations to TSE as being the cause. you have shown us nothing to date that shows this. which is nothing new

You to chicken to read a book flounder? No, I don't think you're scared to read this book (The Petkau Effect), you probably know all about it already. You're scared that others on this board, etc, will read this book. It is imperative everyone READ THIS BOOK.

Let me give another little quote from it:

In a letter to the author (Ralph Graeub) Petkau summarized the essential results of his research work as follows: (my emphasis added)

"The inverse dose rate effect that I have described in refereed journals applies to 1) Radiation induced breakage of model phospholipid membranes by Na22 (Health Physics, (1972) 239-244). The phospholipids were extracted from fresh beef brain. The membranes were planar in structure. These types of membranes were also used to show that superoxide radicals are attracted to their surfaces (Can J. Chem. 49 (1971) 1187-1195). The collection of superoxide radicals at the membrane surfaces also changed the radiation chemistry in the water phase nearby. This insight led to the next series of experiments.

2) Radiation-induced lipid peroxidation in spherical shaped model membranes made from phospholipids extracted from soybean (Biochem biophy Acta 433 (1976) 445-446). Irradiation was done with an external Cs137 source. The inverse dose rate effect was observed when the membranes were unprotected by superoxide dismutase (SOD), a scavenger of superoxide radicals. However, when SOD was added, the membranes did not undergo a measurable amount of lipid peroxidation. Hence, no dose rate responses were observed. These results clearly implicated superoxide radicals in radiation induced lipid peroxidation of phospholipid membranes. A concurrent Hungarian study on mice showed that SOD also fully protected against lipid peroxidation in the liver induced by an external source of X-rays. Thus, these in-vitro results were consistent with each other.

When tritiated water was used to irradiate these membranes, I found that the dose rate relationship could be extended down to background levels, thus demonstrating for the first time a specific radiation-induced chemical process at background dose rates in a biologically relevant system. The tritiated water was in effect an internal source of radiation. I found that the inverse dose rate effect was modified by SOD but, in contrast with the Cs137 study, not totally eliminated. Thus, these studies showed up a fundamental difference in response of the membrane to external and internal radiation."

Remember the Dr. Margaret Plews, and Dr. RE Mitchel study (Canada):


PA-43
THE ROLE OF OXIDATIVE STRESS IN PRION PROVOKED NEUROTOXICTY
M. Plews1,2, S.L.R. Simon2, D.R. Boreham3, R.E. Mitchel4, S. Czub5, J.D. Knox1,2
1Department of Medical Microbiology, Faculty of Medicine, University of Manitoba, Winnipeg, Canada
2Division of Host Genetics and Prion Diseases, Public Health Agency of Canada, Winnipeg, Canada
3 Department of Medical Physics and Applied Radiation Sciences, McMaster University, Hamilton, Ontario, Canada.
4 Radiation Biology and Health Physics Branch, Atomic Energy of Canada Limited, Chalk River Laboratories, Stn 51, Chalk River, Canada5National BSE Reference Laboratory, National Centre for Foreign Animal Disease/Canadian Food Inspection Agency, Winnipeg, Canada
[email protected]
There is a wealth of evidence implicating oxidative stress in the pathology of many neurodegenerative diseases. In prion diseases the accumulation of PrPsc correlates with disease progression and coincides with the appearance of markers of oxidative stress in the brains of infected mice. This suggests that the disease-associated neurodegeneration may in part be due to oxidative damage. To investigate the role of oxidative stress in prion provoked neurotoxicity the influence of a dietary supplement on oxidative stress and disease progression was determined. Brains and body fluids were collected at various time points throughout the course of the disease and markers of antioxidant capacity, DNA damage and lipid peroxidation were measured. Scrapie infected mice displayed reduced total glutathione levels as compared to control mice. The appearance of decreased total glutathione levels relative to control was delayed in infected mice fed the anti-oxidant diet. Later stages of the disease were marked by an increase in 8-OHdG levels. The anti-oxidant diet caused a reduction in 8-OHdG levels, but they remained elevated relative to that observed in agematched controls. Infection did not alter 4-HNE levels. The data demonstrates that oxidative stress is associated with prion disease well before clinical signs are apparent. Though the anti-oxidant diet may have ameliorated adverse effects resulting from the disease-associated oxidative stress the onset of terminal stage disease was not delayed.
link: http://www.neuroprion.com/pdf_docs/conferences/prion2006/abstract_book.pdf

Tritium - is radioactive Hydrogen, produced in minute amounts by cosmic rays in the atmosphere, and in larger concentrations by nuclear power stations.
links:
http://en.wikipedia.org/wiki/Tritium
http://www.physics.isu.edu/radinf/tritium.htm
http://www.ccnr.org/tritium_1.html
Recent US news article:
http://www.thestate.com/news/story/197626.html

Tritium level high in water at S.C. plant
Radioactive material at Catawba nuclear site above EPA safe-drinking standard

By SAMMY FRETWELL - [email protected]
State and federal authorities are investigating the discovery of radioactive tritium in groundwater at a Duke Energy nuclear power plant in York County.
(see link for whole story).

Tex wrote:
One thing is for sure. If Kathy's theory of depleted uranium being a factor in bse is true, we should start seeing it in Iraq.

Not to say forget Iraq, I already see the consequences of DU via DVDs such as "The Doctor, The Children and the DU" ... very sad.
Those children that don't die in the womb, are born with the most horrific birth defects; and even if they look normal - they are internally damaged and will likely go onto develop leukemia or cancers, as well as having brain damage. Dr. Ernest Sternglass, quoted in The Petkau Effect, and in his own book "Secret Fallout" (available on line) showed how SAT scores in the USA dropped significantly after atmospheric atomic bomb testing in Nevada (Utah was hit hardest).

Start worrying not just about Iraq, but about your own backyards. The USA military still wants to take over millions of acres at Pinon Canyon Manuever Base in Colorado. One of the reasons for this, though not likely the most important (since USA [and Canadian] officials have effectively restricted BSE testing, and work diligently to prevent those like Creekstone from doing private testing)...One reason is live fire exercises using DU at this practice range (like in Hawaii and at Suffield, Wainwright, Cold Lake, Namao in Alberta) has already contaminated the region and it is only a matter of time before the ranchers in the area get wise and decide to test their soils, and have a class action law-suit against the military for ruining their lives and livelihoods. Then again, this may never come to fruition, as the best defence is to completely ignore the charges.

The documentary "Blowin In the Wind" from Australia is another good one. Shows how USA is using DU weapons there (though they deny it). The effects are showing up already. Depending on the levels of contamination, the mineral deficiencies and other sources of oxidative free radicals (like chemicals), BSE could show up down under soon as well.
 
kathy,

your wrong, admit it, your blowing smoke.

BSE peaked out about 1992 with around 170,000+ confirmed cases.
The feed ban was implemented. and it has been downhill every since where
these feed bans were adhered to. your nukes, metals, and or ops, had nothing
to do with it. transmission studies do not lie, only folks that have agendas do $$$
you should really hit the books kathy (not the comic books your reading).


http://www.defra.gov.uk/animalH/bse/statistics/weeklystats.html#pass


http://www.defra.gov.uk/animalh/bse/controls-eradication/index.html


tss


Kathy said:
flounder says:
your lack of knowledge on the cause of TSE shows your ignorance kathy, and you never answered my question. make your mink up kathy, which is it, nukes, ops', or metals? you flip flop about like some politicians i know. i would have a bit more respect for your postings if they made any sense in relations to TSE as being the cause. you have shown us nothing to date that shows this. which is nothing new

You to chicken to read a book flounder? No, I don't think you're scared to read this book (The Petkau Effect), you probably know all about it already. You're scared that others on this board, etc, will read this book. It is imperative everyone READ THIS BOOK.

Let me give another little quote from it:

snip...........NOT INTERESTED///
 
Not Interested,.... I'm not that interested in YOU reading this book either, flounder. The good people in the cattle industry that come to this message board, are the ones I am encouraging to read this very enlightening book. I hope that they are less closed-minded than you, and actually want to find the cause of these diseases.

The arguements we have had have been very good for people to see that all you can do is cut and paste, no attempt to relate the information in your own words.

Feed bans not only halted the massive bio-accumulation of heavy metals, radionuclides and chemicals (like Phosmet) in the animal food chain, they also got chicken poop with high levels of manganese and arsenic out of the animal food chain.

Don't forget to get Mark Purdey's new book, "Animal Pharm" when it comes out in November 2007, ask your local book store to bring it in.
www.markpurdey.com for more details.

The countries with the most BSE and CWD are nuclear countries. Canada has the unfortunate problem of having huge natural deposits of uranium, we need to ensure that no more radiation goes into the atmosphere - and that will take alot of work and refitting of many energy facilities. Nuclear facilities will always, always cause more radiation to enter the atmosphere and our environment (air, water, soil, food)....
 
Kathy said:
Not Interested,.... I'm not that interested in YOU reading this book either, flounder. snip....


kathy, your flip flopping again ;


kathy wrote;




>>>You to chicken to read a book flounder? No, I don't think you're scared to read this book (The Petkau Effect), you probably know all about it already.<<<


that's what i am talking about, you just cannot make your mind up.


[/quote]Don't forget to get Mark Purdey's new book, "Animal Pharm" when it comes out in November 2007, ask your local book store to bring it in.
www.markpurdey.com for more details.

The countries with the most BSE and CWD are nuclear countries. Canada has the unfortunate problem of having huge natural deposits of uranium, we need to ensure that no more radiation goes into the atmosphere - and that will take alot of work and refitting of many energy facilities. Nuclear facilities will always, always cause more radiation to enter the atmosphere and our environment (air, water, soil, food)....[/quote]



yep, i would expect nothing else from you kathy. disregard all proven transmisson studies and go ahead with some junk science that has already been proven wrong, time and time again. your nuclear proliferation theory on TSEs is wrong, and so was purdey. anybody can
write a book. does not make it correct. i suppose too that you consider iCJD as a nuclear transmission of TSE as well :? go ahead and ignore the transmission studies, go ahead and dream on, i am through with this thread. your hopeless. i really don't even believe that YOU believe your own junk science. but i will remind you of the transmission studies one more time, and then you can paste all you want about nuclear proliferation, ops, metals, and what ever else you can dream up, but the facts. ...



P04.27

Experimental BSE Infection of Non-human Primates: Efficacy of the Oral Route


Holznagel, E1; Yutzy, B1; Deslys, J-P2; Lasmézas, C2; Pocchiari, M3;
Ingrosso, L3;
Bierke, P4; Schulz-Schaeffer, W5; Motzkus, D6; Hunsmann, G6; Löwer, J1
1Paul-Ehrlich-Institut, Germany; 2Commissariat à l´Energie Atomique, France;
3Instituto
Superiore di Sanità, Italy; 4Swedish Institute for Infectious Disease
control, Sweden;
5Georg August University, Germany; 6German Primate Center, Germany


Background:

In 2001, a study was initiated in primates to assess the risk for humans
to contract BSE through contaminated food. For this purpose, BSE brain was
titrated in cynomolgus monkeys.


Aims:

The primary objective is the determination of the minimal infectious dose
(MID50)
for oral exposure to BSE in a simian model, and, by in doing this, to assess
the risk for
humans. Secondly, we aimed at examining the course of the disease to
identify
possible biomarkers.


Methods:


Groups with six monkeys each were orally dosed with lowering amounts of
BSE brain: 16g, 5g, 0.5g, 0.05g, and 0.005g. In a second titration study,
animals were intracerebrally (i.c.) dosed (50, 5, 0.5, 0.05, and 0.005 mg).


Results:


In an ongoing study, a considerable number of high-dosed macaques already
developed simian vCJD upon oral or intracerebral exposure or are at the
onset of the
clinical phase. However, there are differences in the clinical course
between orally and
intracerebrally infected animals that may influence the detection of
biomarkers.


Conclusions:


Simian vCJD can be easily triggered in cynomolgus monkeys on the oral
route using less than 5 g BSE brain homogenate. The difference in the
incubation
period between 5 g oral and 5 mg i.c. is only 1 year (5 years versus 4
years). However,
there are rapid progressors among orally dosed monkeys that develop simian v
CJD as
fast as intracerebrally inoculated animals.


The work referenced was performed in partial fulfilment of the study "BSE in
primates"
supported by the EU (QLK1-2002-01096).


http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf


P03.137


Transmission of BSE to Cynomolgus Macaque, a Non-human Primate; Development
of Clinical Symptoms and Tissue Distribution of PrPSC


Yamakawa, Y1; Ono, F2; Tase, N3; Terao, K3; Tannno, J3; Wada, N4; Tobiume,
M5; Sato, Y5; Okemoto-Nakamura, Y1; Hagiwara, K1; Sata, T5 1National
Institure of Infectious diseases, Cell biology and Biochemistry, Japan;
2Corporation for Production and Research Laboratory Primates., Japan;
3National Institure of Biomedical Innovation, Tsukuba Primate Reserch
Center, Japan; 4Yamauchi Univ., Veterinary Medicine, Japan; 5National
Institure of Infectious diseases, Pathology, Japan

Two of three cynomolgus monkeys developed abnormal neuronal behavioral signs
at
30-(#7) and 28-(#10) months after intracerebral inoculation of 200ul of 10%
brain
homogenates of BSE affected cattle (BSE/JP6). Around 30 months post
inoculation
(mpi), they developed sporadic anorexia and hyperekplexia with squeal
against
environmental stimulations such as light and sound. Tremor, myoclonic jerk
and
paralysis became conspicuous during 32 to 33-mpi, and symptoms become
worsened
according to the disease progression. Finally, one monkey (#7) fell into
total paralysis
at 36-mpi. This monkey was sacrificed at 10 days after intensive veterinary
care
including infusion and per oral supply of liquid food. The other monkey
(#10) had to
grasp the cage bars to keep an upright posture caused by the sever ataxia.
This
monkey was sacrificed at 35-mpi. EEG of both monkeys showed diffuse slowing.
PSD
characteristic for sporadic CJD was not observed in both monkeys. The result
of
forearm movement test showed the hypofunction that was observed at onset of
clinical
symptoms. Their cognitive function determined by finger maze test was
maintained at
the early stage of sideration. However, it was rapidly impaired followed by
the disease
progression. Their autopsied tissues were immunochemically investigated for
the
tissue distribution of PrPSc. Severe spongiform change in the brain together
with heavy
accumulation of PrPSc having the type 2B/4 glycoform profile confirmed
successful
transmission of BSE to Cynomolgus macaques. Granular and linear deposition
of
PrPSC was detected by IHC in the CNS of both monkeys. At cerebral cortex,
PrPSC was prominently accumulated in the large plaques. Sparse accumulation
of PrPSc
was detected in several peripheral nerves of #7 but not in #10 monkey, upon
the WB
analysis. Neither #7 nor #10 monkey accumulated detectable amounts of PrPSc
in their
lymphatic organs such as tonsil, spleen, adrenal grands and thymus although
PrPSc
was barely detected in the submandibular lymph node of #7 monkey. Such
confined
tissue distribution of PrPSc after intracerebral infection with BSE agent is
not
compatible to that reported on the Cynomolgus macaques infected with BSE by
oral
or intra-venous (intra-peritoneal) routs, in which PrPSc was accumulated at
not only
CNS but also widely distributed lymphatic tissues.

http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf



P04.49


Case Report of Variant Creutzfeldt-Jakob Disease in a Macaque after Blood
Transfusion


Lescoutra-Etchegaray, N1; Ruchoux, MM1; Correia, E1; Jolit, A1; Freire, S1;
Lasmezas,
CI2; Deslys, JP1; Comoy, E1 1CEA/DSV/IMETI/SEPIA, France; 2Scripps Florida,
USA



A fourth human case of probable transmission of vCJD through transfusion has
now
been reported but a number of features affecting transfusion-related
infection remain
imprecise, including infectious dose, length of incubation period and
critical infectious
window of blood donors.


We report here the first case of experimental transmission of vCJD in
primates by
blood transfusion. Experimental infection of Cynomolgus macaque has been
demonstrated to be a sensitive model for the investigation of human prion
diseases,
inducing similar distribution of infectivity in peripheral lymphoid tissues
and equivalent
brain pathology. In our study, transfusion was performed with 40 ml of whole
blood
drawn from a vCJD-infected macaque at the terminal stage of the disease.
Clinical
symptoms of vCJD appeared in the recipient animal after five years of
incubation. The
total amount of infectivity in the transfused blood was approximately 106
fold lower
than in the brain (titration still in progress). In several animals infected
intravenously
with brain homogenate, the presence of PrPres in serial lymph nodes biopsies
and in
other organs at autopsy was examined and results will be presented.


http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf




P04.51


Atypical Presentation of Variant Creutzfeldt-Jakob Disease in a 73 Year Old
Blood Transfusion Recipient


Wroe, S1; Pal, S1; Webb, T1; Alner, K2; Hewitt, P3; Brander, S4; Wadsworth,
JD5; Collinge, J1 1National Hospital for Neurology and Neurosurgery,
National Prion Clinic,
UK; 2National Hospital for Neurology and Neurosurgery, Department of
Neuropsychology, UK;
3Health Protection Agency, UK; 4National Hospital for Neurology and
Neurosurgery,
Department of Neuropathology, UK; 5Institute of Neurology, UCL, UK



We report atypical presentation of variant Creutzfeldt-Jakob Disease (vCJD)
identified
ante-mortem in a 73 year-old recipient of blood products. This patient was
transfused
following orthopaedic surgery in December 1997. Tracing of blood products
identified
a single unit of non-leucodepleted red cells from an individual who
developed
neuropathologically confirmed vCJD eleven months after donation. Nine years
post
transfusion, this individual was referred to the National Prion Clinic for
specialist
investigation. Six years post transfusion the recipient complained of
fluctuating fatigue
and impaired concentration. At this time neurological examination and MRI
brain
(T1/T2 weighted/DWI) were normal. Progressive symptoms emerged six months
later
with imbalance and deteriorating cognition. Examination two months after
onset of
neurological symptoms demonstrated cognitive deficits, dyspraxia or
visuospatial
dysfunction and normal motor, sensory and gait examination. Six weeks later
cognitive
impairment was identified alongside tremulousness, impaired manual dexterity
and
limb ataxia. Serological investigations were normal. MRI (T1/T2
weighted/FLAIR/DWI)
demonstrated prominent signal change throughout the dorsal thalamus,
consistent
with vCJD. PRNP genotyping revealed no mutations and homozygosity for
methionine
at codon 129. The prolonged incubation period of vCJD and possibility of
asymptomatic carrier states pose major public health concerns. This case
highlights
the significant risk encountered by recipients of contaminated blood
products and the
necessity for their specialist monitoring.


http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf



P04.36

Enhanced Surveillance of Persons Identified as at Increased Risk of CJD Due
to
Blood Transfusion or Healthcare Procedures

Brookes, D1; Chow, Y1; Ward, HJT2; Will, RG2; Hewitt, P3; Gill, ON1
1HPA, CJD, UK; 2National CJD Surveillance Unit, UK; 3Colindale, NHS Blood
and Tissue, UK


Introduction:

Reports of four iatrogenic transmissions of variant-CJD (vCJD) infection
in the UK (all due to transfusion of blood from donors who later developed
vCJD),
evidence from iatrogenic transmissions of sporadic CJD and experimental work
on
CJD infectivity in tissues and on healthcare instruments have given rise to
concern
about the risks of iatrogenic transmission of CJD. This risk warrants a)
certain public
health precautions, and b) follow-up of individuals with identified risks in
order to gain
evidence about their risks and ensure appropriate management of these risks.
Evidence of transmission via iatrogenic routes is important to inform public
health
measures and so prevent ongoing transmission of CJD.


Methods:


The Health Protection Agency and Health Protection Scotland holds details
of persons identified as 'at-risk' of vCJD due to blood transfusion and of
persons identified as 'at-risk' of CJD (of any type) from other healthcare
procedures. The GPs/clinicians of all persons identified as 'at-risk' for
public health
purposes are provided with: information; risk assessment updates; advice on
public health
precautions and advice on referral to specialist care. Procedures are being
established to obtain enhanced surveillance data on these individuals,
including:
clinical status updates, date and cause of death, surplus tissue and blood
specimens, and
postmortem investigations.


Results:


Persons 'at-risk' of CJD have experienced a range of exposures. Estimated
risks are uncertain and overlapping. Some individuals - recipients of vCJD
implicated blood components - are considered to be at a clearly higher risk
of
infection: active follow-up is currently conducted for these individuals. In
time, the
enhanced surveillance of persons at increased risk of CJD will provide
estimates of
transmission risks and of the impact of iatrogenic exposures on mortality.
Conclusion: Knowledge about iatrogenic transmission of CJD is being gained
by the follow-up of individuals who have been identified as 'at-risk' of CJD
in the
UK. This enhanced surveillance may need to be sustained for many years.


http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf




Prions in Plasma of Patients with Sporadic Creutzfeldt-Jakob Disease
Safar, J.G1,3, Geschwindm M.D2,3, Letessier, F1,
Kuo, A1, Pomeroy, K1, Deering, C1, Serban, A1,
Groth, D1, Miller, B.L2,3, DeArmond, S.J1,4,
Prusiner, S.B1,3,5
1Institute for Neurodegenerative Diseases,
2Memory and Aging Center, Departments of
3Neurology, 4Pathology, and 5Biochemistry
and Biophysics, University of California,
San Francisco, California 94143


http://www.prion2007.com/pdf/Prion%20Friday.pdf

http://www.prion2007.com/pdf/Prion%20Thursday.pdf

http://www.prion2007.com/pdf/Prion%20Wednesday.pdf




P04.33


Diagnostic Utility of CSF Biomarkers and General CSF Findings in a U.S
Sporadic CJD Cohort


Geschwind, MD; Haman, A; Torres-Chae, C; Raudabaugh, BJ; Devereux, G;
Miller, BL
University of California, San Francisco, USA


Background:

The diagnostic utility of CSF biomarkers, including 14-3-3 protein,
neuron-specific enolase (NSE), AB42, total Tau (T-Tau), and phosphorylated
Tau (PTau)/ T-Tau ratio are often are used for sporadic CJD (sCJD) diagnosis
is
controversial. We have previously reported the CSF 14-3-3 protein to have
poor sensitivity
for CJD diagnosis. In this study, now report the sensitivity and specificity
of
several CSF biomarkers and general characteristics in a U.S. cohort of sCJD
and
non-prion rapidly progressive dementia (RPD) controls (Non-CJD cohort)
subjects.



Design/Methods:


Clinical diagnoses are made through review of medical
records, clinical evaluation, and in many cases pathology. Data is stored in
a secure
clinical relational database, which was queried for various CSF findings,
including
cell count, protein, IgG index, oligoclonal bands (OCBs), 14-3-3, NSE, T-Tau
in patients
with probable or definite sporadic CJD and non-prion rapidly progressive
dementias (RPD),
most of whom were referred to our center with a potential diagnosis of CJD.
For probable sCJD diagnosis, we used UCSF criteria that are modified from
WHO to
substitute MRI for 14-3-3. T-Tau and NSE were considered positive if > 1300
pg/ml and > 35 ng/ml, respectively. For this analysis, ambiguous 14-3-3
results were
considered as negative.


Results:

14-3-3 protein (n=149) sensitivity was only 48% (47% for definite; 50% for
probable sCJD). NSE (n=49) sensitivity was 63% (66% for definite; 59% for
probable
sCJD). T-Tau (n=28) was the most sensitive at 68% (69% for definite; 67% for
probable
sCJD). The specificity of these biomarkers among our CJD and RPD controls
(n=72)
was 66% for 14-3-3 (n=47), 81% for NSE (n=21), and 100% for T-Tau (n=7). The
14-3-3 had the lowest sensitivity and specificity. Mildly elevated CSF
protein
(<100 mg/dl) is common in sCJD; High WBC; >20, is uncommon in sCJD.


Conclusions/Relevance:


In a cohort from a major U.S. CJD referral center, the 14-3-3
is neither sensitive nor specific for sCJD. NSE and T-Tau also show poor
sensitivity for
sCJD. T-Tau may be more specific than 14-3-3 and NSE, but our "n" is small.
WHO
sCJD criteria should be revised; by eliminating 14-3-3 and including brain
MRI into the
criteria. We are currently analyzing the effects of disease duration and
codon 129
polymorphism on these CSF biomarker results.



http://www.prion2007.com/pdf/Prion%20Book%20of%20Abstracts.pdf



Subject: FATEPriDE Environmental Factors that Affect the Development of
Prion Diseases
Date: February 18, 2006 at 9:24 am PST

FATEPriDE


Environmental Factors that Affect the Development of Prion Diseases.

Project funded by the European Commission under the Quality of Life
Programme.


Contract No: QLK4-CT-2002-02723

Project No: QLRT-2001-02723

Start Date

1st January 2003

Duration

36 months plus 6 month extension

Partners

1. The University of Bristol, UK (Co-ordinator)
2. National Environment Research Council-The British Geological Society, UK
3. University of Bath, UK
4. Free University of Berlin, Germany
5. University of Iceland, Iceland
6. Universita degli studi di Perugia, Italy
7. Universite Joseph Fourier Grenoble, France
8. Alpine Institute of Environmental Dynamics, France

Introduction

The work proposed here brings together top EU geo and biochemists focusing
on determining the environmental factors that affect the development of
prion diseases such as scrapie, bovine spongiform enchpalitis (BSE), chronic
wasting disease (CWD) and Creutzfeld-Jacobs disease (CJD). First the
geographical distribution of manganese and copper in soils will be
investigated as risk factors. This will be undertaken due to the fact that
prion diseases often are found in clusters. It now has been established that
the normal metal for prion protein is copper but if that metal is replaced
with manganese, the structure of the prion protein is altered. The role of
organophosphate pesticides will also be investigated because it has been
suggested that copper is complexed with organophosphate, preventing copper
absorption.

Objectives

There is clear evidence that the occurrence of prion diseases often has a
non-random distribution, suggesting a link to some environmental factors.
The work proposed here will investigate risk factors, including the role of
trace elements and organophosphates. Analysis of regional variation in local
manganese/copper levels will be determined and compared to the incidence of
the diseases. The ability of manganese and/or organophosphates in
influencing conversion of the prion protein to an abnormal and/or infectious
protein will be determined. In combination with geographical occurrence and
geo-chemical considerations this program will identify whether these
environmental considerations should be acted upon to bring about effective
prevention or at least risk minimalisation of prion diseases in the EU and
further afield.

Description of the Work

Recently it has been suggested that disbalance in dietary trace-elements
and/or exposure to organophosphates might either cause or be a risk factor
for prion disease development. In particular, high incidence of scrapie
(e.g. in Iceland), chronic wasting disease, and in Slovakia and Italy CJD
are associated with regions where soil and foliage are reported to be low in
copper and high in manganese. This proposal will address whether exposure to
a diet that has a high manganese/copper ratio can influence prion disease
will also be addressed. In particular, we shall investigate this theory at
the level of protein, cells, animals as well as geographical and
geo-chemical associations with prion diseases. Animal models of prion
disease and sheep from farms in regions of high scrapie will be investigated
for a possible influence of level of manganese and copper on incidence or
onset of these diseases. Bio-chemical and biophysical techniques will be
used to investigate interaction of the prion protein with copper and
manganese to determine the mechanism by which Mn substitution for Cu
influences conversion to the abnormal isoform of the protein and whether
such conversion results in protein that is infectious in mouse bioassay for
infectivity. Additionally, a cell culture model will be used to generate
abnormal prion protein by exposure to manganese. Cell culture model of
infection will be used to assay whether prion disease alters manganese
metabolism and transport of manganese into cells. The level of expression of
the prion protein is in itself a risk factor for prion disease as it
shortens the incubation time for the disease. This research will result in
understanding of the role of disbalance in the trace elements Cu and Mn on
the onset and mechanisms behind the occurrence of prion diseases and will
for the first time define whether there are environmental risk factors for
prion diseases.

Milestones and Expected Results

The study proposed here will produce a geo-chemical map of Europe for
manganese and copper. These maps will be used to target field areas where
prion diseases have occurred as clusters. The bio-chemical studies will
establish whether the replacement of manganese for copper in prion protein
is a risk factor for the disease _development_. Organophosphate will also be
investigated as a risk factor. The study aims at minimising the risk of
prion diseases for humans and animals in the EU.



http://www.arp-manchester.org.uk/FatePride.htm


SINCE THEN ;


Subject: FATEPriDE KEY FINDINGS ORGANOPHOSPHATE NO RELATIONSHIP TO CAUSE TSE
Date: May 3, 2007 at 8:41 am PST

KEY FINDINGS

Organophosphate Studies

6. Studies using phosmet (an organophosphate pesticide) were
carried out throughout the project. No relationship between this
compound and the potential to cause a TSE were identified. In
studies with oral dosing of rats, it was shown that PrP expression
levels increased in the brain but there was no association between
this and formation of proteinase K (PK) resistant PrP.


snip...


12. A model of seed protein aggregation and fibril formation was
established using PrP charged with Mn2+. PrP-Mn2+ was found to
form small circular aggregates able to catalyse further protein
aggregation and fibrilisation of PrP. This model unlike other
published models (for example those of Baskakov et al.1) does not
require the presence of denaturants and is not an autocatalytic
process (i.e. the substrate of the reaction did not aggregate). The
results suggest that Mn2+ may play a role in the formation of prion
seeds

__although further studies showed that this material was not
infectious in mouse bioassay.__

snip...

24. The project also generated information concerning the relation of
TSEs to environmental factors:
• __Potentially no role for organophosphates in TSEs.__
• Increased Mn in the diet results in higher PrP levels in the
brain.
• No conclusion is yet possible in terms of the relationship
between environmental trace element concentrations and the
geographical occurrence of TSEs (classical scrapie or BSE).
• Some confirmation was provided that in some specific farms
occurrence of classical scrapie correlates with high Mn levels.


http://www.seac.gov.uk/papers/97-4.pdf



a) As regards the involvement of organophosphates in the origin of BSE, no
new scientific
information providing evidence or supporting the hypothesis by valid data
became
available after the adoption of the last opinion of the SSC on this issue.
Consequently
there is no reason for modifying the existing opinions.
b) Regarding the possibility of OP poisoning, the European legislation for
registration of
plant protection products and veterinary medicines – addressed in the
enquiries – provide
the basis for safe use of registered compounds and their formulations.
Regarding the
alleged intoxication cases reported and OP exposure it must be concluded
that safety
measures may not have been strictly followed.
References
Brown, D.R., Qin, K., Herms, J.W., Madlung, A., Manson, J., Strome, R.,
Fraser, P.E., Kruck, T., von
Bohlen, A., Schulz- Schaeffer, W., Giese, A., Westaway, D. and Kretzschmar,
H. (1997) The Cellular
Prion Protein Binds Copper In Vivo, Nature, 390, 684-7.
Purdey, M. (2000) Ecosystems Supporting Clusters of Sporadic TSEs
Demonstrate Excesses of the Radical-
Generating Divalent Cation Manganese and Deficiencies of Antioxidant
Co-Factors Cu, Se, Fe, Zn Medical
Hypotheses, 54, 278-306.
Scientific Steering Committee, 1998. Opinion on possible links between BSE
and Organophosphates. Adopted
on 25-26 June 1998
Scientific Steering Committee, 2001. Opinion on Hypotheses on the origin and
transmission of BSE. Adopted
on 29-30 November 2001.

http://europa.eu.int/comm/food/fs/sc/ssc/out356_en.pdf



OP'S MEETING WITH PURDEY

http://www.bseinquiry.gov.uk/files/yb/1994/02/09001001.pdf



transmission studies do not lie, amplification and transmission!


1: J Infect Dis 1980 Aug;142(2):205-8


Oral transmission of kuru, Creutzfeldt-Jakob disease, and scrapie to
nonhuman primates.

Gibbs CJ Jr, Amyx HL, Bacote A, Masters CL, Gajdusek DC.

Kuru and Creutzfeldt-Jakob disease of humans and scrapie disease of
sheep and goats were transmitted to squirrel monkeys (Saimiri
sciureus) that were exposed to the infectious agents only by their
nonforced consumption of known infectious tissues. The asymptomatic
incubation period in the one monkey exposed to the virus of kuru was
36 months; that in the two monkeys exposed to the virus of
Creutzfeldt-Jakob disease was 23 and 27 months, respectively; and
that in the two monkeys exposed to the virus of scrapie was 25 and
32 months, respectively. Careful physical examination of the buccal
cavities of all of the monkeys failed to reveal signs or oral
lesions. One additional monkey similarly exposed to kuru has
remained asymptomatic during the 39 months that it has been under
observation.

PMID: 6997404

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6997404&dopt=Abstract



look at the table and you'll see that as little as 1 mg (or 0.001 gm) caused
7% (1 of 14) of the cows to come down with BSE;

Risk of oral infection with bovine spongiform encephalopathy agent in
primates

Corinne Ida Lasmézas, Emmanuel Comoy, Stephen Hawkins, Christian Herzog,
Franck Mouthon, Timm Konold, Frédéric Auvré, Evelyne Correia, Nathalie
Lescoutra-Etchegaray, Nicole Salès, Gerald Wells, Paul Brown, Jean-Philippe
Deslys
Summary The uncertain extent of human exposure to bovine spongiform
encephalopathy (BSE)--which can lead to variant Creutzfeldt-Jakob disease
(vCJD)--is compounded by incomplete knowledge about the efficiency of oral
infection and the magnitude of any bovine-to-human biological barrier to
transmission. We therefore investigated oral transmission of BSE to
non-human primates. We gave two macaques a 5 g oral dose of brain homogenate
from a BSE-infected cow. One macaque developed vCJD-like neurological
disease 60 months after exposure, whereas the other remained free of disease
at 76 months. On the basis of these findings and data from other studies, we
made a preliminary estimate of the food exposure risk for man, which
provides additional assurance that existing public health measures can
prevent transmission of BSE to man.


snip...


BSE bovine brain inoculum

100 g 10 g 5 g 1 g 100 mg 10 mg 1 mg 0·1 mg 0·01 mg

Primate (oral route)* 1/2 (50%)

Cattle (oral route)* 10/10 (100%) 7/9 (78%) 7/10 (70%) 3/15 (20%) 1/15 (7%)
1/15 (7%)

RIII mice (ic ip route)* 17/18 (94%) 15/17 (88%) 1/14 (7%)

PrPres biochemical detection

The comparison is made on the basis of calibration of the bovine inoculum
used in our study with primates against a bovine brain inoculum with a
similar PrPres concentration that was

inoculated into mice and cattle.8 *Data are number of animals
positive/number of animals surviving at the time of clinical onset of
disease in the first positive animal (%). The accuracy of

bioassays is generally judged to be about plus or minus 1 log. ic
ip=intracerebral and intraperitoneal.

Table 1: Comparison of transmission rates in primates and cattle infected
orally with similar BSE brain inocula


Published online January 27, 2005

http://www.thelancet.com/journal/journal.isa


It is clear that the designing scientists must also have shared Mr Bradley's
surprise at the results because all the dose levels right down to 1 gram
triggered infection.


http://www.bseinquiry.gov.uk/files/ws/s145d.pdf



and for Gods sake, if someone is smearing this cr@p all over there kids
heads for lice and did not come up with a TSE, i would say this is good case
study;


UK FARMER WITH BSE


1) None of our animals that contracted BSE were treated with OP's, even
in utero.
2) My kids were treated with OP's as infants to control head lice. This
seems to be endemic as infection waves in UK primary schools (and
possibly elsewhere).
3) One might argue if the continued use of british beef in the UK was
ethical, none the less it happened. We have a duty to learn from it, not
least a duty to learn on behalf of those people who died so horribly....



TSS
 
Kathy, it seems that some of the arguments that you and flounder make on bse seem to be similar. The similarities are the transmission routes, maybe not the method of transmission, but at least there seems to be some agreement that bovine material fed to bovines is the probable transmission route.

I would like to point out that this transmission route was one that was promoted by slaughter houses in their efforts to increase their profits by making by-products salable without making sure feeding bovines to bovines was safe.

Unfortunately, this untested food safety and animal safety example shows that the AMI just gives mouth service to the belief that its members should not compete on food safety. Feeding cattle guts o cattle was an example of how AMI members competed with each other when it came to food safety.

The cold cruel fact is that food companies do compete against each other in whatever way they can, even if it means competing on food safety, regardless of what the AMI says. The AMI's reputation should be viewed on its actions not on its words.

There are some who might say that the feeding of cattle parts to cattle just lowers the cost of meat for consumers. They conveniently forget the costs for decisions like that to the markets and to consumers.

This is the reason regulatory agencies are required. The decisions of industry (and their profit motive) often leaves out other, just as important decisions, on food and animal safety.

It is also the reason these agencies should not be run by the industry or unduly influenced by them. It seems that industry has been able to use its profits to "buy" laxity and the absence of good judgment in the name of either making a buck or out competing rivals.

Some say the trade off is fine. To them, I say: "Why don't you put your money where your mouth is and eat what is being fed to you in the name of profits or competition? " I doubt the AMI would serve bse infected cattle or cattle fed other cattle in their executive meetings. Why should they profit by it by selling their line to others?
 

Latest posts

Back
Top