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Border Reopening Needs More Analysis?

Mike

Well-known member
NMPF: Border reopening needs more analysis
By Dairy Herd news source (Monday, August 20, 2007)


The National Milk Producers Federation has asked the White House’s Office of Management and Budget to better analyze the economic impacts of a reopened Canadian border.

The Bush Administration is in the final stages of reopening the U.S. border to all types of Canadian cattle — including dairy animals — born after March 1, 1999. The proposed regulatory change includes milk cows to be used for breeding purposes.

NMPF believes that the USDA’s cursory review of the potential economic impacts of the cattle trade “is inadequate, and doesn’t fully account for the economic losses that could occur as a result of a reopened border,” said Jerry Kozak, president and CEO of NMPF, in a letter sent Aug. 17 to the Office of Management and Budget. The Office of Management and Budget is responsible for conducting an economic review of all major regulatory changes proposed by the federal government.

NMPF estimates that additional annual imports of approximately 47,000 Canadian dairy heifers could increase milk production by 0.5 percent per year over the next five years, reducing farm-level milk prices by 18 percent and dairy producer revenue by $5 billion, on average, during that time period.

In addition, a surge in Canadian dairy animals will reduce the current value of a producer’s dairy herd, “substantially reducing” his net worth, Kozak said.

Because Canada’s government has continued to find cattle that have bovine spongiform encephalopathy, the USDA is estimating that up to 700 BSE-infected cattle could be exported to the U.S. during the next 20 years. Such a development could reduce beef prices — and thus the revenue that dairy producers derive from cattle sold for meat packing — as a result of the resumption in Canadian exports.

“The existence of BSE-infected animals could substantially undercut demand for beef, as it has done in Europe. It could also lead to greater discounts for dairy cows at slaughter,” Kozak said.

The letter goes on to state that while NMPF does not object to the proposed regulation’s review of Canadian cattle designated for immediate slaughter, the regulatory analysis for dairy breeding animals is incomplete “and does not justify that part of the proposed rule.”

NMPF is asking for an opportunity to further assist the Office of Management and Budget with a full review of the potential impact of this proposed regulation.



National Milk Producers Federation
 

Kathy

Well-known member
What dietary supplementation did this study use? (a form of anti-oxidant)

http://www.neuroprion.com/pdf_docs/conferences/prion2006/abstract_book.pdf
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.

Dr. Brown showed this before, and has spent years proving that oxidative stress is a precursor before clinical signs of disease. Look him up:

Folia Neuropathol. 2005;43(4):229-43. Links
Neurodegeneration and oxidative stress: prion disease results from loss of antioxidant defence.Brown DR.
Department of Biology and Biochemistry, University of Bath, Bath, BA2 7AY, UK. [email protected]

Prion diseases or transmissible spongiform encephalopathies (TSEs) are rare neurodegenerative disorders that can be acquired either by direct transmission, inherited through dominant mutations in the prion protein gene or via an unknown sporadic cause. This latter group constitutes the vast majority of cases. Like many neurodegenerative diseases the hallmarks of oxidative damage can be readily detected throughout the brain of the affected individual. However, unlike most other neurodegenerative diseases, prion diseases are connected with a dramatic loss of antioxidant defence. As abnormal protein accumulates in the diseased brain there is both an increase of oxidative substances and a loss of the defences that keep them in check. In particular the normal cellular prion protein has been shown to be an antioxidant. Conversion of this protein to the protease resistant isoform is accompanied by a loss of this antioxidant activity. This change creates a paradox as the loss of activity is not accompanied by a loss of protein expression. It is likely that this prevents other cellular defences from responding sufficiently to protect neurons from the heightened oxidative burden. Recent experiments with transgenic mice have shown that when prion protein expression is switched off during the course of prion disease, cell death is dramatically halted and the mouse recovers from the disease. This result clearly illustrates that the continued expression of non-function prion protein is essential for disease progression. This implies that the presence of this abnormal protein during prion disease causes a failure of cellular antioxidant defence. This failed defence is the fundamental cause of the massive neurodegeneration that results in the fatal nature of TSEs. The role of oxidative stress in TSEs and other neurodegenerative disorders are discussed in this review. PMID: 16416388

This is free online if you search hard enough for it.


Mike, I suspect that the SPP "security and prosperity partnership" which is fast tracking the integration of all of our commerce, military, health, ETC. (and which a meeting between Canada, USA and Mexico is taking place right now in Montebello Quebec) is being pushed - partly - because:

if I am correct, and Depleted uranium weapons, nuclear fallout and certain metal nanoclusters ARE responsible for BSE, CWD and other neurological disorders - then the USA has it in their herds big-time, already. Just as Canada probably has more cases than CFIA is willing to say.

By integrating our economies and health issues under one umbrella of regulations the 'discovery' of these cases will not have as big an impact in North America. Of course, it will completely close our over-seas markets - but since the economic, political and military goal is to fully mesh these three countries into the North American Union - we will have to be happy to just trade meat among ourselves. [that is if anyone still wants to buy it].

Now you can slam me for this prediction, and I will be happy if it doesn't come to pass - but given the probability - I prefer to head off mis-information about "infectious proteins" and identify the true causative agent that is causing the disease. As Dr. Vodyanoy claims, metal nanoclusters are misfolding, polymerizing and aggregating proteins. Dr. Hamir shoed lead fed to dogs caused spongiform of the brain. DU preferentially accumulates in the Peyer's Patches of the distal ileum (a specified risk material), uranium accumulates in the brain. Cesium 134/137 accumulates in the muscle and decays into barium. Most radionuclides accumulate in the bone (major source) ie: Meat and Bone Meal- fed to cows was a bad idea.

Read Mark Purdey's ecodetective papers, his peer-reviewed medical papers and connect the dots. When a metal contaminates the brain, then starts to decay because it is radio-active, the disease associated with this trauma would cause massive oxidative stress, decreased immune status and eventually (if enough damage takes place) will kill the affected.

Gotta get to work.
 
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