Health knowledge made personal
Join this community!
› Share page:
Go
Search posts:

Who killed my son?: book exposes "biggest health scandal of our times"

Posted Aug 03 2013 12:24pm
Monday, July 29 2013

 

Who killed my son? book exposes "biggest health scandal of our times"

 

Christine Lord's son Andrew was killed by the human form of mad cow disease (vCJD) aged 24 years old.

 

She said: "When he was dying he begged me to find out who did this to him and expose them. Since then I have investigated the BSE scandal and campaigned relentlessly for all victims of human BSE, the thousands that continue to be affected and the millions of us exposed to BSE-infected meat.

 

"My beloved son Andrew need never have died: vCJD should never have existed in humans. Andrew was a rising star in the media. He was handsome, healthy with a bright future. He worked for TalkSPORT, Sky and BBC as a producer/researcher. In March 2007, Andrew produced his last live national radio show and by December he was blind, quadriplegic, unable to move, swallow or recognise his friends.

 

"My five-year investigation has resulted in my book Who Killed my Son? which exposes the UK's biggest political and health scandal of modern times.'"

 

Christine, a freelance journalist, is launching her book at a press conference at NUJ headquarters, Headland House, 308-312 Gray's Inn Road, London WC1X 8DP on Monday 9 September, 11.00-12.30.

 

If you would like to attend, please contact campaigns@nuj.org.uk

 


 

 

 

Monday, October 10, 2011

 

EFSA Journal 2011 The European Response to BSE: A Success Story

 

snip...

 

EFSA and the European Centre for Disease Prevention and Control (ECDC) recently delivered a scientific opinion on any possible epidemiological or molecular association between TSEs in animals and humans (EFSA Panel on Biological Hazards (BIOHAZ) and ECDC, 2011). This opinion confirmed Classical BSE prions as the only TSE agents demonstrated to be zoonotic so far but the possibility that a small proportion of human cases so far classified as "sporadic" CJD are of zoonotic origin could not be excluded. Moreover, transmission experiments to non-human primates suggest that some TSE agents in addition to Classical BSE prions in cattle (namely L-type Atypical BSE, Classical BSE in sheep, transmissible mink encephalopathy (TME) and chronic wasting disease (CWD) agents) might have zoonotic potential.

 

snip...

 


 


 

 see follow-up here about North America BSE Mad Cow TSE prion risk factors, and the ever emerging strains of Transmissible Spongiform Encephalopathy in many species here in the USA, including humans ;

 


 

 

 

Thursday, August 12, 2010

 

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

 

snip...

 


 

 

 

Saturday, June 25, 2011

 

Transmissibility of BSE-L and Cattle-Adapted TME Prion Strain to Cynomolgus Macaque

 

"BSE-L in North America may have existed for decades"

 


 

 

 

Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME.

 

snip...

 

The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle...

 


 

 

 

Monday, September 26, 2011

 

L-BSE BASE prion and atypical sporadic CJD

 


 

 

 

CANADA SEE STEADY INCREASE OF THE SPORADIC CJD’S AND THE VPSPR’S (sporadic CJD’s). ...tss

 

 PLEASE NOTE, type determination pending Creutzfeldt Jakob Disease (tdpCJD) in Canada is also on a steady increase.

 

 please see ;

 

> 3. Final classification of 50 cases from 2009, 2010, 2011 and 2012 is pending.

 

 CJD Deaths Reported by CJDSS1, 1994-20122

 

 As of May 31, 2012

 

 Deaths of Definite and Probable CJD

 

 Year Sporadic Iatrogenic Familial GSS FFI vCJD Total

 

 1994 2 0 0 1 0 0 3

 

 1995 3 0 0 0 0 0 3

 

 1996 13 0 0 0 0 0 13

 

 1997 16 0 1 1 0 0 18

 

 1998 22 1 0 1 0 0 24

 

 1999 26 2 2 1 0 0 31

 

 2000 32 0 0 3 0 0 35

 

 2001 27 0 2 1 0 0 30

 

 2002 31 0 2 2 0 1 36

 

 2003 27 1 1 0 0 0 29

 

 2004 42 0 1 0 0 0 43

 

 2005 42 0 0 2 0 0 44

 

 2006 39 0 1 3 1 0 44

 

 2007 35 0 0 4 0 0 39

 

 2008 48 0 1 0 0 0 49

 

 2009 48 0 3 2 0 0 53

 

 2010 34 0 3 0 0 0 37

 

 2011 37 0 2 1 0 1 41

 

 2012 1 0 0 0 0 0 1

 

 Total 525 4 19 22 1 2 573

 

 1. CJDSS began in 1998

 

 2. Data before 1998 are retrospective and partial, data from 1998 to 2008 are complete, and data for 2009 - 2012 are provisional

 

 3. Final classification of 50 cases from 2009, 2010, 2011 and 2012 is pending.

 

 CJD Deaths Reported by CJDSS1, 1994-20122

 

 

 

 As of May 31, 2012

 


 


 

 SEE DECEMBER 2012 CANADA

 


 

 

 

USA SEE STEADY INCREASE OF THE SPORADIC CJD’S AND THE VPSPR’S (sporadic CJD’s). ...tss

 

 National Prion Disease Pathology Surveillance Center

 

 Cases Examined1

 

 (May 18, 2012)

 

 Year Total Referrals2 Prion Disease Sporadic Familial Iatrogenic vCJD

 

 1996 & earlier 50 32 28 4 0 0

 

 1997 114 68 59 9 0 0

 

 1998 88 52 44 7 1 0

 

 1999 123 74 65 8 1 0

 

 2000 145 103 89 14 0 0

 

 2001 210 120 110 10 0 0

 

 2002 248 149 125 22 2 0

 

 2003 266 168 137 31 0 0

 

 2004 326 187 164 22 0 13

 

 2005 344 194 157 36 1 0

 

 2006 382 196 166 28 0 24

 

 2007 377 213 185 28 0 0

 

 2008 396 232 206 26 0 0

 

 2009 423 256 212 43 1 0

 

 2010 413 257 216 41 0 0

 

 2011 410 257 213 43 0 0

 

 2012 153 82 51 15 0 0

 

 TOTAL 44685 26406 2227 387 6 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 14 cases in which the diagnosis is pending, and 18 inconclusive cases;

 

 6 Includes 17 (16 from 2012) cases with type determination pending in which the diagnosis of vCJD has been excluded. The Sporadic cases include 16 cases of sporadic Fatal Insomnia (sFI) and 42 cases of Variably Protease-Sensitive Prionopathy (VPSPr) and 2118 cases of sporadic Creutzfeldt-Jakob disease (sCJD).

 

 Rev 5/18/2012

 

 

 


 

 

 

 

 

 > 6 Includes

 

 > 17 (16 from 2012) cases with type determination pending in which the diagnosis of vCJD has been excluded.

 

 > The Sporadic cases include 16 cases of sporadic Fatal Insomnia (sFI) and 42 cases of Variably Protease-Sensitive Prionopathy (VPSPr) and 2118 cases of sporadic Creutzfeldt-Jakob disease (sCJD).

 

 

 

 WELL, it seems the USA mad cow strains in humans classified as type determination pending tdpCJD, VPSPr, sFFI, and sCJD) have steadily increased over the years, and the same old song and dance continues with sporadic CJD cases $$$

 


 

 

 

Thursday, April 4, 2013

 

 Variably protease-sensitive prionopathy in the UK: a retrospective review 1991–2008

 

 Brain (2013) 136 (4): 1102-1115. doi: 10.1093/brain/aws366

 


 

 

 

*** The discovery of previously unrecognized prion diseases in both humans and animals (i.e., Nor98 in small ruminants) demonstrates that the range of prion diseases might be wider than expected and raises crucial questions about the epidemiology and strain properties of these new forms. We are investigating this latter issue by molecular and biological comparison of VPSPr, GSS and Nor98.

 

VARIABLY PROTEASE-SENSITVE PRIONOPATHY IS TRANSMISSIBLE ...price of prion poker goes up again $

 

OR-10: Variably protease-sensitive prionopathy is transmissible in bank voles

 

Romolo Nonno,1 Michele Di Bari,1 Laura Pirisinu,1 Claudia D’Agostino,1 Stefano Marcon,1 Geraldina Riccardi,1 Gabriele Vaccari,1 Piero Parchi,2 Wenquan Zou,3 Pierluigi Gambetti,3 Umberto Agrimi1 1Istituto Superiore di Sanità; Rome, Italy; 2Dipartimento di Scienze Neurologiche, Università di Bologna; Bologna, Italy; 3Case Western Reserve University; Cleveland, OH USA

 

Background. Variably protease-sensitive prionopathy (VPSPr) is a recently described “sporadic”neurodegenerative disease involving prion protein aggregation, which has clinical similarities with non-Alzheimer dementias, such as fronto-temporal dementia. Currently, 30 cases of VPSPr have been reported in Europe and USA, of which 19 cases were homozygous for valine at codon 129 of the prion protein (VV), 8 were MV and 3 were MM. A distinctive feature of VPSPr is the electrophoretic pattern of PrPSc after digestion with proteinase K (PK). After PK-treatment, PrP from VPSPr forms a ladder-like electrophoretic pattern similar to that described in GSS cases. The clinical and pathological features of VPSPr raised the question of the correct classification of VPSPr among prion diseases or other forms of neurodegenerative disorders. Here we report preliminary data on the transmissibility and pathological features of VPSPr cases in bank voles.

 

Materials and Methods. Seven VPSPr cases were inoculated in two genetic lines of bank voles, carrying either methionine or isoleucine at codon 109 of the prion protein (named BvM109 and BvI109, respectively). Among the VPSPr cases selected, 2 were VV at PrP codon 129, 3 were MV and 2 were MM. Clinical diagnosis in voles was confirmed by brain pathological assessment and western blot for PK-resistant PrPSc (PrPres) with mAbs SAF32, SAF84, 12B2 and 9A2.

 

Results. To date, 2 VPSPr cases (1 MV and 1 MM) gave positive transmission in BvM109. Overall, 3 voles were positive with survival time between 290 and 588 d post inoculation (d.p.i.). All positive voles accumulated PrPres in the form of the typical PrP27–30, which was indistinguishable to that previously observed in BvM109 inoculated with sCJDMM1 cases.

 

In BvI109, 3 VPSPr cases (2 VV and 1 MM) showed positive transmission until now. Overall, 5 voles were positive with survival time between 281 and 596 d.p.i.. In contrast to what observed in BvM109, all BvI109 showed a GSS-like PrPSc electrophoretic pattern, characterized by low molecular weight PrPres. These PrPres fragments were positive with mAb 9A2 and 12B2, while being negative with SAF32 and SAF84, suggesting that they are cleaved at both the C-terminus and the N-terminus. Second passages are in progress from these first successful transmissions.

 

Conclusions. Preliminary results from transmission studies in bank voles strongly support the notion that VPSPr is a transmissible prion disease. Interestingly, VPSPr undergoes divergent evolution in the two genetic lines of voles, with sCJD-like features in BvM109 and GSS-like properties in BvI109.

 

The discovery of previously unrecognized prion diseases in both humans and animals (i.e., Nor98 in small ruminants) demonstrates that the range of prion diseases might be wider than expected and raises crucial questions about the epidemiology and strain properties of these new forms. We are investigating this latter issue by molecular and biological comparison of VPSPr, GSS and Nor98.

 


 

 Monday, January 14, 2013

 

Gambetti et al USA Prion Unit change another highly suspect USA mad cow victim to another fake name i.e. sporadic FFI at age 16 CJD Foundation goes along with this BSe

 


 

 Monday, December 31, 2012

 

Creutzfeldt Jakob Disease and Human TSE Prion Disease in Washington State, 2006–2011-2012

 


 

 Saturday, December 29, 2012

 

MAD COW USA HUMAN TSE PRION DISEASE DECEMBER 29 2012 CJD CASE LAB REPORT

 


 

 Saturday, July 6, 2013

 

Small Ruminant Nor98 Prions Share Biochemical Features with Human Gerstmann-Sträussler-Scheinker Disease and Variably Protease-Sensitive Prionopathy

 

Research Article

 


 

 Sunday, July 21, 2013

 

As Chronic Wasting Disease CWD rises in deer herd, what about risk for humans?

 


 

 Tuesday, June 26, 2012

 

Creutzfeldt Jakob Disease Human TSE report update North America, Canada, Mexico, and USDA PRION UNIT as of May 18, 2012

 

type determination pending Creutzfeldt Jakob Disease (tdpCJD), is on the rise in Canada and the USA

 


 

 Saturday, March 5, 2011

 

MAD COW ATYPICAL CJD PRION TSE CASES WITH CLASSIFICATIONS PENDING ON THE RISE IN NORTH AMERICA

 


 

 Sunday, February 12, 2012

 

National Prion Disease Pathology Surveillance Center Cases Examined1 (August 19, 2011) including Texas

 


 

 Monday, August 9, 2010

 

Variably protease-sensitive prionopathy: A new sporadic disease of the prion protein or just more Prionbaloney ?

 


 

 Wednesday, March 28, 2012

 

VARIABLY PROTEASE-SENSITVE PRIONOPATHY IS TRANSMISSIBLE ...price of prion poker goes up again $

 

OR-10 15:25 - 15:40 VARIABLY PROTEASE-SENSITIVE PRIONOPATHY IS TRANSMISSIBLE IN BANK VOLES Nonno

 


 

 Sunday, August 09, 2009

 

CJD...Straight talk with...James Ironside...and...Terry Singeltary... 2009

 


 

 Tuesday, August 18, 2009

 

BSE-The Untold Story - joe gibbs and singeltary 1999 – 2009

 


 

 

 

 TSS
Post a comment
Write a comment: