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Test EVERY Cow in the Food Chain

Test EVERY Cow in the Food Chain
Like Other Countries Do
Showing posts with label atypical BSE. Show all posts
Showing posts with label atypical BSE. Show all posts

Saturday, January 1, 2011

USDA Creates Bill to Compell Japan to Buy Our Beef, Lies to Congress about Mad Cow

Lies highlighted in bold italics

S. Res. 452

RESOLUTION

Supporting increased market access for exports of United States beef and beef products to Japan.

Whereas, in 2003, Japan was the largest market for United States beef, with exports valued at $1,400,000,000;

Whereas, after the discovery of 1 Canadian-born cow infected with bovine spongiform encephalopathy (BSE) disease in the State of Washington in December of 2003, Japan closed its market to United States beef, and still restricts access to a large number of safe United States beef products;

Whereas for years the Government of the United States has developed and implemented a multilayered system of interlocking safeguards to ensure the safety of United States beef, and after the 2003 discovery, the United States implemented further safeguards to ensure beef safety;

Whereas a 2006 study by the United States Department of Agriculture found that BSE was virtually nonexistent in the United States
; ( I would like to see a copy of this "study")

Whereas the internationally recognized standard-setting body, the World Organization for Animal Health (OIE), has classified the United States as a controlled risk country for BSE, which means that United States beef is safe for export and consumption. (Oh yes and we believe anything the WHO has to say......we KNOW they would never lie to U.S. (not.)

Full text; http://www.govtrack.us/congress/billtext.xpd?bill=sr111-452

Saturday, December 4, 2010

Wednesday, December 1, 2010

Counsil Conclusions on TSE / USA the Worst

The U.S. has lower sanitary and phyto-sanitary standards (SPS) for imports than many other countries, especially those concerning bovine spongiform encephalopathy (BSE). These low standards have made the U.S. a dumping ground for beef from the countries that have experienced BSE problems.

Full article; http://transmissiblespongiformencephalopathy.blogspot.com/2010/11/council-conclusions-on-tse-road-map-2.html

Sunday, October 25, 2009

Taiwan lifts ban on importing US bone-in beef

Guess Taiwan didnt hear about Chinas banning US Beef Imports because of "banned organs" found in the cow carcasses. Recently, both Tyson and Cargill Beef Products have been guilty of failure to remove these banned parts from the carcasses of the beef we are exporting and/or are selling to our own American consumers.

By Pawan Shukla | 24/10/2009 | in

The Taiwan government has announced that it will lift a ban on imports of a range of U. S. ‘beef in bone’ products including Porterhouse steak.

Taiwan has ended a six year long ban on import that was in place over fears of mad cow disease, and ushering improving ties with the U. S.

The import is likely to start in November this year.

Meanwhile, the health department announced all imported beef products will have to carry a label of approval from the U. S. Agriculture Department.

During the meeting of Taiwan and US officials, a retired US diplomat in Taipei, Syd Goldsmith said, “It removes an irritant that's been nagging for as long as I can remember.”

A source from US official told reporters that the deal is finalized and it allows import of all beef products from cattle under 30 months old. He also added that imports from older cattle will be allowed only after the young ones are found safe.

While talking to reporters, the Taiwan government official said, “After a strict appraisal and risk analysis proving the safety of U. S. beef, the Department of Health today announces that in addition to the boneless products now allowed, it will open to other beef.”

The United States is Taiwan’s second largest trading partner and it generates an annual trade of about $57 billion.

Click on title above for original article and place to comment; http://topnews.com.sg/content/2384-taiwan-lifts-ban-importing-us-beef-bone

SEE ALSO, Related;

Taiwan minister offers to quit over US beef decision
(AFP) – 1 day ago

TAIPEI — Taiwan's health minister on Saturday offered to resign over the controversial decision to lift the ban on US beef on the bone despite mad cow disease concerns.

"Of course I will resign if there is a demand. I will take the responsibility," health minister Yang Chih-liang told reporters.

The health department announced Friday that it would allow imports of US bone-in beef and intestines in a move blasted by some lawmakers and consumer rights advocates.

The ruling Kuomintang caucus demanded Yang step down for lifting the ban without the parliament's consent and threatened to freeze the health department's budget.

Meanwhile, the Consumers' Foundation accused the government of bowing to pressure from Washington despite health risks and urged the authorities to put warning labels on US beef products.

Local media said the new measure would take effect in late October and the first shipment of US beef on the bone is expected to arrive in the island as early as November 10.

Taiwan banned US beef imports in December 2003 due to reports of mad cow disease in the country but opened up to boneless beef products in 2006.

Beef affected by the disease is feared to cause in humans a variant of Creutzfeldt-Jakob disease.


http://www.google.com/hostednews/afp/article/ALeqM5hkNOLNffaZFNGZYSZ5Jk_6YXFYiA

Monday, October 12, 2009

Japan Suspends Beef Imports from Tyson / Finds Banned Cattle-parts in Carcasses / Nice Going USDA

October 10, 2009

Japan suspends beef imports from US plant

By MARI YAMAGUCHI Associated Press Writer

Japan suspended beef shipments from an American meatpacker Saturday over its failure to remove cattle parts banned under a bilateral agreement, as officials here raised concerns about U.S. safeguards against mad cow disease.

Japanese quarantine inspectors found bovine spinal columns in one of 732 boxes shipped from Tyson Fresh Meats Inc., which arrived in Japan in late September, the Ministry of Agriculture, Forestry and Fisheries said. The box contained 35 pounds (16 kilograms) of chilled short loin with spinal bones, which were not released commercially, said ministry official Goshi Nakata.

The suspension only affects Tyson's factory in Lexington, Nebraska, one of 46 meatpacking plants approved to export beef to Japan.

It was the second suspension for the Lexington factory, Nakata said. Japan slapped a four-month ban on beef shipments from the same plant in February 2007 after finding two boxes of beef lacking verifications to show they came from cattle that met Japan's safety standards.

"It's extremely regrettable," said Agriculture Minister Hirotaka Akamatsu, who has just returned from meetings in Washington with U.S. trade and farm officials. "We need to closely examine if it was just a careless mistake or there is a systematic problem."

Japan's new ruling Democratic Party has proposed a tough response to any violation to a bilateral safety agreement, including a blanket ban on U.S. beef shipments.

The Japanese ministry has asked the U.S. Department of Agriculture to investigate how the box containing the banned parts ended up in Japan.

Japan will await results of a U.S. investigation to determine the penalty for the Tyson factory, the ministry said.

Gary Mickelson, a spokesman for Tyson, called the delivery of that box a mix-up. He said the Springdale, Ark.-based company is investigating it and will work with the Agriculture Department to "take corrective measures" so the plant can start supplying Japanese customers again.

He said Tyson has seven other beef plants approved to ship meat to Japan. It was not immediately clear how much meat Tyson ships to Japan, but Mickelson said it was not among its top five international markets in 2008.

The problem surfaced just one day after U.S. Trade Representative Ron Kirk urged Akamatsu on Thursday to lower Japan's strict safety standards in line with international standards.

"It was bad timing," said another Japanese agricultural official, Yusuke Hirata, referring to the Tyson shipment. "I hope the U.S. side would see it as an embarrassment and try to make an improvement."

Washington has repeatedly criticized Japan for its tough import restrictions, which authorities say have no scientific basis.

Under the bilateral trade agreement, U.S. exporters must remove spinal columns, brain tissue and other parts considered linked to mad cow disease. U.S. beef shipments to Japan must also come only from cattle age 20 months or younger, which are believed to pose less of a risk.

U.S. officials have urged Japan to allow imports of beef from cattle aged at least up to 30 months, a widely used safety standard elsewhere, and possibly scrap age restrictions.

"We don't have a deadline, and we have not made any decisions as to whether we should change any safety standards," Hirata said. He said, however, a decision could be further delayed "if the latest incident was found to have involved serious violations."

Japan banned all U.S. beef imports in 2003 after the first case of mad cow disease was discovered in the United States. Japan resumed buying American beef in 2006 after the bilateral trade agreement setting new safety standards.

Mad cow disease, formally known as bovine spongiform encephalopathy, is a degenerative nerve disease in cattle. In humans, eating meat products contaminated with the illness is linked to variant Creutzfeldt-Jakob disease, a rare and fatal malady.


http://license.icopyright.net/user/viewContent.act?clipid=376091587&mode=cnc&tag=3.5721%3Ficx_id%3D20091010-pf1onfile-V804

Tuesday, November 18, 2008

Alabama Mad Cows / June 2006

Report: 2006

Statement by Wenonah Hauter, executive director, Food & Water Watch



Today’s news report that a third cow with mad cow disease has been found in Alabama brings us once again to questions we’ve been asking for more than five years now: Why isn’t there a mandatory system in place to report suspect animals? When is the Animal and Plant Inspection Service going to address the problems with the sampling in its surveillance program? Why isn’t the U.S. Food and Drug Administration fixing the loopholes in the animal feed ban that would prevent mad cow from even being an issue?


We applaud the farmer who did the right thing by turning over the sick cow in question to a veterinarian for testing. But this is still a voluntary system that must be made mandatory for the sake of public health. Without a mandatory reporting system, who knows what else is out there?


The USDA surveillance system still has problems – even the U.S. Department of Agriculture’s own inspector general deeply criticized the system, and still there has been little action taken to fix the identified problems.


We urge USDA to continue its heightened surveillance program and to fight for more money in its 2007 budget for continued testing. As it currently stands, the fiscal budget for 2007 only provides for 40,000 tests. This is insufficient.


Mad cow disease will not go away on its own. The government must admit there’s a problem and take the necessary steps to fix the problems and protect all consumers.


Click on title above to see article;
http://www.foodandwaterwatch.org/press/releases/mad-cow-in-alabama-article03142006/?searchterm=mad%20cow

Tuesday, November 11, 2008

Mapping CJD: Human Mad Cow Disease

Creutzfeldt-Jakob disease, commonly known as CJD, is a brain disease that progresses rapidly and generally results in the death of the patient. It probably came to the public notice following the outbreaks of mad cow disease in Europe in the 1990s because the agent that causes bovine spongiform encephalopathy (BSE) in cows is thought by some to be responsible for the onset of variant CJD in humans. Yet, despite the swathe of publicity, CJD is a rare disease.

Of the various types, sporadic CJD is the most common, accounting for about 85% of cases in the US. The symptoms only show their faces around the age of 60 and most patients die within a year. Hereditary CJD, accounting for 5-10% of US cases, and acquired CJD, which is transmitted by exposure and accounts for 1% of cases, are the other major categories. The rapid progression and fatal outcome of the disease point to the fact that there is no cure for CJD.

The conventional way to confirm CJD in humans is to carry out a brain biopsy. This occurs in post-mortem examinations but biopsies on suspected patients are generally discouraged because, even if the disease is diagnosed, there is no treatment. So, the medical world needs a reliable test for live patients. Currently, one available test looks for the 14-3-3 proteins in cerebrospinal fluid (CSF). These are indicative of CJD but the immunoblot procedure gives a false positive rate of 5-10%, so is unsuitable for screening. In addition, a high proportion of patients with variant CJD do not produce these proteins. A second test, developed by Amorfix Life Sciences Ltd. and currently undergoing validation in the UK, detects prion proteins associated with vCJD in human blood and has given promising results.

A team of scientists in Germany has adopted a different approach, looking for a panel of proteins in CSF which are indicative of CJD and can differentiate it from other neurodegenerative diseases in the largest study of this type. Markus Otto from the University of Ulm with colleagues from six other institutions analysed CSF from a total of 72 patients: 36 diagnosed as having probable CJD (according to WHO criteria), 24 with Alzheimer's disease, 6 with dementia with Lewy bodies and 6 non-demented controls.

The samples were subjected to an optimised sample preparation procedure for analysis by 2D differential gel electrophoresis using the CyDyes 2, 3, and 5. This method has the potential to separate thousands of proteins on a single gel and is a popular choice for comparative, quantitative proteomics studies.

Following 20-fold concentration, CSF was depleted of the abundant proteins albumin and immunoglobulin G, which tend to mask less abundant proteins. There is always a risk that some less abundant proteins will be co-depleted, or reduced in volume so that there is insufficient quantity remaining on the gels for subsequent identification. However, the advantage gained by removing albumin and IgG were considered to outweigh these disadvantages.

The depleted CSF was mixed with acetone to induce protein precipitation and the dried proteins were lysed in buffer to get at the soluble proteins. Then, proteins from the different disease groups were labelled with the respective dyes and subjected to gel electrophoresis. An initial separation at pH 4-10 showed that few proteins were resolved in the pH 7-10 region, so the samples were run at pH 4-7. In this way, about 2200 spots were resolved.

The use of an internal standard allowed normalisation and comparison between the various gels. Using stringent criteria, five protein spots were found to be statistically different in the CJD samples compared with the others. These were cut from the gel to identify the proteins by mass spectrometry, although one protein remained a mystery because there was insufficient sample for identification. The team regarded this protein as one with high diagnostic potential for CJD and will aim to identify it in the future.

Two of the other four proteins were members of the 14-3-3 family, which was not unexpected. The remaining two were L-lactate dehydrogenase B-chain and gamma-enolase. Their suitability as biomarkers has yet to be validated but their discovery presents more possibilities for developing a diagnostic test that is more reliable than the current 14-3-3 immunoblotting test.

Other proteins that have been proposed previously as candidate markers for CJD, such as transthyretin, serotransferrin and gelsolin, were regulated on some gels but did not fulfil the stringent criteria for selection.

Otto and the team have demonstrated the validity of their approach for differentiating CJD from other neurodegenerative diseases and have presented several new candidates for biomarkers. The technique should also be applicable to other brain diseases, especially those in which brain proteins are transferred into CSF but the limitations with regard to low abundance proteins should be taken into account.

Related links:

Proteomics 2008, 8, 4357-4366: "Cerebrospinal fluid-optimized two-dimensional difference gel electrophoresis (2-D DIGE) facilitates the differential diagnosis of Creutzfeldt-Jakob disease"
Article by Steve Down


Click on title above to see full article with pics; http://www.spectroscopynow.com/coi/cda/detail.cda?id=19726&type=Feature&chId=10&page=1

Friday, November 7, 2008

Mad Cow Horse Discovered in UpState NY!



Is this what a horse looks like with "Mad Cow" or is it just a "New York Cow Horse?" Hard to tell these days with all them mutant prions going around taking new shape and form in every species they infect.

Had ya going there a minute, didnt I, USDA? lol

Friday, October 24, 2008

Canada Close to Live Testing Methods

Canadian and German scientists have discovered that a single protein can accurately distinguish between healthy cows and those with mad cow disease, or bovine spongiform encephalopathy (BSE). This finding should hopefully lead to the development of a test for diagnosing BSE in live cattle, says lead researcher David Knox from the University of Manitoba, Winnipeg.

First detected in the UK in 1985, BSE is a degenerative neurological disease that affects cows. Like scrapie in sheep and Creutzfeld-Jakob Disease (CJD) in humans, BSE is a type of a transmissible spongiform encephalopathy (TSE) disease, caused by the build-up in the brain of an abnormal protein known as a prion.

Following the BSE epidemic among UK cows in the 1980s and 1990s and the discovery that humans could contract the so-called new variant CJD by eating BSE-infected meat, many countries implemented monitoring programmes to detect cows with BSE. This usually involves testing for the presence of prions in the brains of all cows older than a certain age or showing possible signs of BSE.

Understandably, this kind of test can only be conducted after the cows have been killed, which is sort of shutting the stable door after the cow has bolted. In contrast, a test that could detect BSE in live cows would permit the routine testing of all cattle. This would allow any BSE outbreak to be detected at an earlier stage and give much greater confidence that a country's cow population was entirely free of BSE.

Unfortunately, although prions are found at high concentrations in brains and spinal cords, they're present at much lower concentrations in easily testable bodily fluids such as cerebrospinal fluid, blood and urine. This has helped to stymie attempts to develop just such a live test.

But detecting prions is not the only way to diagnose BSE. Like any other disease, BSE induces a whole host of biochemical changes in infected cows, which should be reflected in the presence of characteristic protein biomakers in their bodily fluids. So Knox and his colleagues set out to find these biomarkers.

Using two-dimensional gel electrophoresis, they searched for proteins present at different concentrations in urine from four healthy and four BSE-infected cows. Finding that 56 of the over 1,300 protein spots on each of the subsequent gels were present at different concentrations in the two groups, Knox and his colleagues then used a range of multivariate statistical techniques to determine which spots were best at distinguishing between healthy and infected cows.

This uncovered a single protein spot that was able to distinguish between the two groups with perfect accuracy. Analysing this protein using mass spectrometry revealed it to be the glycoprotein clusterin, which is commonly found in a wide range of different biological tissues. Unfortunately, high concentrations of clusterin have already been linked to neurodegenerative diseases such as Alzheimer's disease, suggesting that it might not make a particularly specific BSE biomarker.

However, Knox and his team actually detected two versions of clusterin in cow urine, perhaps reflecting two different post-translational modifications of the protein, and only one of these versions was able to distinguish between the healthy and infected groups. This raises the possibility that this particular version of clusterin could make a more accurate biomarker.

Furthermore, by analysing proteins in the cow urine at six different times during the course of the BSE infection, Knox and his team discovered that changes in the concentrations of 16 of the protein spots accurately matched the progression of the disease.

'Our work shows that it is possible to identify biomarkers in urine that could be useful in the diagnosis and monitoring of disease progression in BSE,' says Knox. In addition to developing a live BSE test, Knox hopes that this work will lead to live tests for other TSE diseases, including CJD


Click on title above for article;
http://www.separationsnow.com/coi/cda/detail.cda?id=19656&type=Feature&chId=2&page=1

Thursday, October 23, 2008

UK Announces New Blood Test for Human BSE (CJD)

The first ever diagnosis for variant CJD, which is currently undergoing clinical trials and could be available within 18 months, is seen as an important step in finally stamping out the incurable disease and preventing it from becoming endemic in society.

But medical experts on an advisory committee to the government are worried that the test may have an unexpected downside including reducing the number of blood donors. There are also fears it could increase insurance premiums.

The doctors worry that donors will be reluctant to give blood if they risk being told that they have the possibility of developing the disease which causes an agonising death.

“You would think that the development of a test was a good news story ,” said John Forsythe, chair of the Advisory Committee on the Safety of Blood Tissues and Organs (SABTO) and a transplant surgeon at the Royal Infirmary of Edinburgh.

“But its does have a significant downsides. There is a worry it could put anyone off from donations.”

Despite fears that the disease could become widespread in the UK, only four of the 167 people who have died from variant CJD caught it through infected blood.

However, surveys suggest that one in 4,000 people carry the infection and although 95 per cent of them may never actually develop the full blown disease, being told you have the disease would be a terrifying blow.

Mr Forsythe said that the problem is compounded because around one per cent of the positive tests could be wrong. With two million people donating blood every year that could amount to 250 people being told they have the infection, and up to three or four of them falsely diagnosed.

Professor Marc Turner, who is also on SABTO, said that both legally and ethically the donors would have to be told they are incubating the disease even though only a few could develop it fully.

“They would have to be told that they could develop a really rather horrible condition,” he said.

It is not the first time vCJD has had an impact on blood supplies.

Four years ago the number of blood donors dropped by 52,000 when anybody who had received blood transfusion in the previous two decades was banned.

At the moment blood is screened for HIV, syphillis and hepatitus B and C, but a number of companies are on the verge of developing a blood test for vCJD.

The difference is that vCJD is not curable or even treatable and many donors may prefer to not know they could develop an ultimately fatal progressive degenerative brain disease.

At present vCJD is tested for by performing post mortem biopsies on the brain.

Professor Turner said that blood donations were currently sufficient because of better management of supplies.

“We can survive a small reduction but a substantive hit would give us major problems,” he said.

SABTO, which is holding a major meeting today, is also expected to recommend that those receiving blood donations be asked for consent for the first time.

A spokesman for the Association of British Insurers said: “The industry looks at any medical development and individual companies will make their own decision.”

Click on title above for article:
http://www.telegraph.co.uk/news/newstopics/politics/health/3230094/Test-for-human-form-of-mad-cow-disease-sparks-fears-of-a-blood-donor-shortage.html

Thursday, October 16, 2008

FDA Bans Brains & Spinal Cords from Petfood

It is well to remember that the nasty little mal-formed pirons that are generally concentrated in the brains and spinal cords of infected animals,---have also been known to show up in the meat and muscle of some of them. Therefore, banning these parts from the food chain ALONE is NOT enough: studies show its in the meat of the animals too!

(NaturalNews)

Effective April 23, 2009, the FDA has banned a series of
cattle products from all animal feed and pet food in attempt to
prevent the spread of bovine spongiform encephalopathy (BSE), also
known as mad cow disease.

BSE is a fatal, degenerative disease of the brain cause by defective
proteins known as prions. These prions can be acquired by consuming
the flesh of infected animals and lead to a similarly fatal human
version of the disease, known as variant Creutzfeldt-Jakob Disease.

Federal regulations already prohibit using ruminant protein as part of
the feed given to other ruminants. These measures were instituted in
the United States and Canada in 1997, after a mad cow outbreak in the
United Kingdom.

--
Click on title above for full story:
http://www.naturalnews.com/024489.html

STAPLES supports this: http://www.youtube.com/watch?v=88kMJXphN0k

Thursday, October 9, 2008

Study Shows New Forms of BSE

And its NOT JUST COWS anymore!

The study shows that a distinctive neurological disorder of cattle which has some clinical similarities to BSE, is associated with abnormal PrP accumulation in brain but the pathology and biochemistry of IBNC are distinct from BSE. The study is important either because it raises the possibility of a significant increase in the scope of prion disease or because it demonstrates that widespread and consistent PrP alterations may not be confined to prion diseases. Transmission experiments are needed to establish whether IBNC is a condition in which prion protein is abnormally regulated or is yet a further example of an infectious cattle prion disease.

Click title above for full article;
http://www.biomedcentral.com/1746-6148/4/38/abstract