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From: TSS (216-119-156-132.ipset36.wt.net)
-------- Original Message -------- MCG takes surgical precautions By DAVID WAHLBERG MCG officials said they were being "overly cautious" and that no one Those are symptoms of CJD, a form of which is known to come from Monday night, MCG closed its 22 operating rooms, Caruana said. The MCG officials have not formally notified patients of the situation Creutzfeldt-Jakob disease has two main forms: variant CJD, the human Both forms of the disease are caused by prions, abnormal proteins The MCG patient had unusual neurological symptoms but no obvious On Monday, hospital officials interviewing operating room staff To do that, the officials shut down the 22 operating rooms, canceling Caruana said MCG was convinced the patient didn't have CJD and that http://www.ajc.com/metro/content/metro/0105/12cjd.html final transmission, please reply...... -------- Original Message -------- Greetings Danielle, my name is Terry S. Singeltary Sr. and I belong to several groups, could you please tell us what the Definitive test was and what the findings kind regards, Terry S. Singeltary > But the patient, now receiving steroid treatments, is getting better, http://www.fortunecity.com/healthclub/cpr/349/part1cjd.htm DOES not seem they are willing to discuss this. I find this rather disturbing; > Caruana said MCG was convinced the patient didn't have CJD and that FOR them to act as if there was really a risk, while pretending there was J Neurol Neurosurg Psychiatry 1994 Jun;57(6):757-8 Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC. Laboratory of Central Nervous System Studies, National Institute of Stereotactic multicontact electrodes used to probe the cerebral PMID: 8006664 [PubMed - indexed for MEDLINE] http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8006664&dopt=Abstract Docket: 02N-0370 - Neurological Devices; Classification of Human Dura Mater Comment Number: EC -1 Accepted - Volume 1 Ref: MRC/62/04 Under strict embargo until 19.00 British Time Thursday 11 November 2004 GENETIC MAKE-UP MAY DETERMINE WHAT TYPE OF CJD OCCURS WHEN HUMANS ARE INFECTED WITH BSE New research published today (19.00 hours Thursday 11th November) by a team from the Medical Research Council (MRC) Prion Unit offers an explanation about why only people with a particular genetic make-up have so far developed vCJD. It also provides evidence that other types of BSE-derived prion infection with a different pattern of symptoms might occur in humans. The findings are published in the journal Science. Variant CJD (vCJD) is the human disease thought to be caused by eating food contaminated with the infectious agent, known as a prion, responsible for the epidemic of BSE or mad cow disease in cattle. So far, everyone known to have developed vCJD has been of a particular genetic type known as MM. Until now it has been a mystery why everyone that has developed vCJD is of the MM type and one possibility is that they are simply the first to develop the disease when infected with BSE, and that people with the other genetic types1 (known as VV and MV) infected with BSE prions will also develop vCJD, but some years later. In a series of experiments spanning more than ten years, the MRC team has been studying mice genetically modified so that they make human prion proteins which are used to model human susceptibility to BSE. The team has now shown that mice with the human VV genetic type do become infected when given BSE or vCJD prions, but manifest a different form of the disease which looks quite different to vCJD and has a novel prion strain type. Remarkably, when these novel prions were used to infect mice of the MM genetic type, the mice either developed a disease very like vCJD, or else a pattern of disease that looks like so-called sporadic CJD the classical form of CJD. This form has been known about for many years, is seen all over the world and has not hitherto been associated with BSE. However, the new strain identified in the mice, being called type 5, has not been seen yet in people and we do not know what pattern of disease it would cause. It could look like one of the forms of classical or sporadic CJD or perhaps be yet another different variant form. The work from the MRC team suggests that type 4 prions, the type associated with vCJD, can only propagate themselves in people that make the M form of the protein. It seems the V form of the protein just cannot adopt the particular molecular shape that characterises type 4. The studies in mice also suggest that if these prions were to pass from person to person (for example by blood transfusion) then, depending on the genetic type of the person becoming infected, at least three different patterns of disease might result: type 2 (which is seen in sporadic CJD); type 4 (which causes vCJD) or type 5 (which may cause a new pattern of disease). Professor John Collinge, Director of the MRC Prion Unit, which is based at University College London, said: These mouse studies give us vital clues about the behaviour of prions and how they appear to modify and adapt depending on the genetic makeup of the individual they are infecting. We always have to be cautious about making direct comparison to the human condition, but our work strongly suggests that we can not assume only those with one genetic profile are vulnerable to BSE infection. At this stage it is not possible to say how this should alter estimates of those likely to become ill, but our findings do suggest we should be taking steps to draw up a more sophisticated system of categorizing the disease so that we dont mistake BSE related infection for a version of sporadic CJD. ENDS For more information call the MRC press office on 020 7 637 6011 Notes to Editors 1The human prion protein comes in two common forms, known as M and V. Because everyone has two copies of this gene, there are three possible genetic types: MM, MV and VV. Paper - Human Prion protein v129 prevent expression of vCJD phenotype Science On line 11.11.04 Prions are rogue forms of one of the bodys own proteins known as the prion protein which are misshapen. There are several different rogue or misshapen forms that can infect humans, and these different types of prions are known as strains . This is analogous to different strains of other germs such flu virus causing influenza or strains of salmonella causing different forms of food poisoning for example. The strain of prion causing vCJD is known as type 4, types 1-3 cause the different forms of sporadic or classical CJD. Each strain causes a different pattern or type of disease. It is known that prion strains can change or mutate when they pass between different animals. The Medical Research Council (MRC) is a national organisation funded by the UK tax-payer. Its business is medical research aimed at improving human health; everyone stands to benefit from the outputs. The research it supports and the scientists it trains meet the needs of the health services, the pharmaceutical and other health-related industries and the academic world. MRC has funded work which has led to some of the most significant discoveries and achievements in medicine in the UK. About half of the MRCs expenditure of £430 million is invested in its 40 Institutes, Units and Centres. The remaining half goes in the form of grant support and training awards to individuals and teams in universities and medical schools. Web site at: http://www.mrc.ac.uk . Send Post-Publication Peer Review to journal: Re: RE-Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States Email Terry S. Singeltary: flounder@wt.net 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/cgi/eletters/60/2/176#535 Docket No. 2003N-0312 Animal Feed Safety System [TSS SUBMISSION] http://www.fda.gov/ohrms/dockets/dockets/03n0312/03N-0312_emc-000001.txt Terry S. Singeltary Sr. P.O. Box 42 Bacliff, TEXAS USA 77518 ######### https://listserv.kaliv.uni-karlsruhe.de/warc/bse-l.html ##########
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