UNITED STATES OF AMERICA VS GALEN J. NIEHUES FAKED MAD COW FEED TEST ON 92 BSE INSPECTION REPORTS FOR APPROXIMATELY 100 CATTLE OPERATIONS
UNITED STATES OF AMERICA VS GALEN J. NIEHUES FAKED MAD COW FEED TEST ON 92 BSE INSPECTION REPORTS FOR APPROXIMATELY 100 CATTLE OPERATIONS
4:10-cr-03119-RGK -CRZ Doc # 1 Filed: 11/16/10 Page 1 of 4 - Page ID #1
FILED
U.S. DISTRICT COURT
DISTRICT OF NEBRASKA
10 NOV 16 PM 4:16
OFFICE OF THE CLERK
IN THE UNITED STATES DISTRICT COURT
FOR THE DISTRICT OF NEBRASKA
UNITED STATES OF AMERICA,
Plaintiff,
vs.
GALEN J. NIEHUES,
Defendant.
INDICTMENT
18 U.S.C. § 1001
18 U.S.C. § 1341
The Grand Jury charges that:
INTRODUCTION
At all times material to this Indictment:
I. The U.S. Food and Drug Administration (FDA) was an agency within the U.S. Department of Health and Human Services, a part of the executive branch of the Government of the United States.
2. The FDA provided $250,000.00 in grant funds annually to the Nebraska Department of Agriculture (NDA) to perform inspections at cattle producing sites within the state to detect and identify the possible existence of Bovine Spongiform Encephalopathy (BSE), also known as "Mad Cow Disease".
3. The FDA published a final regulation designed to prevent the spread ofBSE through animal feed. The rule prohibited use of most mammalian protein, such as meat meal, bone meal, and hydrolyzed hair, in the manufacture of animal feeds given to cows, sheep and goats. The regulation also required process and control systems to ensure that feed for these animals does not contain prohibited mammalian tissue.
4. Defendant Galen J. Niehues was employed by NDA between approximately July 1, 2009 and March 31, 2010. Niehues' job duties included identifying cattle producers, performing on
-1-
4:10-cr-03119-RGK -CRZ Doc # 1 Filed: 11/16/10 Page 2 of 4 - Page ID # 2
site inspections of the farm site and cattle operations, interviewing cattle producers, taking samples of cattle feed and submitting the feed samples for laboratory analysis for the possible presence of BSE contaminants, and completing reports to document his on-site inspections and feed sample collection.
5. Between approximately July 1,2009 and March 31, 2010, Defendant Galen J. Niehues submitted reports he had completed and feed samples to NDA, for approximately 100 cattle operations within Nebraska as well as travel, per diem, lodging and miscellaneous expenses, by delivering-and placing the reports and related documents and forms to post offices in Lexington, Nebraska and Cozad, Nebraska, to be sent or delivered by the postal service to NDA in Lincoln, Nebraska, and knowingly causing the reports, documents and forms to be delivered by mail.
6. During the time of his employment, Defendant Galen J. Niehues was paid a total of $35,409.65 by NDA in salary and benefits.
7. Title 18 USC §IOOI (False Statement) prohibits anyone, in any matter, within the executive branch of the government of the United States, from making or using any false writing or document, knowing the same to contain any materially false, fictitious, or fraudulent statement or entry.
8. Title 18 USC § 1341 (Mail Fraud) prohibits anyone, having devised or intended to devise a scheme or artifice to defraud, or for obtaining money or property by means of materially false pretenses, representations, or promises, for the purpose of executing such scheme or artifice or attempting to do so, from placing in any post office or authorized depository for mail, any written matter or thing to be sent or delivered by the postal service, or knowingly causing any such matter or thing to be delivered by mail.
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COUNT 1 - FALSESTATEMENT
9. Paragraphs 1 - 8 of this Indictment are realleged and incorporated as fully set forth herein.
10. On or about September 10, 2009, in the District of Nebraska, Defendant Galen Niehues, did knowingly and intentionally make, in a matter within the jurisdiction of the U.S. Department of Health and Human Services, a false BSE report, #EIR 3007935397, knowing the same to contain a materially false and fictitious statement in that the information and data contained in the reporthe prepared and submitted to NDA represented he had made contact with and interviewed the cattle owner, inspected the cattle owner's premises, and collected a sample of cattle feed, when in fact, Defendant Niehues, at the time he submitted the report on or about September 10,2009, then and there knew he had not made contact nor interviewed the owner or anyone associated with the cattle operation, nor had he obtained a sample of feed from the cattle operation as he represented in his report.
In violation of Title 18 United States Code §1001
COUNT II - MAIL FRAUD
11. Paragraphs 1 - 8 of this Indictment are realleged and incorporated as fully set forth herein.
12. Between approximately July 1, 2009, and March 31, 20 10, in the District of Nebraska, and elsewhere, Defendant Galen J. Niehues, devised and intended to devise a scheme and artifice to defraud, and to obtain money and property by means of material and false pretenses and representations.
13. It was part of the scheme and artifice to defraud, that in connection with his job duties and responsibilities with NDA, Defendant Galen 1. Niehues completed and submitted
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approximately 92 BSE inspection reports and related documents which he knew contained materially false, fictitious and fraudulent statements. Specifically, the inspection reports were materially false, in that, they represented that the defendant had made contact with and interviewed the cattle owners, inspected the cattle owners' premises, and collected samples of cattle feed, when, in fact, he had not.
14. On or about September 11, 2009, Defendant Galen J. Niehues, as part of his scheme and artifice to defraud, and for the purpose of executing such scheme and artifice, and attempting to do so, placed copies of fabricated BSE reports and related documents in a post office and authorized depository for mail matter, in Cozad, Nebraska, to be sent and delivered by the postal service to NDJ\. in Lincoln, Nebraska, knowing such reports and related documents were to be delivered by mail.
In violation of Title 18 United States Code §1341.
The United States of America requests that trial of this case be held at Lincoln, Nebraska, pursuant to the rules of this Court.
WILLIAM W. MICKLE, II Assistant United States Attorney
FILED U.S. DISTRICT COURT DISTRICT OF NEBRASKA 10 NOV 16 PM 4:17 OFFICE OF THE CLERK
-4-...END...TSS
Wednesday, November 17, 2010
MAD COW TESTING FAKED IN USA BY Nebraska INSPECTOR Senator Mike Johanns STATE
http://madcowtesting.blogspot.com/2010/11/mad-cow-testing-faked-in-usa-by.html
Tuesday, November 02, 2010
IN CONFIDENCE
The information contained herein should not be disseminated further except on the basis of "NEED TO KNOW".
BSE - ATYPICAL LESION DISTRIBUTION (RBSE 92-21367) statutory (obex only) diagnostic criteria CVL 1992
http://bse-atypical.blogspot.com/2010/11/bse-atypical-lesion-distribution-rbse.html
Seven main threats for the future linked to prions
The NeuroPrion network has identified seven main threats for the future linked to prions.
First threat
The TSE road map defining the evolution of European policy for protection against prion diseases is based on a certain numbers of hypotheses some of which may turn out to be erroneous. In particular, a form of BSE (called atypical Bovine Spongiform Encephalopathy), recently identified by systematic testing in aged cattle without clinical signs, may be the origin of classical BSE and thus potentially constitute a reservoir, which may be impossible to eradicate if a sporadic origin is confirmed.
*** Also, a link is suspected between atypical BSE and some apparently sporadic cases of Creutzfeldt-Jakob disease in humans. These atypical BSE cases constitute an unforeseen first threat that could sharply modify the European approach to prion diseases.
Second threat
In small ruminants, a new atypical form of scrapie currently represents up to 50% of detected cases and even involves sheep selected for resistance to classical scrapie. The consequences for animal and human health are still unknown and there may be a potential connection with atypical BSE. These atypical scrapie cases constitute a second threat not envisioned previously which could deeply modify the European approach to prion diseases.
Third threat
The species barrier between human and cattle might be weaker than previously expected and the risk of transmission of prion diseases between different species has been notoriously unpredictable. The emergence of new atypical strains in cattle and sheep together with the spread of chronic wasting disease in cervids renders the understanding of the species barrier critical. This constitutes a third threat not properly envisioned previously that could deeply modify the European approach to prion diseases.
Fourth threat
Prion infectivity has now been detected in blood, urine and milk and this has potential consequences on risk assessments for the environment and food as well as for contamination of surfaces including medical instruments. Furthermore the procedures recommended for decontamination of MBM (Meat and Bone Meal), which are based on older methodologies not designed for this purpose, have turned out to be of very limited efficacy and compromise current policies concerning the reuse of these high value protein supplements (cross-contamination of feed circuits are difficult to control). It should be noted that the destruction or very limited use of MBM is estimated to still cost 1 billion euros per year to the European economy,
whereas other countries, including the US,
Brazil, and Argentine do not have these constraints.
However, many uncertainties remain concerning the guarantees that can be reasonably provided for food and feed safety and scientific knowledge about the causative agents (prions) will continue to evolve. This decontamination and environmental issue is a fourth threat that could modify deeply the European approach to prion diseases.
Fifth threat The precise nature of prions remains elusive. Very recent data indicate that abnormal prion protein (PrPTSE) can be generated from the brains of normal animals, and under some conditions (including contaminated waste water) PrPTSE can be destroyed whereas the BSE infectious titre remains almost unchanged, a finding that underlines the possibility of having BSE without any detectable diagnostic marker. These are just two areas of our incomplete knowledge of the fundamental biology of prions which constitute a fifth threat to the European approach to prion diseases.
Sixth threat The absence of common methods and standardisation in the evaluation of multiple in vivo models with different prion strains and different transgenic mice expressing PrP from different species (different genotypes of cattle, sheep, cervids, etc) renders a complete and comprehensive analysis of all the data generated by the different scientific groups almost impossible. This deeply impairs risk assessment. Moreover, the possibility of generating PrPTSE de novo with new powerful techniques has raised serious questions about their appropriateness for use as blood screening tests. The confusion about an incorrect interpretation of positive results obtained by these methods constitutes a sixth threat to European approach to prion diseases.
Seventh Threat The detection of new or re-emerging prion diseases in animals or humans which could lead to a new crisis in consumer confidence over the relaxation of precautionary measures and surveillance programmes constitutes a seventh threat that could modify the European approach to prion diseases.
http://www.neuroprion.org/en/np-neuroprion.html
Thursday, August 12, 2010
Seven main threats for the future linked to prions
http://prionpathy.blogspot.com/2010/08/seven-main-threats-for-future-linked-to.html
http://prionpathy.blogspot.com/
ALABAMA MAD COW g-h-BSEalabama
In this study, we identified a novel mutation in the bovine prion protein gene (Prnp), called E211K, of a confirmed BSE positive cow from Alabama, United States of America. This mutation is identical to the E200K pathogenic mutation found in humans with a genetic form of CJD. This finding represents the first report of a confirmed case of BSE with a potential pathogenic mutation within the bovine Prnp gene. We hypothesize that the bovine Prnp E211K mutation most likely has caused BSE in "the approximately 10-year-old cow" carrying the E221K mutation.
http://www.plospathogens.org/article/info%3Adoi%2F10.1371%2Fjournal.ppat.1000156
http://www.plospathogens.org/article/fetchObjectAttachment.action?uri=info%3Adoi%2F10.1371%2Fjournal.ppat.1000156&representation=PDF
Saturday, August 14, 2010
BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and VPSPr PRIONPATHY
(see mad cow feed in COMMERCE IN ALABAMA...TSS)
http://prionpathy.blogspot.com/2010/08/bse-case-associated-with-prion-protein.html
Wednesday, July 28, 2010
re-Freedom of Information Act Project Number 3625-32000-086-05, Study of Atypical BSE UPDATE July 28, 2010
http://bse-atypical.blogspot.com/2010/07/re-freedom-of-information-act-project.html
Monday, August 9, 2010
Variably protease-sensitive prionopathy: A new sporadic disease of the prion protein or just more PRIONBALONEY ?
http://prionunitusaupdate2008.blogspot.com/2010/08/variably-protease-sensitive-prionopathy.html
PLEASE SEE the dramatic increase in sporadic CJD cases in documented BSE countries, then think, BSE can propagate as nvCJD and sporadic CJD in the lab ;
TOTAL CASES OF SPORADIC CJD (DEATHS) DEFINITE AND PROBABLE CASES
Australia Austria Canada France Germany Italy Netherlands Slovakia Spain Switzerland UK
http://www.eurocjd.ed.ac.uk/sporadic.htm
USA
5 Includes 16 cases in which the diagnosis is pending, and 18 inconclusive cases;
6 Includes 21 (19 from 2010) cases with type determination pending in which the diagnosis of vCJD has been excluded.
2010
PLEASE NOTE REFERENCE LINES 5. AND 6.
Monday, August 9, 2010
National Prion Disease Pathology Surveillance Center Cases Examined (July 31, 2010) Year Total Referrals2 Prion Disease Sporadic Familial Iatrogenic vCJD
1996 & earlier 51 33 28 5 0 0
1997 114 68 59 9 0 0
1998 88 52 44 7 1 0
1999 120 72 64 8 0 0
2000 146 103 89 14 0 0
2001 209 119 109 10 0 0
2002 248 149 125 22 2 0
2003 274 176 137 39 0 0
2004 325 186 164 21 0 1(3)
2005 344 194 157 36 1 0
2006 383 197 166 29 0 2(4)
2007 377 214 187 27 0 0
2008 394 231 204 25 0 0
2009 425 259 216 43 0 0
2010 204 124 85 20 0 0
TOTAL 3702(5) 2177(6) 1834 315 4 3
1 Listed based on the year of death or, if not available, on year of referral;
2 Cases with suspected prion disease for which brain tissue and/or blood (in familial cases) were submitted;
3 Disease acquired in the United Kingdom;
4 Disease was acquired in the United Kingdom in one case and in Saudi Arabia in the other case;
5 Includes 16 cases in which the diagnosis is pending, and 18 inconclusive cases;
6 Includes 21 (19 from 2010) cases with type determination pending in which the diagnosis of vCJD has been excluded.
http://www.cjdsurveillance.com/pdf/case-table.pdf
Monday, August 9, 2010
National Prion Disease Pathology Surveillance Center Cases Examined (July 31, 2010)
(please watch and listen to the video and the scientist speaking about atypical BSE and sporadic CJD and listen to Professor Aguzzi)
http://prionunitusaupdate2008.blogspot.com/2010/08/national-prion-disease-pathology.html
Atypical BSE in Cattle
BSE has been linked to the human disease variant Creutzfeldt Jakob Disease (vCJD). The known exposure pathways for humans contracting vCJD are through the consumption of beef and beef products contaminated by the BSE agent and through blood transfusions. However, recent scientific evidence suggests that the BSE agent may play a role in the development of other forms of human prion diseases as well. These studies suggest that classical type of BSE may cause type 2 sporadic CJD and that H-type atypical BSE is connected with a familial form of CJD.
To date the OIE/WAHO assumes that the human and animal health standards set out in the BSE chapter for classical BSE (C-Type) applies to all forms of BSE which include the H-type and L-type atypical forms. This assumption is scientifically not completely justified and accumulating evidence suggests that this may in fact not be the case. Molecular characterization and the spatial distribution pattern of histopathologic lesions and immunohistochemistry (IHC) signals are used to identify and characterize atypical BSE. Both the L-type and H-type atypical cases display significant differences in the conformation and spatial accumulation of the disease associated prion protein (PrPSc) in brains of afflicted cattle. Transmission studies in bovine transgenic and wild type mouse models support that the atypical BSE types might be unique strains because they have different incubation times and lesion profiles when compared to C-type BSE. When L-type BSE was inoculated into ovine transgenic mice and Syrian hamster the resulting molecular fingerprint had changed, either in the first or a subsequent passage, from L-type into C-type BSE. In addition, non-human primates are specifically susceptible for atypical BSE as demonstrated by an approximately 50% shortened incubation time for L-type BSE as compared to C-type. Considering the current scientific information available, it cannot be assumed that these different BSE types pose the same human health risks as C-type BSE or that these risks are mitigated by the same protective measures.
snip...see full text ;
http://www.prionetcanada.ca/detail.aspx?menu=5&dt=293380&app=93&cat1=387&tp=20&lk=no&cat2
14th ICID International Scientific Exchange Brochure -
Final Abstract Number: ISE.114
Session: International Scientific Exchange
Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009
T. Singeltary
Bacliff, TX, USA
Background:
An update on atypical BSE and other TSE in North America. Please remember, the typical U.K. c-BSE, the atypical l-BSE (BASE), and h-BSE have all been documented in North America, along with the typical scrapie's, and atypical Nor-98 Scrapie, and to date, 2 different strains of CWD, and also TME. All these TSE in different species have been rendered and fed to food producing animals for humans and animals in North America (TSE in cats and dogs ?), and that the trading of these TSEs via animals and products via the USA and Canada has been immense over the years, decades.
Methods:
12 years independent research of available data
Results:
I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2009. With all the science to date refuting it, to continue to validate this old myth, will only spread this TSE agent through a multitude of potential routes and sources i.e. consumption, medical i.e., surgical, blood, dental, endoscopy, optical, nutritional supplements, cosmetics etc.
Conclusion:
I would like to submit a review of past CJD surveillance in the USA, and the urgent need to make all human TSE in the USA a reportable disease, in every state, of every age group, and to make this mandatory immediately without further delay. The ramifications of not doing so will only allow this agent to spread further in the medical, dental, surgical arena's. Restricting the reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD knows NO age group, TSE knows no boundaries. I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Transmissible Spongiform Encephalopathy is far from an exact science, but there is enough proven science to date that this myth should be put to rest once and for all, and that we move forward with a new classification for human and animal TSE that would properly identify the infected species, the source species, and then the route.
page 114 ;
http://ww2.isid.org/Downloads/14th_ICID_ISE_Abstracts.pdf
The EMBO Journal (2002) 21, 6358 - 6366 doi:10.1093/emboj/cdf653
BSE prions propagate as either variant CJD-like or sporadic CJD-like prion strains in transgenic mice expressing human prion protein
Emmanuel A. Asante1, Jacqueline M. Linehan1, Melanie Desbruslais1, Susan Joiner1, Ian Gowland1, Andrew L. Wood1, Julie Welch1, Andrew F. Hill1, Sarah E. Lloyd1, Jonathan D.F. Wadsworth1 and John Collinge1
1.MRC Prion Unit and Department of Neurodegenerative Disease, Institute of Neurology, University College, Queen Square, London WC1N 3BG, UK Correspondence to:
John Collinge, E-mail: j.collinge@prion.ucl.ac.uk
Received 1 August 2002; Accepted 17 October 2002; Revised 24 September 2002
--------------------------------------------------------------------------------
Abstract
Variant Creutzfeldt–Jakob disease (vCJD) has been recognized to date only in individuals homozygous for methionine at PRNP codon 129. Here we show that transgenic mice expressing human PrP methionine 129, inoculated with either bovine spongiform encephalopathy (BSE) or variant CJD prions, may develop the neuropathological and molecular phenotype of vCJD, consistent with these diseases being caused by the same prion strain. Surprisingly, however, BSE transmission to these transgenic mice, in addition to producing a vCJD-like phenotype, can also result in a distinct molecular phenotype that is indistinguishable from that of sporadic CJD with PrPSc type 2. These data suggest that more than one BSE-derived prion strain might infect humans; it is therefore possible that some patients with a phenotype consistent with sporadic CJD may have a disease arising from BSE exposure.
Keywords:BSE, Creutzfeldt–Jakob disease, prion, transgenic
http://www.nature.com/emboj/journal/v21/n23/abs/7594869a.html
BSE prions propagate as either variant CJD-like or sporadic CJD-like prion strains in transgenic mice expressing human prion protein
Emmanuel A. Asante, Jacqueline M. Linehan, Melanie Desbruslais, Susan Joiner, Ian Gowland, Andrew L. Wood, Julie Welch, Andrew F. Hill, Sarah E. Lloyd, Jonathan D.F. Wadsworth, and John Collinge1 MRC Prion Unit and Department of Neurodegenerative Disease, Institute of Neurology, University College, Queen Square, London WC1N 3BG, UK 1Corresponding author e-mail: j.collinge@prion.ucl.ac.ukReceived August 1, 2002; Revised September 24, 2002; Accepted October 17, 2002.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC136957/?tool=pubmed
TSS
4:10-cr-03119-RGK -CRZ Doc # 1 Filed: 11/16/10 Page 1 of 4 - Page ID #1
FILED
U.S. DISTRICT COURT
DISTRICT OF NEBRASKA
10 NOV 16 PM 4:16
OFFICE OF THE CLERK
IN THE UNITED STATES DISTRICT COURT
FOR THE DISTRICT OF NEBRASKA
UNITED STATES OF AMERICA,
Plaintiff,
vs.
GALEN J. NIEHUES,
Defendant.
INDICTMENT
18 U.S.C. § 1001
18 U.S.C. § 1341
The Grand Jury charges that:
INTRODUCTION
At all times material to this Indictment:
I. The U.S. Food and Drug Administration (FDA) was an agency within the U.S. Department of Health and Human Services, a part of the executive branch of the Government of the United States.
2. The FDA provided $250,000.00 in grant funds annually to the Nebraska Department of Agriculture (NDA) to perform inspections at cattle producing sites within the state to detect and identify the possible existence of Bovine Spongiform Encephalopathy (BSE), also known as "Mad Cow Disease".
3. The FDA published a final regulation designed to prevent the spread ofBSE through animal feed. The rule prohibited use of most mammalian protein, such as meat meal, bone meal, and hydrolyzed hair, in the manufacture of animal feeds given to cows, sheep and goats. The regulation also required process and control systems to ensure that feed for these animals does not contain prohibited mammalian tissue.
4. Defendant Galen J. Niehues was employed by NDA between approximately July 1, 2009 and March 31, 2010. Niehues' job duties included identifying cattle producers, performing on
-1-
4:10-cr-03119-RGK -CRZ Doc # 1 Filed: 11/16/10 Page 2 of 4 - Page ID # 2
site inspections of the farm site and cattle operations, interviewing cattle producers, taking samples of cattle feed and submitting the feed samples for laboratory analysis for the possible presence of BSE contaminants, and completing reports to document his on-site inspections and feed sample collection.
5. Between approximately July 1,2009 and March 31, 2010, Defendant Galen J. Niehues submitted reports he had completed and feed samples to NDA, for approximately 100 cattle operations within Nebraska as well as travel, per diem, lodging and miscellaneous expenses, by delivering-and placing the reports and related documents and forms to post offices in Lexington, Nebraska and Cozad, Nebraska, to be sent or delivered by the postal service to NDA in Lincoln, Nebraska, and knowingly causing the reports, documents and forms to be delivered by mail.
6. During the time of his employment, Defendant Galen J. Niehues was paid a total of $35,409.65 by NDA in salary and benefits.
7. Title 18 USC §IOOI (False Statement) prohibits anyone, in any matter, within the executive branch of the government of the United States, from making or using any false writing or document, knowing the same to contain any materially false, fictitious, or fraudulent statement or entry.
8. Title 18 USC § 1341 (Mail Fraud) prohibits anyone, having devised or intended to devise a scheme or artifice to defraud, or for obtaining money or property by means of materially false pretenses, representations, or promises, for the purpose of executing such scheme or artifice or attempting to do so, from placing in any post office or authorized depository for mail, any written matter or thing to be sent or delivered by the postal service, or knowingly causing any such matter or thing to be delivered by mail.
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COUNT 1 - FALSESTATEMENT
9. Paragraphs 1 - 8 of this Indictment are realleged and incorporated as fully set forth herein.
10. On or about September 10, 2009, in the District of Nebraska, Defendant Galen Niehues, did knowingly and intentionally make, in a matter within the jurisdiction of the U.S. Department of Health and Human Services, a false BSE report, #EIR 3007935397, knowing the same to contain a materially false and fictitious statement in that the information and data contained in the reporthe prepared and submitted to NDA represented he had made contact with and interviewed the cattle owner, inspected the cattle owner's premises, and collected a sample of cattle feed, when in fact, Defendant Niehues, at the time he submitted the report on or about September 10,2009, then and there knew he had not made contact nor interviewed the owner or anyone associated with the cattle operation, nor had he obtained a sample of feed from the cattle operation as he represented in his report.
In violation of Title 18 United States Code §1001
COUNT II - MAIL FRAUD
11. Paragraphs 1 - 8 of this Indictment are realleged and incorporated as fully set forth herein.
12. Between approximately July 1, 2009, and March 31, 20 10, in the District of Nebraska, and elsewhere, Defendant Galen J. Niehues, devised and intended to devise a scheme and artifice to defraud, and to obtain money and property by means of material and false pretenses and representations.
13. It was part of the scheme and artifice to defraud, that in connection with his job duties and responsibilities with NDA, Defendant Galen 1. Niehues completed and submitted
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approximately 92 BSE inspection reports and related documents which he knew contained materially false, fictitious and fraudulent statements. Specifically, the inspection reports were materially false, in that, they represented that the defendant had made contact with and interviewed the cattle owners, inspected the cattle owners' premises, and collected samples of cattle feed, when, in fact, he had not.
14. On or about September 11, 2009, Defendant Galen J. Niehues, as part of his scheme and artifice to defraud, and for the purpose of executing such scheme and artifice, and attempting to do so, placed copies of fabricated BSE reports and related documents in a post office and authorized depository for mail matter, in Cozad, Nebraska, to be sent and delivered by the postal service to NDJ\. in Lincoln, Nebraska, knowing such reports and related documents were to be delivered by mail.
In violation of Title 18 United States Code §1341.
The United States of America requests that trial of this case be held at Lincoln, Nebraska, pursuant to the rules of this Court.
WILLIAM W. MICKLE, II Assistant United States Attorney
FILED U.S. DISTRICT COURT DISTRICT OF NEBRASKA 10 NOV 16 PM 4:17 OFFICE OF THE CLERK
-4-...END...TSS
Wednesday, November 17, 2010
MAD COW TESTING FAKED IN USA BY Nebraska INSPECTOR Senator Mike Johanns STATE
http://madcowtesting.blogspot.com/2010/11/mad-cow-testing-faked-in-usa-by.html
Tuesday, November 02, 2010
IN CONFIDENCE
The information contained herein should not be disseminated further except on the basis of "NEED TO KNOW".
BSE - ATYPICAL LESION DISTRIBUTION (RBSE 92-21367) statutory (obex only) diagnostic criteria CVL 1992
http://bse-atypical.blogspot.com/2010/11/bse-atypical-lesion-distribution-rbse.html
Seven main threats for the future linked to prions
The NeuroPrion network has identified seven main threats for the future linked to prions.
First threat
The TSE road map defining the evolution of European policy for protection against prion diseases is based on a certain numbers of hypotheses some of which may turn out to be erroneous. In particular, a form of BSE (called atypical Bovine Spongiform Encephalopathy), recently identified by systematic testing in aged cattle without clinical signs, may be the origin of classical BSE and thus potentially constitute a reservoir, which may be impossible to eradicate if a sporadic origin is confirmed.
*** Also, a link is suspected between atypical BSE and some apparently sporadic cases of Creutzfeldt-Jakob disease in humans. These atypical BSE cases constitute an unforeseen first threat that could sharply modify the European approach to prion diseases.
Second threat
In small ruminants, a new atypical form of scrapie currently represents up to 50% of detected cases and even involves sheep selected for resistance to classical scrapie. The consequences for animal and human health are still unknown and there may be a potential connection with atypical BSE. These atypical scrapie cases constitute a second threat not envisioned previously which could deeply modify the European approach to prion diseases.
Third threat
The species barrier between human and cattle might be weaker than previously expected and the risk of transmission of prion diseases between different species has been notoriously unpredictable. The emergence of new atypical strains in cattle and sheep together with the spread of chronic wasting disease in cervids renders the understanding of the species barrier critical. This constitutes a third threat not properly envisioned previously that could deeply modify the European approach to prion diseases.
Fourth threat
Prion infectivity has now been detected in blood, urine and milk and this has potential consequences on risk assessments for the environment and food as well as for contamination of surfaces including medical instruments. Furthermore the procedures recommended for decontamination of MBM (Meat and Bone Meal), which are based on older methodologies not designed for this purpose, have turned out to be of very limited efficacy and compromise current policies concerning the reuse of these high value protein supplements (cross-contamination of feed circuits are difficult to control). It should be noted that the destruction or very limited use of MBM is estimated to still cost 1 billion euros per year to the European economy,
whereas other countries, including the US,
Brazil, and Argentine do not have these constraints.
However, many uncertainties remain concerning the guarantees that can be reasonably provided for food and feed safety and scientific knowledge about the causative agents (prions) will continue to evolve. This decontamination and environmental issue is a fourth threat that could modify deeply the European approach to prion diseases.
Fifth threat The precise nature of prions remains elusive. Very recent data indicate that abnormal prion protein (PrPTSE) can be generated from the brains of normal animals, and under some conditions (including contaminated waste water) PrPTSE can be destroyed whereas the BSE infectious titre remains almost unchanged, a finding that underlines the possibility of having BSE without any detectable diagnostic marker. These are just two areas of our incomplete knowledge of the fundamental biology of prions which constitute a fifth threat to the European approach to prion diseases.
Sixth threat The absence of common methods and standardisation in the evaluation of multiple in vivo models with different prion strains and different transgenic mice expressing PrP from different species (different genotypes of cattle, sheep, cervids, etc) renders a complete and comprehensive analysis of all the data generated by the different scientific groups almost impossible. This deeply impairs risk assessment. Moreover, the possibility of generating PrPTSE de novo with new powerful techniques has raised serious questions about their appropriateness for use as blood screening tests. The confusion about an incorrect interpretation of positive results obtained by these methods constitutes a sixth threat to European approach to prion diseases.
Seventh Threat The detection of new or re-emerging prion diseases in animals or humans which could lead to a new crisis in consumer confidence over the relaxation of precautionary measures and surveillance programmes constitutes a seventh threat that could modify the European approach to prion diseases.
http://www.neuroprion.org/en/np-neuroprion.html
Thursday, August 12, 2010
Seven main threats for the future linked to prions
http://prionpathy.blogspot.com/2010/08/seven-main-threats-for-future-linked-to.html
http://prionpathy.blogspot.com/
ALABAMA MAD COW g-h-BSEalabama
In this study, we identified a novel mutation in the bovine prion protein gene (Prnp), called E211K, of a confirmed BSE positive cow from Alabama, United States of America. This mutation is identical to the E200K pathogenic mutation found in humans with a genetic form of CJD. This finding represents the first report of a confirmed case of BSE with a potential pathogenic mutation within the bovine Prnp gene. We hypothesize that the bovine Prnp E211K mutation most likely has caused BSE in "the approximately 10-year-old cow" carrying the E221K mutation.
http://www.plospathogens.org/article/info%3Adoi%2F10.1371%2Fjournal.ppat.1000156
http://www.plospathogens.org/article/fetchObjectAttachment.action?uri=info%3Adoi%2F10.1371%2Fjournal.ppat.1000156&representation=PDF
Saturday, August 14, 2010
BSE Case Associated with Prion Protein Gene Mutation (g-h-BSEalabama) and VPSPr PRIONPATHY
(see mad cow feed in COMMERCE IN ALABAMA...TSS)
http://prionpathy.blogspot.com/2010/08/bse-case-associated-with-prion-protein.html
Wednesday, July 28, 2010
re-Freedom of Information Act Project Number 3625-32000-086-05, Study of Atypical BSE UPDATE July 28, 2010
http://bse-atypical.blogspot.com/2010/07/re-freedom-of-information-act-project.html
Monday, August 9, 2010
Variably protease-sensitive prionopathy: A new sporadic disease of the prion protein or just more PRIONBALONEY ?
http://prionunitusaupdate2008.blogspot.com/2010/08/variably-protease-sensitive-prionopathy.html
PLEASE SEE the dramatic increase in sporadic CJD cases in documented BSE countries, then think, BSE can propagate as nvCJD and sporadic CJD in the lab ;
TOTAL CASES OF SPORADIC CJD (DEATHS) DEFINITE AND PROBABLE CASES
Australia Austria Canada France Germany Italy Netherlands Slovakia Spain Switzerland UK
http://www.eurocjd.ed.ac.uk/sporadic.htm
USA
5 Includes 16 cases in which the diagnosis is pending, and 18 inconclusive cases;
6 Includes 21 (19 from 2010) cases with type determination pending in which the diagnosis of vCJD has been excluded.
2010
PLEASE NOTE REFERENCE LINES 5. AND 6.
Monday, August 9, 2010
National Prion Disease Pathology Surveillance Center Cases Examined (July 31, 2010) Year Total Referrals2 Prion Disease Sporadic Familial Iatrogenic vCJD
1996 & earlier 51 33 28 5 0 0
1997 114 68 59 9 0 0
1998 88 52 44 7 1 0
1999 120 72 64 8 0 0
2000 146 103 89 14 0 0
2001 209 119 109 10 0 0
2002 248 149 125 22 2 0
2003 274 176 137 39 0 0
2004 325 186 164 21 0 1(3)
2005 344 194 157 36 1 0
2006 383 197 166 29 0 2(4)
2007 377 214 187 27 0 0
2008 394 231 204 25 0 0
2009 425 259 216 43 0 0
2010 204 124 85 20 0 0
TOTAL 3702(5) 2177(6) 1834 315 4 3
1 Listed based on the year of death or, if not available, on year of referral;
2 Cases with suspected prion disease for which brain tissue and/or blood (in familial cases) were submitted;
3 Disease acquired in the United Kingdom;
4 Disease was acquired in the United Kingdom in one case and in Saudi Arabia in the other case;
5 Includes 16 cases in which the diagnosis is pending, and 18 inconclusive cases;
6 Includes 21 (19 from 2010) cases with type determination pending in which the diagnosis of vCJD has been excluded.
http://www.cjdsurveillance.com/pdf/case-table.pdf
Monday, August 9, 2010
National Prion Disease Pathology Surveillance Center Cases Examined (July 31, 2010)
(please watch and listen to the video and the scientist speaking about atypical BSE and sporadic CJD and listen to Professor Aguzzi)
http://prionunitusaupdate2008.blogspot.com/2010/08/national-prion-disease-pathology.html
Atypical BSE in Cattle
BSE has been linked to the human disease variant Creutzfeldt Jakob Disease (vCJD). The known exposure pathways for humans contracting vCJD are through the consumption of beef and beef products contaminated by the BSE agent and through blood transfusions. However, recent scientific evidence suggests that the BSE agent may play a role in the development of other forms of human prion diseases as well. These studies suggest that classical type of BSE may cause type 2 sporadic CJD and that H-type atypical BSE is connected with a familial form of CJD.
To date the OIE/WAHO assumes that the human and animal health standards set out in the BSE chapter for classical BSE (C-Type) applies to all forms of BSE which include the H-type and L-type atypical forms. This assumption is scientifically not completely justified and accumulating evidence suggests that this may in fact not be the case. Molecular characterization and the spatial distribution pattern of histopathologic lesions and immunohistochemistry (IHC) signals are used to identify and characterize atypical BSE. Both the L-type and H-type atypical cases display significant differences in the conformation and spatial accumulation of the disease associated prion protein (PrPSc) in brains of afflicted cattle. Transmission studies in bovine transgenic and wild type mouse models support that the atypical BSE types might be unique strains because they have different incubation times and lesion profiles when compared to C-type BSE. When L-type BSE was inoculated into ovine transgenic mice and Syrian hamster the resulting molecular fingerprint had changed, either in the first or a subsequent passage, from L-type into C-type BSE. In addition, non-human primates are specifically susceptible for atypical BSE as demonstrated by an approximately 50% shortened incubation time for L-type BSE as compared to C-type. Considering the current scientific information available, it cannot be assumed that these different BSE types pose the same human health risks as C-type BSE or that these risks are mitigated by the same protective measures.
snip...see full text ;
http://www.prionetcanada.ca/detail.aspx?menu=5&dt=293380&app=93&cat1=387&tp=20&lk=no&cat2
14th ICID International Scientific Exchange Brochure -
Final Abstract Number: ISE.114
Session: International Scientific Exchange
Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America update October 2009
T. Singeltary
Bacliff, TX, USA
Background:
An update on atypical BSE and other TSE in North America. Please remember, the typical U.K. c-BSE, the atypical l-BSE (BASE), and h-BSE have all been documented in North America, along with the typical scrapie's, and atypical Nor-98 Scrapie, and to date, 2 different strains of CWD, and also TME. All these TSE in different species have been rendered and fed to food producing animals for humans and animals in North America (TSE in cats and dogs ?), and that the trading of these TSEs via animals and products via the USA and Canada has been immense over the years, decades.
Methods:
12 years independent research of available data
Results:
I propose that the current diagnostic criteria for human TSEs only enhances and helps the spreading of human TSE from the continued belief of the UKBSEnvCJD only theory in 2009. With all the science to date refuting it, to continue to validate this old myth, will only spread this TSE agent through a multitude of potential routes and sources i.e. consumption, medical i.e., surgical, blood, dental, endoscopy, optical, nutritional supplements, cosmetics etc.
Conclusion:
I would like to submit a review of past CJD surveillance in the USA, and the urgent need to make all human TSE in the USA a reportable disease, in every state, of every age group, and to make this mandatory immediately without further delay. The ramifications of not doing so will only allow this agent to spread further in the medical, dental, surgical arena's. Restricting the reporting of CJD and or any human TSE is NOT scientific. Iatrogenic CJD knows NO age group, TSE knows no boundaries. I propose as with Aguzzi, Asante, Collinge, Caughey, Deslys, Dormont, Gibbs, Gajdusek, Ironside, Manuelidis, Marsh, et al and many more, that the world of TSE Transmissible Spongiform Encephalopathy is far from an exact science, but there is enough proven science to date that this myth should be put to rest once and for all, and that we move forward with a new classification for human and animal TSE that would properly identify the infected species, the source species, and then the route.
page 114 ;
http://ww2.isid.org/Downloads/14th_ICID_ISE_Abstracts.pdf
The EMBO Journal (2002) 21, 6358 - 6366 doi:10.1093/emboj/cdf653
BSE prions propagate as either variant CJD-like or sporadic CJD-like prion strains in transgenic mice expressing human prion protein
Emmanuel A. Asante1, Jacqueline M. Linehan1, Melanie Desbruslais1, Susan Joiner1, Ian Gowland1, Andrew L. Wood1, Julie Welch1, Andrew F. Hill1, Sarah E. Lloyd1, Jonathan D.F. Wadsworth1 and John Collinge1
1.MRC Prion Unit and Department of Neurodegenerative Disease, Institute of Neurology, University College, Queen Square, London WC1N 3BG, UK Correspondence to:
John Collinge, E-mail: j.collinge@prion.ucl.ac.uk
Received 1 August 2002; Accepted 17 October 2002; Revised 24 September 2002
--------------------------------------------------------------------------------
Abstract
Variant Creutzfeldt–Jakob disease (vCJD) has been recognized to date only in individuals homozygous for methionine at PRNP codon 129. Here we show that transgenic mice expressing human PrP methionine 129, inoculated with either bovine spongiform encephalopathy (BSE) or variant CJD prions, may develop the neuropathological and molecular phenotype of vCJD, consistent with these diseases being caused by the same prion strain. Surprisingly, however, BSE transmission to these transgenic mice, in addition to producing a vCJD-like phenotype, can also result in a distinct molecular phenotype that is indistinguishable from that of sporadic CJD with PrPSc type 2. These data suggest that more than one BSE-derived prion strain might infect humans; it is therefore possible that some patients with a phenotype consistent with sporadic CJD may have a disease arising from BSE exposure.
Keywords:BSE, Creutzfeldt–Jakob disease, prion, transgenic
http://www.nature.com/emboj/journal/v21/n23/abs/7594869a.html
BSE prions propagate as either variant CJD-like or sporadic CJD-like prion strains in transgenic mice expressing human prion protein
Emmanuel A. Asante, Jacqueline M. Linehan, Melanie Desbruslais, Susan Joiner, Ian Gowland, Andrew L. Wood, Julie Welch, Andrew F. Hill, Sarah E. Lloyd, Jonathan D.F. Wadsworth, and John Collinge1 MRC Prion Unit and Department of Neurodegenerative Disease, Institute of Neurology, University College, Queen Square, London WC1N 3BG, UK 1Corresponding author e-mail: j.collinge@prion.ucl.ac.ukReceived August 1, 2002; Revised September 24, 2002; Accepted October 17, 2002.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC136957/?tool=pubmed
TSS
posted by Terry S. Singeltary Sr. at
1:13 PM
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