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China clones BSE resistant calf

Mike

Well-known member
Mad-cow-resistant calf cloned
26/04/2006 11:56 - (SA)


Beijing - Chinese scientists have cloned a calf that may be resistant to mad cow disease, state press reported on Wednesday.

The calf, weighing 55kg, was born on Tuesday in eastern China's Shandong province with genes that are resistant to mad cow disease, Xinhua news agency said, citing a local science institute.

Two scientists from Shandong who cloned China's first two healthy cows in 2001 led the project to produce the mad cow-resistant calf, according to Xinhua.

However the report, which gave few other details, cautioned that further tests were needed to confirm whether the cloning was a success.

Mad cow disease, known also as bovine spongiform encephalopathy, has been connected to the fatal brain-wasting disease in humans called variant Creutzfeldt-Jakob disease.

Mad cow disease decimated Britain's cattle industry in the 1990s, and has also impacted stocks in the United States, Canada and Japan.
 

TimH

Well-known member
See any implications here,Mike??

What if someone does develop a strain of "BSE Resistant" cattle?
What if a company like Monsanto, Dow Chemical or anybody else obtains a patent on these cattle? (It's already happened with grains ,oilseeds and lab mice.)

Then what if the BSE fear mongers make it impossible to sell any cattle that are not of this "Patented BSE Resistant" strain????

You and I will be paying a "licensing fee" to the owner of the patent for every "BSE Resistant" animal that we raise. Or we could just quit the cattle biz.

And all because of fear about a disease that has NO PROVEN LINK TO vCJD.

:cry: :cry: :cry: :cry:
 

Mike

Well-known member
TimH said:
See any implications here,Mike??

What if someone does develop a strain of "BSE Resistant" cattle?
What if a company like Monsanto, Dow Chemical or anybody else obtains a patent on these cattle? (It's already happened with grains ,oilseeds and lab mice.)

Then what if the BSE fear mongers make it impossible to sell any cattle that are not of this "Patented BSE Resistant" strain????

You and I will be paying a "licensing fee" to the owner of the patent for every "BSE Resistant" animal that we raise. Or we could just quit the cattle biz.

And all because of fear about a disease that has NO PROVEN LINK TO vCJD.

:cry: :cry: :cry: :cry:

Like I've been saying all along. The USDA's mistakes have driven the scaremongering press to the dogs.

If a private company had made as many PR mistakes as the USDA has, they would be paying you to own their stock.
 

Kathy

Well-known member
Tim, you have it just right. I have seen patent applications, already, for what are called "prion knock-out" animals (not just cattle). The problem with these animals, is that they aren't OK. They may appear outwardly to be "normal", but they have problems which will cause them to have breeding problems. And, because they have lost the prion protein, they will have problems associated with copper homeostasis and signalling, as well as oxidative stress of the cells/mitochondria. There is recent research which also outlines that the prion protein aids bone-marrow stem cells in becoming whatever new cell they need to be.

If it did come to such a scenario as you have outlined here, there would be alot of people getting out of the cattle business, including me.

Let's do something to stop it from going that far.
 

Big Muddy rancher

Well-known member
Had a discussion like this about even a patented tenderness gene. Could you keep replacements with out paying a royalty? Could a company say they wouldn't buy any cattle that weren't carrying their Gene?
 

Kathy

Well-known member
I'm no patent expert, but, from what I understand you cannot patent something which already exists.

If you mess with genes by "blocking" the genes which code for, say the prion protein, you have created something new and novel. If you insert a gene into a creature which never could have possibly had that gene, say like a fish gene in a tomato, this is also new and novel.

If genes for tenderness already exist within cattle, and you are able to breed your cattle in a manner that maximizes this genes presence, no one can make you pay for something which already existed.

They could not, therefore, patent a tenderness gene in/from cattle, because that gene already exists in cattle around the world and it is not a new and novel idea/product.

This does not mean that down the road, some big company like McDonalds couldn't say that they would pay a premium for cattle which have been identified to have some tenderness gene. But since, genetics only makes for a fraction of meat quality and the manner they are raised, fed and slaughtered also contributes to tenderness, I don't foresee that this selective type of genetic purchasing would necessarily guarantee the end product.

As I have always stated, we all need cattle that survive in our specific environmental conditions best. What works for someone in northern Alberta won't necessarily work well for our area.

Many patent applications are made, but to my knowledge there have been no approved patents which give rights to existing features/qualities.
 

flounder

Well-known member
"BSE Resistant" ?????????


2004 Society for General Microbiology

Neuronal accumulation of abnormal prion protein in sheep carrying a
scrapie-resistant genotype (PrPARR/ARR)
Anne Buschmann1, Gesine Lühken2, Julia Schultz1, G. Erhardt2 and Martin H.
Groschup1

1 Federal Research Centre for Virus Diseases of Animals, Institute for Novel
and Emerging Infectious Diseases, Boddenblick 5a, 17493 Greifswald - Insel
Riems, Germany
2 Department of Animal Breeding and Genetics, Justus-Liebig-University
Gießen, Ludwigstraße 21B, 35390 Gießen, Germany


Correspondence
Martin H. Groschup
[email protected]

The susceptibility of sheep to scrapie infection is influenced by prion gene
alleles, which are modulated by polymorphic variations corresponding to
amino acid positions 136, 154 and 173 of the prion protein (PrP). As no
unquestioned report of a diseased sheep carrying homozygous alleles encoding
alanine, arginine and arginine (PrPARR) at these sites has been published to
date, sheep of this genotype are believed to be scrapie resistant. After the
introduction of large-scale rapid testing for scrapie, a number of so-called
'atypical' scrapie cases have been found in Germany and elsewhere. Among
those cases were two supposedly scrapie-resistant sheep. Brain samples from
these animals tested positive for abnormal PrP (PrPSc) in one of four rapid
tests available. Moreover, scrapie-associated fibril (SAF)-immunoblotting
and immunohistochemistry, which are the generally accepted diagnostic
techniques for scrapie, revealed prominent PrPSc deposition in the
cerebellum. SAF immunoblotting also revealed PrPSc deposition in the obex,
frontal cortex and brainstem. Transmission experiments to investigate the
infectivity of scrapie propagated from these sheep have been initiated.

snip...


Taken together, the findings reported here indicate that
sheep homozygous for the PrPARR allele may not be fully
resistant to natural scrapie infections and may exhibit
diagnostic features that fit the most recently discovered
'atypical' scrapie case definition. 'Atypical' scrapie cases
occur predominantly in sheep carrying a scrapie-resistance
PrP allele in heterozygous or homozygous form. If
transmission studies indeed show that the PrPSc depositions
in these cases are infectious and that such infections are able
to spread from sheep under natural conditions, these
findings would question the large-scale sheep genotyping
and scrapie-resistant breeding programmes that have been
introduced in several EU member states over the last 5 years.


http://vir.sgmjournals.org/cgi/reprint/85/9/2727


TSS
 

flounder

Well-known member
The central molecular event in transmissible spongiform encephalopathies,
such as scrapie in sheep, is the accumulation in tissues of an abnormal
isoform of the cellular prion protein. A previous investigation of 26 sheep
showed that the accumulation of PrPres in brain correlated more with the
prnp genotype than with the severity of the clinical disease. Here, the
ability of a sandwich ELISA to detect PrPres distribution in the brain was
demonstrated. Immunohistochemistry also strongly supported the hypothesis
that the dorsal motor nucleus of the vagus nerve is the possible entry site
in the brain for the scrapie agent. Remarkably, three asymptomatic (or
possibly asymptomatic for scrapie) sheep carrying an allele known to be
associated with clinical scrapie resistance (ARR), which were negative for
the detection of PrPres by Western blotting and immunohistochemistry, were
positive for the presence of PrPres by ELISA, raising the possibility of
carriers resistant to the disease and possibly contributing to the
persistence of scrapie in certain flocks.


snip...

All 12 sheep were diagnosed as negative for the detection
of PrPres by IHC. However, four animals were positive for
the detection of PrPres in the cerebellum by ELISA, and two
were also positive by ELISA for detection of PrPres in the
brain stem and/or mesencephalon (giving a specific signal
2?5 times greater than the cut-off level in three separate
experiments). All positive results were obtained using pure
20% homogenates and negative results were obtained at a
1 : 10 dilution, thus indicating low levels of accumulated
PrPres. Two of these four sheep, including one VRQ/ARR
sheep (S18), had been classified as having possible symptoms
(Madec et al., 2000), including some wool loss and
emaciation but no trembling, hyperexcitability or paresthesias.
However, since marked clinical signs can be associated
with a low amount of brain PrPres (as in sheep S9), it was
reasonable to assume that a less obvious clinical status might
also be associated with a very low level of PrPres accumulation,
possibly only detectable by ELISA. By comparison,
the two animals in which PrPSc was only found in the
DMNV (S9 and S14, see above) by IHC displayed OD values
by ELISA at least 2?5-fold higher than those obtained for the
two IHC-negative sheep with possible symptoms (S18 and
S22). These results suggested that ELISA may have a higher
sensitivity than IHC for the detection of PrPres in these sheep
and under these experimental conditions, whereas Western
blotting and IHC may have a comparable sensitivity, as also
suggested by other studies (Jeffrey et al., 2002).
Interestingly, three of these four asymptomatic (or possibly
Table 1. Detection of PrPres in sheep brain using Western blotting, IHC and
ELISA
Results were classified with regard to the prnp genotypes of the animals and
their clinical status at the time of sacrifice, as defined
previously (Madec et al., 2000). Three different combinations (+/+/+, 2/2/2
and 2/2/+) were observed for the results obtained using
Western blotting, IHC and ELISA, respectively (+, PrPres-positive sheep; 2,
PrPres-negative sheep). Genotypes are given using the singleletter
code for amino acids corresponding to codons 136, 154 and 171 of the prnp
gene, respectively.
Genotype Sheep No. sheep Clinical status
Highly affected Possible symptoms No symptoms
VRQ/VRQ S4, S5 2 +/+/+
VRQ/ARQ S6, S7, S8 3 +/+/+
VRQ/ARQ S12, S13, S14 3 +/+/+
VRQ/ARH S9 1 +/+/+
VRQ/ARH S10, S11 2 +/+/+
ARQ/ARQ S15 1 2/2/2
ARQ/ARH S16 1 2/2/2
ARQ/ARH S17 1 2/2/+
VRQ/ARR S18 1 2/2/+
VRQ/ARR S19 1 2/2/2
ARQ/ARR S20, S21 2 2/2/2
ARH/ARR S22 1 2/2/+
ARH/ARR S23 1 2/2/+
ARH/ARR S24, S25, S26 3 2/2/2
Total 23
3484 Journal of General Virology 85
J.-Y. Madec and others
asymptomatic for scrapie) and ELISA-positive animals
carried the ARR allele (Table 1). The ARR allele is associated
with a protective effect against, if not resistance to, clinical
scrapie. Our results thus raise some concern that PrPSc can
be found not only in preclinical stages of the disease in
susceptible animals, but also in relatively resistant animals.
It is generally considered that ARH/ARR animals are either
not expected to develop scrapie during their life span or
that they will develop the disease only after 70 months
(Andre´oletti et al., 2000; van Keulen et al., 1996). Therefore,
these findings suggest that scrapie-infected sheep with
genetic resistance may behave as healthy carriers or as only
very slightly affected animals in flocks. The possibility of a
carrier state has already been suggested in certain rodent
models (Collis & Kimberlin, 1985; Race & Chesebro, 1998;
Race et al., 2001) and this could help to explain the persistence
of the natural disease in some cases. It may also have
significance for breeding and lambing management programmes
for the eradication of scrapie.
It is not known whether both PrPs encoded by the ARH and
ARR alleles or only the PrP encoded by the most susceptible
alleles (ARH or VRQ) are converted into a pathological form
in these sheep during the natural process of scrapie infection.
It is notable that the sheep PrP encoded by the ARR allele was
successfully converted into its pathological counterpart in
experimental BSE challenge of sheep (Houston et al., 2003).
A recent study also reported that some atypical ELISApositive
sheep remained negative using either Western
blotting or, in some cases, IHC (Buschmann et al., 2003),
and this work also included a number of sheep carrying the
ARR or AHQ allele associated with a relatively high resistance
to clinical scrapie. Similar observations were also made by
another group in sheep with so-called Nor98 scrapie carrying
the AHQ allele, displaying clinical signs of scrapie (Benestad
et al., 2003). The data presented here on asymptomatic
animals with partial genetic resistance to the disease reinforce
the possible association between these alleles and an unusual
biochemical behaviour or low levels of PrPSc, according to
the method used for its identification. Attempts to transmit
the disease to ovine-transgenic mice, which have been shown
to be more susceptible to scrapie than conventional rodents
(Crozet et al., 2001; Vilotte et al., 2001), will help to determine
the potential infectivity of these samples.
Acknowledgements.............
http://vir.sgmjournals.org/cgi/reprint/85/11/3483

TSS


tse resistant anything??? hope so though, but to early to tell if this is for real. ...TSS
 
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