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

JAPAN SUSPECTS MAD COWS IN 6 YEAR OLD COW AND A 20 MONTH OLD

flounder

Well-known member
Subject: JAPAN SUSPECTS MAD COW DISEASE IN 6 YEAR OLD COW AND A 20 MONTH OLD STEER
Date: April 27, 2007 at 3:16 pm PST
Japan suspects mad cow disease in bovine




TOKYO (AP) — Preliminary tests on a 6-year-old cow in western Japan indicate it may be infected with mad cow disease, a health official said Tuesday.

Meat inspectors in Okayama prefecture (state) found late Monday that a dairy cow, intended to be slaughtered for meat, has tested positive for the disease, said prefectural health official Waichiro Kawai. The prefecture has sent samples from the cow to the National Institute of Infectious Diseases for confirmation, which could come as early as Wednesday, Kawai said.

Also on Monday, agriculture ministry officials said a 20-month-old steer in northeastern Japan may have had mad cow disease. If confirmed, that case could affect import restrictions on beef from the U.S. and Canada, said Vice Agriculture Minister Mamoru Ishihara.

Japan in December eased a 2-year-old ban on U.S. beef to allow beef imports from cows aged 20 months or younger - an age at which they’re believed less likely to be infected - as long as the meat does not contain brains, bone marrow or other body parts thought to be especially at risk of carrying the brain-wasting disease.

However, the ban was re-imposed in January, after a U.S. veal shipment was found to contain spinal bones, which are restricted under the requirement. The two countries are still negotiating possible safeguards that might allow Japan to resume U.S. beef imports.

Mad cow is a degenerative nerve disease in cattle. Eating contaminated meat products has been linked to the rare but fatal human variant, Creutzfeldt-Jakob disease, which causes brain tissues to waste.

Japan, which conducts mad cow tests on all cattle killed for meat, has confirmed 24 cases since 2001 — including three cases this year — according to the Agricultural Ministry.

Okayama is about 545 kilometers (340 miles) west of Tokyo.


Programming by Ayten Alizadeh. Copyight by IntraNS. All rights reserved.


http://www.bakusun.az/cgi-bin/ayten/bakusun/show.cgi?code=9512

TSS
 

Kathy

Well-known member
Neurochem Res. 2007 Apr 4; [Epub ahead of print]
Heavy Metals Modulate Glutamatergic System in Human Platelets.

Borges VC, Santos FW, Rocha JB, Nogueira CW.
Departamento de Quimica, Centro de Ciencias Naturais e Exatas, Universidade Federal de Santa Maria, Santa Maria, CEP 97105-900, RS, Brazil, [email protected]

Research strategies have been developed to characterize parameters in peripheral tissues that might easily be measured in humans as surrogate markers of damage, dysfunction or interactions involving neural targets of toxicants. The similarities between platelet and neuron may even be clinically important, as a number of biochemical markers show parallel changes in the central nervous system (CNS) and platelets. The purpose of our research was to investigate the effect of Hg(2+), Pb(2+) and Cd(2+) on the [(3)H]-glutamate binding and [(3)H]-glutamate uptake in human platelets. The involvement of oxidative stress in the modulation of glutamatergic system induced by heavy metals was also investigated. The present study clearly demonstrates that Hg(2+), Cd(2+), and Pb(2+) inhibited [(3)H]-glutamate uptake in human platelets. Hg(2+) inhibited [(3)H]-glutamate binding, while Cd(2+) and Pb(2+) stimulated [(3)H]-glutamate binding in human platelets. Hg(2+), Cd(2+) and Pb(2+) increased lipid peroxidation levels and reactive oxygen species (ROS) measurement in platelets. The present limited results could suggest that glutamatergic system may be used as a potential biomarker for neurotoxic action of heavy metals in humans.

PMID: 17406985

"a potential biomarker for neurotoxic actions of heavy metals in humans" ..... maybe for cows also! (?)

Can't test for BSE.... test for heavy metal intoxication via platelets.

Prions alone cannot cause BSE (TSEs) - the metal nucleating centers are required for the malformed proteins to attach to. The amount of malformed proteins that gather (or surround) the metal PNCs depends on the size of and metal type of the nanocluster centers.
 

flounder

Well-known member
Kathy said:
Prions alone cannot cause BSE (TSEs) - the metal nucleating centers are required for the malformed proteins to attach to. The amount of malformed proteins that gather (or surround) the metal PNCs depends on the size of and metal type of the nanocluster centers.


which is it kathy, OPs or metals, make your mind up. i dont suppose TSE tainted animal feed had anything to do with it ;-)


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


and for Gods sake, if someone is smearing this [email protected] 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


TSS
 

Kathy

Well-known member
Success story: Prion hypothesis challenged by new Sheep study
Despite the fact that the Nobel Prize was awarded for the prion hypothesis, there remains the possibility that the infectious agent behind diseases such as mad cow, scrapie and variant Creutzfeldt-Jakob disease might not necessarily be rogue prion protein. The findings of the SC GUT project, funded for five years via the European Commission’s Fifth Framework Programme, show that there is a need to remain diligent and open minded when investigating the causes of this group of diseases.


© Dr. Arild Espenes ( Norwegian School of Veterinary Science)

Scrapie in sheep is problem through most of the world and is the most widespread TSE in Europe. It is generally considered, but not proven, to be the source of the BSE epidemic and control and eradication of TSE in small ruminants is one of the top priorities in the EU. The SC GUT project, addresses key issues related to the pathogenesis of scrapie and BSE in sheep. By studying the problem of scrapie in sheep, this project helps to provide tools for early detection of TSEs which will be a key to the control of diseases that are a significant threat to human food safety. The confirmation of BSE in a goat in France in January 2005 added greater emphasis to the need for this type of research.

Better knowledge of TSE in sheep

The SC GUT project studies the early pathogenesis of scrapie and of bovine spongiform encephalopathy (BSE) in sheep and mice, using a combination of approaches involving novel experimental methods and includes the experimental oral infection of scrapie-free sheep and access to scrapie-infected flocks of PrP-genotyped sheep. These studies will result in a better understanding of the early pathogenesis of scrapie and BSE and this understanding will, in turn, contribute to the better application of diagnostic methods and control strategies, leading to safer food sources for consumers.

Prion proteins hypothesis in question

The infectious agent behind mad cow, scrapie and variant Creutzfeldt-Jakob disease is generally believed to be rogue prion proteins. Although deformed prions are a characteristic of these diseases however, it is possible that they are not the initial infectious agent. This theory is based on how these proteins are absorbed in the sheep gut. The scientists inoculated sheep intestines with brain extracts containing the abnormal form of the prion protein (PrP) believed to cause the neurodegenerative disease. Surprisingly, the inoculated prion proteins were only detected for a short time (3.5 hours) in the wall of the gut and not in sites where disease generated prion protein accumulated, i.e., prion proteins generated by the disease itself first accumulated one month after inoculation and appeared at sites different from those sites where the inoculated prion protein was seen to be absorbed. In addition, experiments suggest that in the normal animal almost all ingested prions will be digested before it could be absorbed by the gut – supporting the theory that prions do not cause the disease by passing through the gut wall.



Diagram showing relevant anatomical features of distal ileum, and observed routes of transport of inoculum, and a separate, inferred route of transport of infectivity.
Jeffrey, M., Gonzalez, L., Espenes, A., Press, C.M., Martin, S., Chaplin, M., Davis, L., Landsverk, T., MacAldowie, C., Eaton, S. and McGovern, G., Transportation of prion protein across the intestinal mucosa of scrapie-susceptible and scrapie-resistant sheep, Journal of Pathology, 2006, 209 (1): 4-14.
© Pathological Society of Great Britain and Ireland. Permission granted by John Wiley & Sons Ltd on behalf of PathSoc.

New mechanisms of infection

The new discovery does not rule out the possibility that prion proteins, if absorbed in sufficient amounts, might still cause disease, or it may be that prions directly infect nerve endings by some other mechanism. The scientists involved in SC GUT, however, contemplated another intriguing possibility - that the prion hypothesis might not be the correct explanation for TSE infection. Further investigation of the causes of this group of diseases is, therefore, needed.

QLK5-CT-2001-02332, SC-GUT,
STUDIES ON THE ALIMENTARY PATHOGENESIS OF BSE AGENT AND NATURAL SCRAPIE IN SHEEP AND MICE IMPLICATIONS FOR DIAGNOSIS AND CONTROL

PROJECT COORDINATOR
Professor Charles McL. Press
Address:
Norwegian School of Veterinary Science
Box 8146 Dep., 0033 Oslo
Norway
Telephone: (+47) 22597037
Telefax: (+47) 22597086
E-mail address: [email protected]

link: http://ec.europa.eu/research/agriculture/success_prion_en.htm

further, page 18-22 from "Feed Technology Update November 2006"

link: http://www.aquafeed.com/newsletter_pdfs/nl_000237.pdf
"Mad Cow Disease...Results of an E.U. funded sheep study make the case for a re-think on the cause of BSE"
 

Kathy

Well-known member
further, page 18-22 from "Feed Technology Update November 2006"

"Mad Cow Disease...Results of an E.U. funded sheep study make the case for a re-think on the cause of BSE"

link: http://www.aquafeed.com/newsletter_pdfs/nl_000237.pdf

[this was a separate article from the first, and was published last fall. It is falling back on the hypothesis of Mark Purdey. The prion protein is associated with the disease, but not the initiating factor...]
 

flounder

Well-known member
maybe you could tell us why the sudden drop in BSE cases in the U.K. kathy from not feeding them mbm ???


OP'S MEETING WITH PURDEY

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



TSS
 

Kathy

Well-known member
The end of the warble eradication program.

The MBM, in my opinion, contained the heavy metals and OPs.... and it did contribute to the initiation of the disease... not transmission.

The MBM would not likely have had the effect upon the animals, if their mineral status was properly balanced. Unfortunately, the OPs altered that mineral status, as did local environmental mineral/soil conditions.

Children treated with headlice formulas.... what is their immune status, how old are they.... What about treating the pregnant mother with OPs - what effects will that have on a fetus exposed to heavy metals and mineral excesses???

Multifactoral diseases are not simple, and they will take alot of diligence to unravel. The reports want people to keep an open mind - since you never had one on this subject I certainly never expect to see you change or modify your opinion.
 
Top