Thursday, December 1, 2016

PRION2017 DECIPHERING NEURODEGENERATIVE DISORDERS 23 – 26 May 2017 Edinburgh

-----Original Message-----

From: Terry Singeltary <flounder9@verizon.net>

To: prion2017 <>

Cc: amanda.nevitt <>

Sent: Thu, Dec 1, 2016 3:47 pm

Subject: PRION2017 DECIPHERING NEURODEGENERATIVE DISORDERS 23 – 26 May 2017 Edinburgh

Greetings PRION2017 et al,

about the upcoming PRION2017 conference ;


PRION2017 DECIPHERING NEURODEGENERATIVE DISORDERS 23 – 26 May 2017 Edinburgh
 
 
 
Please use the programme below to view each day of the conference. Please note that this is the provisional programme and may be subject to change. For a short biography on each speaker, please click on the speaker’s name.
 
Tuesday 23rd May Wednesday 24th May Thursday 25th May Friday 26th May
 
14:00 Introduction to meeting Professor Sheila Rowan Chief Scientific Advisor, CSO University of Glasgow United Kingdom
 
14:15 Future Public Health challenges in Prion Disease Professor Bob Will National CJD Research& Surveillance Unit, University of Edinburgh United Kingdom
 
14:45 Future scientific challenges in prion disease Professor Bruce Chesebro Rocky Mountain Laboratories, National Institutes of Health, USA United States of America
 
15:15 Coffee-Tea
 
15:45 Post-Doc Formun – 10 short presentations
 
17:45 Welcome Reception
 
 

Sponsorship


This is a fantastic opportunity to network with around 400 professionals from a variety of specialities that include businesses, academics, governments, science institutes and NGOs. Those who have exhibited at previous conferences have commented on the relaxed and collaborative relationship between professionals and industry. This unique environment brings together leading researchers and innovators to kick-start the next wave of ideas and innovation in this field. PRION 2017 will have delegates from over 30 countries and is a unique opportunity to expand contacts and potentially develop new markets. Promote your organisation before, during and after the event through our range of digital and print media channels and partnership packages.
 
Partnership with PRION 2017 will be a key step for your company in fostering partnerships with the International PRION community. This opportunity allows your company, product and brand to be uniquely and actively showcased at this high calibre, innovation driven conference. It will also allow your company to meet new business partners, generate new ideas, gather new knowledge, and foster collaborations. Our all-encompassing themes provides the content for a vast array of industry participation and there is the opportunity to align your core value with those themes outlined. We invite you to be part of PRION 2017 so you can effectively connect with decision makers within your target market.
 
 

Delegates


We expect to welcome more than 400 academics, strategists, innovators, policy makers and researchers from public and private sector across the national and international field of Prion research. We will bring together the people who will deliver action on the ground – from business, industry, NGOs, local government and communities – to share knowledge, ideas and experience with researchers and policymakers.
 
WHO WILL ATTEND?
  • Researchers and educators from leading academic institutions around the world
  • Clinicians and professionals from health and social care
  • Regional, national and international policy makers in health
  • Industry experts from UK, EU and global companies, from SMEs to multinationals
  • Thought leaders and decision makers in healthcare, third sector, governments, and industry; Data scientists and solution developers from public and private sectors
  • Information governance, best practice & regulatory experts
  • The next generation: PhD students; early career researchers and rising stars in industry
 
 
 
Greetings PRION2017 et al,
 
I can't wait for next years PRION Conference from Edinburgh, and the TSE Prion science. Looking forward to reading the abstracts full of TSE Prion science and the latest there from. I hope it is freely accessible to the lay public. This is very important as to help stop this disease, to educate the lay public about this deadly disease, the TSE Prion. Thank you all kindly for your continued work to find cause and cure for the TSE Prion disease, and decipher the science amongst and between them all. ...Good Luck!
 
kindest regards, terry
 
 

Thursday, December 1, 2016

 

The European Union summary report on data of the surveillance of ruminants for the presence of transmissible spongiform encephalopathies (TSEs) in 2015

 
 
Saturday, July 23, 2016

BOVINE SPONGIFORM ENCEPHALOPATHY BSE TSE PRION SURVEILLANCE, TESTING, AND SRM REMOVAL UNITED STATE OF AMERICA UPDATE JULY 2016

http://bovineprp.blogspot.com/2016/07/bovine-spongiform-encephalopathy-bse.html

Tuesday, July 26, 2016

Atypical Bovine Spongiform Encephalopathy BSE TSE Prion UPDATE JULY 2016

http://bse-atypical.blogspot.com/2016/07/atypical-bovine-spongiform.html
 
 
Tuesday, November 29, 2016
 
Transmissibility of Gerstmann–Sträussler–Scheinker syndrome in rodent models: new insights into the molecular underpinnings of prion infectivity
 
 
Self-Propagative Replication of Ab Oligomers Suggests Potential Transmissibility in Alzheimer Disease

*** Singeltary comment PLoS ***

Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic,
what if ?

Posted by flounder on 05 Nov 2014 at 21:27 GMT

http://www.plosone.org/annotation/listThread.action?root=82860

Sunday, November 22, 2015

*** Effect of heating on the stability of amyloid A (AA) fibrils and the intra- and cross-species transmission of AA amyloidosis Abstract

Amyloid A (AA) amyloidosis is a protein misfolding disease characterized by extracellular deposition of AA fibrils. AA fibrils are found in several tissues from food animals with AA amyloidosis. For hygienic purposes, heating is widely used to inactivate microbes in food, but it is uncertain whether heating is sufficient to inactivate AA fibrils and prevent intra- or cross-species transmission. We examined the effect of heating (at 60 °C or 100 °C) and autoclaving (at 121 °C or 135 °C) on murine and bovine AA fibrils using Western blot analysis, transmission electron microscopy (TEM), and mouse model transmission experiments. TEM revealed that a mixture of AA fibrils and amorphous aggregates appeared after heating at 100 °C, whereas autoclaving at 135 °C produced large amorphous aggregates. AA fibrils retained antigen specificity in Western blot analysis when heated at 100 °C or autoclaved at 121 °C, but not when autoclaved at 135 °C. Transmissible pathogenicity of murine and bovine AA fibrils subjected to heating (at 60 °C or 100 °C) was significantly stimulated and resulted in amyloid deposition in mice. Autoclaving of murine AA fibrils at 121 °C or 135 °C significantly decreased amyloid deposition. Moreover, amyloid deposition in mice injected with murine AA fibrils was more severe than that in mice injected with bovine AA fibrils. Bovine AA fibrils autoclaved at 121 °C or 135 °C did not induce amyloid deposition in mice. These results suggest that AA fibrils are relatively heat stable and that similar to prions, autoclaving at 135 °C is required to destroy the pathogenicity of AA fibrils. These findings may contribute to the prevention of AA fibril transmission through food materials to different animals and especially to humans.

Purchase options Price * Issue Purchase USD 511.00 Article Purchase USD 54.00

http://www.tandfonline.com/doi/abs/10.3109/13506129.2015.1095735?journalCode=iamy20

http://betaamyloidcjd.blogspot.com/2015/11/effect-of-heating-on-stability-of.html
 
SWISS MEDICAL WEEKLY

Alzheimer-type brain pathology may be transmitted by grafts of dura mater 26/01/2016 Singeltary comment ;

http://blog.smw.ch/alzheimer-type-brain-pathology-may-be-transmitted-by-grafts-of-dura-mater/#comment-89016

re-Evidence for human transmission of amyloid-β pathology and cerebral amyloid angiopathy

Nature 525, 247?250 (10 September 2015) doi:10.1038/nature15369 Received 26 April 2015 Accepted 14 August 2015 Published online 09 September 2015 Updated online 11 September 2015 Erratum (October, 2015)

snip...see full Singeltary Nature comment here;

http://www.nature.com/nature/journal/v525/n7568/full/nature15369.html#/comments
 
Diagnosis and Reporting of Creutzfeldt-Jakob Disease

Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14, 2001 JAMA

Diagnosis and Reporting of Creutzfeldt-Jakob Disease

To the Editor: In their Research Letter, Dr Gibbons and colleagues1 reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD) has been stable since 1985. These estimates, however, are based only on reported cases, and do not include misdiagnosed or preclinical cases. It seems to me that misdiagnosis alone would drastically change these figures. An unknown number of persons with a diagnosis of Alzheimer disease in fact may have CJD, although only a small number of these patients receive the postmortem examination necessary to make this diagnosis. Furthermore, only a few states have made CJD reportable. Human and animal transmissible spongiform encephalopathies should be reportable nationwide and internationally.

Terry S. Singeltary, Sr Bacliff, Tex

1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323.

http://jama.jamanetwork.com/article.aspx?articleid=1031186

26 March 2003

Terry S. Singeltary, retired (medically) CJD WATCH

I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to comment on the CDC's attempts to monitor the occurrence of emerging forms of CJD. Asante, Collinge et al [1] have reported that BSE transmission to the 129-methionine genotype can lead to an alternate phenotype that is indistinguishable from type 2 PrPSc, the commonest sporadic CJD. However, CJD and all human TSEs are not reportable nationally. CJD and all human TSEs must be made reportable in every state and internationally. I hope that the CDC does not continue to expect us to still believe that the 85%+ of all CJD cases which are sporadic are all spontaneous, without route/source. We have many TSEs in the USA in both animal and man. CWD in deer/elk is spreading rapidly and CWD does transmit to mink, ferret, cattle, and squirrel monkey by intracerebral inoculation. With the known incubation periods in other TSEs, oral transmission studies of CWD may take much longer. Every victim/family of CJD/TSEs should be asked about route and source of this agent. To prolong this will only spread the agent and needlessly expose others. In light of the findings of Asante and Collinge et al, there should be drastic measures to safeguard the medical and surgical arena from sporadic CJDs and all human TSEs. I only ponder how many sporadic CJDs in the USA are type 2 PrPSc?

http://www.neurology.org/content/60/2/176/reply#neurology_el_535

Sent: Monday, January 08,2001 3:03 PM

TO: freas@CBS5055530.CBER.FDA.GOV

FDA CJD BSE TSE Prion Scientific Advisors and Consultants Staff January 2001 Meeting Singeltary Submission

2001 FDA CJD TSE Prion Singeltary Submission

http://www.fda.gov/ohrms/dockets/ac/01/slides/3681s2_09.pdf

2 January 2000

British Medical Journal

U.S. Scientist should be concerned with a CJD epidemic in the U.S., as well

http://www.bmj.com/rapid-response/2011/10/28/us-scientist-should-be-concerned-cjd-epidemic-us-well

15 November 1999

British Medical Journal

vCJD in the USA * BSE in U.S.

http://www.bmj.com/rapid-response/2011/10/28/re-vcjd-usa-bse-us ;;
 
 
Terry S. Singeltary Sr.
Bacliff, Texas USA 77518

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