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I wonder . . .

burnt

Well-known member
. . .whatever became of the BSE test?

And Shaft?

And TimH?

And Rainie?

And Angus Bull?

http://www.ranchers.net/forum/viewtopic.php?t=24320&postdays=0&postorder=asc&start=0
 

per

Well-known member
I wonder who wrote the book of love. :shock: I know you like music, not really trying to hijack your wonderment. Read something about an approved urine test the other day. I will try to find it. These guys will all show back up eventually.
 

burnt

Well-known member
Some of the best ones don't come back. It's like they said "bye, bye, Miss American Pie . . ." :wink:

Shaft was a truly brilliant mind who seemed to be there to serve the people and the truth rather than himself.

A true voice of reason.
 

flounder

Well-known member
burnt said:
. . .whatever became of the BSE test?

And Shaft?

And TimH?

And Rainie?

And Angus Bull?

http://www.ranchers.net/forum/viewtopic.php?t=24320&postdays=0&postorder=asc&start=0




The identification of disease-induced biomarkers in the urine of BSE infected cattle Sharon LR Simon1 , Lise Lamoureux1 , Margot Plews1 , Michael Stobart1,2 , Jillian LeMaistre3 , Ute Ziegler4 , Catherine Graham5 , Stefanie Czub5 , Martin Groschup4 and J David Knox1,2

1Prion Diseases Program, Public Health Agency of Canada, Winnipeg, R3E 3P6, Canada

2Department of Medical Microbiology, University of Manitoba, Winnipeg, R3E 0W3, Canada

3Department of Pharmacology, University of Manitoba, Winnipeg, R2H 2A6, Canada

4Institute for Novel and Emerging Infectious Diseases at the Friedrich-Loeffler Institut, 17493 Greifswald-Insel Riems, Germany

5Animal Diseases Research Institute, Canadian Food Inspection Agency, Lethbridge, T1J 3Z4, Canada

author email corresponding author email

Proteome Science 2008, 6:23doi:10.1186/1477-5956-6-23

The electronic version of this article is the complete one and can be found online at: http://www.proteomesci.com/content/6/1/23

Received: 9 May 2008 Accepted: 5 September 2008 Published: 5 September 2008

© 2008 Simon et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract Background The bovine spongiform encephalopathy (BSE) epidemic and the emergence of a new human variant of Creutzfeldt-Jakob Disease (vCJD) have led to profound changes in the production and trade of agricultural goods. The rapid tests currently approved for BSE monitoring in slaughtered cattle are all based on the detection of the disease related isoform of the prion protein, PrPd, in brain tissue and consequently are only suitable for post-mortem diagnosis. Objectives: In instances such as assessing the health of breeding stock for export purposes where post-mortem testing is not an option, there is a demand for an ante-mortem test based on a matrix or body fluid that would permit easy access and repeated sampling. Urine and urine based analyses would meet these requirements.

Results Two dimensional differential gel eletrophoresis (2D-DIGE) and mass spectrometry analyses were used to identify proteins exhibiting differential abundance in the urine of BSE infected cattle and age matched controls over the course of the disease. Multivariate analyses of protein expression data identified a single protein able to discriminate, with 100% accuracy, control from infected samples. In addition, a subset of proteins were able to predict with 85% ± 13.2 accuracy the time post infection that the samples were collected.

Conclusion These results suggest that in principle it is possible to identify biomarkers in urine useful in the diagnosis, prognosis and monitoring of disease progression of transmissible spongiform encephalopathy diseases (TSEs).

http://www.proteomesci.com/content/6/1/23



Nucleic Acids Research, 2009, Vol. 37, No. 2 550-556 © 2008 The Author(s) This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited.

--------------------------------------------------------------------------------

Molecular Biology

Disease-specific motifs can be identified in circulating nucleic acids from live elk and cattle infected with transmissible spongiform encephalopathies

Paul M. K. Gordon1, Ekkehard Schütz2,3, Julia Beck2, Howard B. Urnovitz2, Catherine Graham4, Renee Clark4, Sandor Dudas4, Stefanie Czub4, Maria Sensen1, Bertram Brenig3, Martin H. Groschup5, Robert B. Church6 and Christoph W. Sensen1,*

1Department of Biochemistry and Molecular Biology, Faculty of Medicine, Sun Center of Excellence for Visual Genomics, University of Calgary, Calgary, AB, Canada T2N 4N1, 2Chronix Biomedical GmbH, Goethealle 8, D-37073 Göttingen, 3Institute of Veterinary Medicine, Georg-August-Universität, Burckhardtweg 2, D-37077 Göttingen, Germany, 4Canadian Food Inspection Agency, Animal Diseases Research Institute, National and OIE BSE Reference Laboratories, Lethbridge, AB, Canada T1J 3Z4, 5Institute for Novel and Emerging Infectious Diseases at the Friedrich-Loeffler-Institut, Federal Research Institute for Animal Health, Südufer 10, D-17439 Greifswald—Insel Riems, Germany and 6Faculty of Medicine, University of Calgary, Calgary, AB, Canada T2N 4N1

*To whom correspondence should be addressed. Tel: +1 403 220 4301; Fax: +1 403 210 9538; Email: [email protected]

Received August 19, 2008. Revised November 11, 2008. Accepted November 12, 2008.

To gain insight into the disease progression of transmissible spongiform encephalopathies (TSE), we searched for disease-specific patterns in circulating nucleic acids (CNA) in elk and cattle. In a 25-month time-course experiment, CNAs were isolated from blood samples of 24 elk (Cervus elaphus) orally challenged with chronic wasting disease (CWD) infectious material. In a separate experiment, blood-sample CNAs from 29 experimental cattle (Bos taurus) 40 months post-inoculation with clinical bovine spongiform encephalopathy (BSE) were analyzed according to the same protocol. Next-generation sequencing provided broad elucidation of sample CNAs: we detected infection-specific sequences as early as 11 months in elk (i.e. at least 3 months before the appearance of the first clinical signs) and we established CNA patterns related to BSE in cattle at least 4 months prior to clinical signs. In elk, a progression of CNA sequence patterns was found to precede and correlate with macro-observable disease progression, including delayed CWD progression in elk with PrP genotype LM. Some of the patterns identified contain transcription-factor-binding sites linked to endogenous retroviral integration. These patterns suggest that retroviruses may be connected to the manifestation of TSEs. Our results may become useful for the early diagnosis of TSE in live elk and cattle.

SNIP...

DISCUSSION

EVI1 is a common site for retroviral integration in mammalian genomes, where viral integration can promote protein expression of EVI1 (18). The EVI1 protein has been shown to act as a transcriptional promoter for a small number of genes, protecting the binding sites from DNAse I digestion (19). The transcription factor's protective effect (20) may explain the occurrence of motif A in the blood CNAs, especially if EVI1 is being expressed beyond what is normally required for its limited functions in adults (21). One of the genes promoted by EVI1 is the transcription factor PLZF, whose target is found in motif B, thus the function of motifs A and B can be directly linked.

EVI1 expression has thus far not been linked to TSE processes in the literature, but single-stranded RNA retroviruses that preferentially integrate into EVI1 have been. Endogenous murine leukemia virus, which is known to re-integrate into EVI1, has been shown in vivo to replicate upon introduction of scrapie (22). Conversely, Moloney murine leukemia virus infection has been shown in vitro to strongly enhance scrapie infectivity (23). Instances of Moloney-like DNA sequences are also found throughout the latest version of the bovine genome assembly (13 September 2007), with 26 genome regions having a BLAST e-value <10–100. Retroviruses may therefore act as cofactors for TSE pathogenesis (24,25). Retrovirus-induced activation of EVI1 during the course of CWD infection could provide a biological basis for the pair of motifs that we detected in elk. These results are also well aligned with our previous findings of human endogenous retroviral associations with progressive neurologic diseases (26).

Growing evidence [e.g. (27,28)] shows that PrPres alone has dramatically lower infectivity than TSE agent particles. A link between general retroviral activity and TSEs was first proposed almost twenty years ago (29). While such a link is speculative, two types of data specifically support an endogenous retroviral cofactor theory. First, the prion agent is released into cell culture in association with exosome-like structures and viral particles of endogenous origin (8). Second, a growing body of literature suggests an antiretroviral role for the PrP protein (30–32). More specifically, recent results (32) show that PrP is highly up-regulated in response to increased activity of murine endogenous retroviruses. The mRNA level of PrP also increases after scrapie agent inoculation in lymphoid tissue (33). If PrPcwd-prompted lymphoid retroviral activity is responsible for EVI1 detection in CNAs, this could explain its early detectability: lymphoid tissues accumulate PrPcwd before the central nervous system (34).

The nucleic-acid-binding properties of PrP (35), and the presence of PrPcwd in cervid blood (36) mean that alternative explanations for the presence of the motifs are possible. Retroviral RNA may play a role in the transformation of PrPc to PrPd (37), or may conversely reduce PrPc availability (38). While an aptamer role is possible, a Smith–Waterman search of both the motifs and common C-type retroviruses against 87 prion-targeting nucleic-acid aptamers found in the literature and patents does not yield any matches. The possibility remains that the motif sequences may bind PrP in a non-sequence-specific manner (39). A simple present/absent criteria was used for unbiased motif discovery in a randomly sequenced CNA dataset: these motifs will inform our targeted characterization and quantification of disease-specific CNAs and any associated complexes going forward.

The biological mechanism by which the CNAs originate still remains uncertain, but our data support the idea that it is possible to detect host reaction to the CWD and BSE infectious agents via CNAs in live animals, and importantly, before clinical signs appear. Further studies will help to validate the specificity of patterns for TSEs versus brain trauma and other neurological diseases, as well as the consistency of the patterns in naturally occurring CWD and BSE cases. The information from the elk study demonstrates that a time course analysis of the blood CNAs can greatly improve our ability to determine the diagnostic signals present in slowly developing, poorly understood diseases such as TSEs. We consider that the patterns described here provide a starting point for the development of a relatively simple, cost-effective live animal test. For instance, in the future PCR-based tests, pooled samples could be used on a large scale to eliminate infected animals from the human food chain, even before the onset of clinical signs. In this context, it is also interesting that we were able to identify a combination of patterns in elk, which was only found in control animals and animals up to 5 months after infection, and patterns in cattle that were only present in the controls (when compared to animals 40 months after infection). Adding these patterns to the eventual screening strategy could certainly enhance the accuracy of a live animal testing system.

http://nar.oxfordjournals.org/cgi/content/abstract/37/2/550?maxtoshow=&HITS=10&hits=10&RESULTFORMAT=1&andorexacttitle=and&andorexacttitleabs=and&fulltext=BSE%2C+PRION&andorexactfulltext=and&searchid=1&FIRSTINDEX=0&sortspec=relevance&fdate=1/1/2009&resourcetype=HWCIT


Monday, May 4, 2009 Back to the Past With New TSE Testing Agricultural Research/May-June 2009

http://madcowtesting.blogspot.com/2009/05/back-to-past-with-new-tse-testing.html



Wednesday, August 19, 2009

CFIA Enhances Animal Disease Reporting


http://madcowtesting.blogspot.com/



FDA Strengthens BSE Safeguards Animal Feed


http://madcowfeed.blogspot.com/



bottom line, a test is only the beginning. certifying and then using that test in enough numbers to find a case, the integrity and honesty to do something about it when you find these cases, i.e. reporting it, testing and disposal in a timely matter, NOT 7 + months, NOT 4 + months, NOT NTAA i.e. No Test At All policy, NOT the SSS policy of the USDA et al. until USDA et al decide that the SSS policy is a flawed policy, a test is meaningless. ...



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