Tuesday, April 06, 2010

Organ distribution of prion proteins in variant Creutzfeldt-Jakob disease

The Lancet Infectious Diseases, Volume 3, Issue 4, Pages 214 - 222, April 2003

doi:10.1016/S1473-3099(03)00578-4Cite or Link Using DOI

Organ distribution of prion proteins in variant Creutzfeldt-Jakob disease

Original Text

Dr I Ramasamy a , M Law b, S Collins c, F Brook a

Summary

In this article we give an overview of the transmissible spongiform encephalopathies, with emphasis on the evidence for the distribution of abnormal prions in tissues. The normal prion protein is distributed ubiquitously throughout human body tissues. Endogenous expression of the normal prion protein, as well as auxiliary proteins, plays a part in accumulation of the abnormal prion protein. As exemplified by variant Creutzfeldt-Jakob disease (vCJD) the abnormal prion protein can accumulate in the host lymphoid system, in particular the follicular dendritic cells. The route for the disease-related prion neuroinvasion is likely to involve the peripheral nervous system. An alternative route may involve blood constituents. Both animal studies and studies on vCJD patients suggest a potential for abnormal prion distribution in several peripheral tissues other than the lymphoreticular system. In human beings the abnormal prion has been reported in the brain, tonsils, spleen, lymph node, retina, and proximal optic nerve. Infectivity, although present in peripheral tissues, is at lower levels than in the central nervous system (CNS). Animal models suggest that the growth of infectivity in the CNS is likely to be gradual with maximum values during the clinical phase of disease. That tissues may harbour the abnormal prion, at different levels of infectivity, during the incubation period of the disease raises concerns of iatrogenic transmission of the disease either after surgery, blood transfusion, or accidental organ transplantation from donors in the preclinical phase of the disease.


http://www.thelancet.com/journals/laninf/article/PIIS1473-3099(03)00578-4/fulltext#article_upsell


Cadaver corneal transplants -- without family permission

Houston, Texas channel 11 news 28 Nov 99

Reported by Terry S. Singeltary Sr. son of CJD victim

"It was a story about how the Lions eye bank were harvesting corneas from victims in the Morgue, without their consent. Under Texas law, this appears to be legal (remember Texas has the Veggie liable law). Even if Family says no, this appears to happen, from what the news story said. They said the only way to prevent this, is to fill out a form, stating not to have this done. So if you don't fill out the form, they can do this. How many people don't know about the form?

This is not only disgusting and appalling, it could be highly infectious. Without proper background checking of the donors, on their physical history, checking on past dementia, and/or family history, some of these unfortunate victims, could be passing a human TSE.

Response Jill Spitler Clevelland Eye Bank:

"No, we are not stealing.........Yes, you do have such a law in the state of Texas, but not all your state Eye Banks utilize the law. The Eye Bank that you're speaking of is only one of 43 certified Eye Bank throughout the USA.

And there are measure taken per the Medical Standards of the Eye Bank Association of America, the certifying body for eye banks and per FDA regulations to address those concerns that you speak of.

I would suggest that those interested/concern with transplant contact their local agencies. The Eye Bank Association of America has a web. site . Further if anyone has problems contacting or finding out about their local organization(s), call me or e-mail me I would be glad to help. My e-mail address is jill@clevelandeyebank.org"

Terry Singeltary responds:

"Explain this to the family in Houston who went to their loved ones funeral, only to find out that the loved one that was in the casket, had their corneas removed without their permission, without the consent of the victim or it's family. They would not have known it, only for the funny look the victim had. So, they questioned, only to find out, the corneas, had in fact, been removed without consent.

I call that stealing, regardless what the law states. This type of legal grave robbing is not a logical thing to do without knowing any type of background of the victims medical past, which really will not prove anything due to the incubation period. Eye tissue being potentially a highly infective source, there are risks here.

Should they not at least know of the potential ramifications of TSE's (the person receiving the corneas)?

Should there not be some sort of screening?

Should there be some sort of moral issue here? If this is the case, and in fact, they can come take your corneas, without your consent, then what will they start taking next, without your consent?

Lets look at a hypothetical situation: What would happen if my Mom (DOD 12-14-97 hvCJD) would have gotten into a car wreck and died, before the symptoms of CJD appeared. Not much money, so there was no autopsy. What would have happened to that recipient of those infecting corneas?"

Comment (webmaster): Actual transmission of CJD by means of corneal transplant may or may not be rare. The incidence of infectivity in older people could be fairly high; this is not to be confused with the lower incidence of symptomatic (clinical) CJD. It is very unlikely that familial CJD would have been diagnosed in earlier generations; however, without interviewing the family even known kindreds would not be excluded.

In blood donation, a much stricter policy is followed, even though corneal transplant may be far more dangerous (being a direct link to the brain and not going through purification steps).

Since highly sensitive tests for pre-clinical CJD are now available, it would make sense to screen corneas for CJD, just as they are screened for AIDS, hepatitus, and a host of other conditions.


http://mad-cow.org/~tom/dec99_news.html#bbb


please see full text here ;

Monday, August 31, 2009

HUMAN BODY PARTS FOR SALE TO THE HIGHEST BIDDER Inside a Creepy Global Body Parts Business


http://creutzfeldt-jakob-disease.blogspot.com/2009/08/human-body-parts-for-sale-to-highest.html


THE LEGALITY OF STEALING ORGAN/TISSUE...

TEXAS STATUTES

Sec. 693.012. Removal of Corneal Tissue Permitted Under Certain Circumstances.

On a request from an authorized official of an eye bank for corneal tissue, a justice of the peace or medical examiner may permit the removal of corneal tissue if:

(1) the decedent from whom the tissue is to be removed died under circumstances requiring an inquest by the justice of the peace or medical examiner;

(2) no objection by a person listed in Section 693.013 is known by the justice of the peace or medical examiner; and

(3) the removal of the corneal tissue will not interfere with the subsequent course of an investigation or autopsy or alter the decedent's postmortem facial appearance.

Acts 1989, 71st Leg., ch. 678, Sec. 1, eff. Sept. 1, 1989.

Note: This information includes legislation enacted through the 75th Congress. The 76th session of the Texas Legislature has concluded. The State of Texas has not yet made the new codes available to the public. Until they do, search the bill text for any changes or amendments.

Search 1999 Legislation for: 693.012

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TEXAS STATUTES Sec. 693.003. Consent Required in Certain Circumstances.

(a) A medical examiner or a person acting on the authority of a medical examiner may not remove a visceral organ unless the medical examiner or person obtains the consent of a person listed in Section 693.004.

(b) If a person listed in Section 693.004 is known and available within four hours after death is pronounced, a medical examiner or a person acting on the authority of a medical examiner may not remove a nonvisceral organ or tissue unless the medical examiner or person obtains that person's consent.

(c) If a person listed in Section 693.004 cannot be identified and contacted within four hours after death is pronounced and the medical examiner determines that no reasonable likelihood exists that a person can be identified and contacted during the four-hour period, the medical examiner may permit the removal of a nonvisceral organ or tissue.

Acts 1989, 71st Leg., ch. 678, Sec. 1, eff. Sept. 1, 1989.

Note: This information includes legislation enacted through the 75th Congress. The 76th session of the Texas Legislature has concluded. The State of Texas has not yet made the new codes available to the public. Until they do, search the bill text for any changes or amendments.

Search 1999 Legislation for: 693.003

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PLEASE NOTE; the bottom would only pertain to those who know of the law. if you don't know about it, you cannot dispute, so in four hours, they can legally remove body organs, as long as they don't disfigure. and who is to know the difference? makes me wonder of some of my dead relatives, and if they were burried with their eye's and or any of their organs. This is very disturbing, if not for moral reasons, but for the risk of dangerous pathogens (human TSE's, etc.) to be transmitted. only time will tell, but i am very disturbed. these laws are not morally correct. They should be re-written as to they cannot so easily take your organs, with no one knowing. The Family or Victim, must consent. There should be some kind of research on donor/family medical history... TSS

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Sec. 693.013. Persons Who May Object to Removal.

The following persons may object to the removal of corneal tissue:

(1) the decedent's spouse;

(2) the decedent's adult children, if there is no spouse;

(3) the decedent's parents, if there is no spouse or adult child; or

(4) the decedent's brothers or sisters, if there is no spouse, adult child, or parent.

Acts 1989, 71st Leg., ch. 678, Sec. 1, eff. Sept. 1, 1989.

Note: This information includes legislation enacted through the 75th Congress. The 76th session of the Texas Legislature has concluded. The State of Texas has not yet made the new codes available to the public. Until they do, search the bill text for any changes or amendments.

Search 1999 Legislation for: 693.013

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to cover one's butt....



Sec. 693.014. Immunity From Damages in Civil Action.

(a) In a civil action brought by a person listed in Section 693.013 who did not object before the removal of corneal tissue, a medical examiner, justice of the peace, or eye bank official is not liable for damages on a theory of civil recovery based on a contention that the person's consent was required before the corneal tissue could be removed.

(b) Chapter 104, Civil Practice and Remedies Code, applies to a justice of the peace, medical examiner, and their personnel who remove, permit removal, or deny removal of corneal tissue under this subchapter as if the justice of the peace, medical examiner, and their personnel were state officers or employees.

Acts 1989, 71st Leg., ch. 678, Sec. 1, eff. Sept. 1, 1989.

Note: This information includes legislation enacted through the 75th Congress. The 76th session of the Texas Legislature has concluded. The State of Texas has not yet made the new codes available to the public. Until they do, search the bill text for any changes or amendments.

Search 1999 Legislation for: 693.014

[[[as you can see, they knew it was wrong when they wrote the laws. or they would not have covered the rear-ends so well...TSS]]]

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thanks again, kind regards, Terry S. Singeltary Sr.


############ http://mailhost.rz.uni-karlsruhe.de/warc/bse-l.html ############


full text ;

Saturday, January 26, 2008

CJD HGH BODY SNATCHERS


http://creutzfeldt-jakob-disease.blogspot.com/2008/01/cjd-hgh-body-snatchers.html



URGENT DATA ON ATYPICAL BSE RISK FACTORS TO HUMANS AND ANIMALS OIE REFUSE TO ACKNOWLEDGE $

position: Post Doctoral Fellow Atypical BSE in Cattle

Closing date: December 24, 2009

Anticipated start date: January/February 2010

Employer: Canadian and OIE Reference Laboratories for BSE CFIA Lethbridge Laboratory, Lethbridge/Alberta

snip...

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...


http://www.prionetcanada.ca/detail.aspx?menu=5&dt=293380&app=93&cat1=387&tp=20&lk=no&cat2



please see full text ;

Wednesday, March 31, 2010

Atypical BSE in Cattle


http://bse-atypical.blogspot.com/2010/03/atypical-bse-in-cattle-position-post.html


Wednesday, February 24, 2010

Transmissible Spongiform encephalopathy (TSE) animal and human TSE in North America 14th

ICID International Scientific Exchange Brochure -


http://transmissiblespongiformencephalopathy.blogspot.com/2010/02/transmissible-spongiform-encephalopathy.html



TSE


http://transmissiblespongiformencephalopathy.blogspot.com/



Monday, October 19, 2009

Atypical BSE, BSE, and other human and animal TSE in North America Update October 19, 2009

snip...

I ask Professor Kong ;

Thursday, December 04, 2008 3:37 PM Subject: RE: re--Chronic Wating Disease (CWD) and Bovine Spongiform Encephalopathies (BSE): Public Health Risk Assessment

''IS the h-BSE more virulent than typical BSE as well, or the same as cBSE, or less virulent than cBSE? just curious.....''

Professor Kong reply ;

.....snip

''As to the H-BSE, we do not have sufficient data to say one way or another, but we have found that H-BSE can infect humans. I hope we could publish these data once the study is complete.

Thanks for your interest.''

Best regards,

Qingzhong Kong, PhD Associate Professor Department of Pathology Case Western Reserve University Cleveland, OH 44106 USA

END...TSS

I look forward to further transmission studies, and a true ENHANCED BSE/atypical BSE surveillance program put forth testing all cattle for human and animal consumption for 5 years. a surveillance program that uses the most sensitive TSE testing, and has the personnel that knows how to use them, and can be trusted. I look forward to a stringent mad cow feed ban being put forth, and then strictly enforced. we need a forced, not voluntary feed ban, an enhanced feed ban at that, especially excluding blood. we need some sort of animal traceability. no more excuses about privacy. if somebody is putting out a product that is killing folks and or has the potential to kill you, then everybody needs to know who they are, and where that product came from. same with hospitals, i think medical incidents in all states should be recorded, and made public, when it comes to something like a potential accidental transmission exposure event. so if someone is out there looking at a place to go have surgery done, if you have several hospitals having these type 'accidental exposure events', than you can go some place else. it only makes sense. somewhere along the road, the consumer lost control, and just had to take whatever they were given, and then charged these astronomical prices. some where along the line the consumer just lost interest, especially on a long incubating disease such as mad cow disease i.e. Transmissible Spongiform Encephalopathy. like i said before, there is much more to the mad cow story than bovines and eating a hamburger, we must start focusing on all TSE in all species. ...TSS



http://bse-atypical.blogspot.com/2009/10/atypical-bse-bse-and-other-human-and.html



TSS

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Thursday, January 28, 2010

Multiorgan Detection and Characterization of Protease-Resistant Prion Protein in a Case of Variant CJD Examined in the United States

PLoS One. 2010; 5(1): e8765. Published online 2010 January 19. doi: 10.1371/journal.pone.0008765. PMCID: PMC2808239

Copyright Notari et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Multiorgan Detection and Characterization of Protease-Resistant Prion Protein in a Case of Variant CJD Examined in the United States

Silvio Notari,#1 Francisco J. Moleres,#1 Stephen B. Hunter,2 Ermias D. Belay,3 Lawrence B. Schonberger,3 Ignazio Cali,1 Piero Parchi,4 Wun-Ju Shieh,3 Paul Brown,5 Sherif Zaki,3 Wen-Quan Zou,1 and Pierluigi Gambetti1* 1Institute of Pathology, Case Western Reserve University, Cleveland, Ohio, United States of America 2Department of Pathology and Laboratory Medicine, Emory University Hospital, Atlanta, Georgia, United States of America 3National Center for Zoonotic, Vector-Borne, and Enteric Diseases, Center for Disease Control and Prevention, Atlanta, Georgia, United States of America 4Dipartimento di Scienze Neurologiche, Universita' di Bologna, Italy 5CEA/DSV/iMETI/SEPIA, France Delia Goletti, Editor National Institute for Infectious Diseases L. Spallanzani, Italy #Contributed equally. * E-mail: pxg13@case.edu Conceived and designed the experiments: SN FJM PG. Performed the experiments: SN FJM IC. Analyzed the data: SN FJM PB WQZ PG. Contributed reagents/materials/analysis tools: SBH WJS SZ PG. Wrote the paper: SN FJM SBH EDB LBS IC PP WJS PB SZ WQZ PG. Received October 19, 2009; Accepted December 18, 2009.

ABSTRACT

Background Variant Creutzfeldt–Jakob disease (vCJD) is a prion disease thought to be acquired by the consumption of prion-contaminated beef products. To date, over 200 cases have been identified around the world, but mainly in the United Kingdom. Three cases have been identified in the United States; however, these subjects were likely exposed to prion infection elsewhere. Here we report on the first of these subjects.

Methodology/Principal Findings Neuropathological and genetic examinations were carried out using standard procedures. We assessed the presence and characteristics of protease-resistant prion protein (PrPres) in brain and 23 other organs and tissues using immunoblots performed directly on total homogenate or following sodium phosphotungstate precipitation to increase PrPres detectability. The brain showed a lack of typical spongiform degeneration and had large plaques, likely stemming from the extensive neuronal loss caused by the long duration (32 months) of the disease. The PrPres found in the brain had the typical characteristics of the PrPres present in vCJD. In addition to the brain and other organs known to be prion positive in vCJD, such as the lymphoreticular system, pituitary and adrenal glands, and gastrointestinal tract, PrPres was also detected for the first time in the dura mater, liver, pancreas, kidney, ovary, uterus, and skin.

Conclusions/Significance Our results indicate that the number of organs affected in vCJD is greater than previously realized and further underscore the risk of iatrogenic transmission in vCJD.

snip...

The oral route of prion infection in vCJD raised the possibility that tissues and organs, beside the central nervous system (CNS), might also be affected. To date, PrPres has been reported in several tissues and organs outside the CNS of vCJD patients (Table 1) [14–19, P. Brown, unpublished data].

Although the amount of PrPres in non-neural tissues is small compared to that in the brain, the risk posed by the spread of even small amounts of PrPres has been underscored by the iatrogenic transmission of vCJD from blood donors in the preclinical phase of the disease [20].

We examined the main characteristics and tissue distribution of PrPres in a case of vCJD, in which the disease was most likely acquired in the UK but which is officially referred to as an American case because illness onset occurred in the US [21]. In an extensive autopsy examination, sodium phosphotungstate (NaPTA) precipitation, a highly sensitive method of PrPres detection [14,22], was used to establish the presence and estimate the relative amounts of PrPres in several organs and tissues made available to the National Prion Disease Pathology Surveillance Center (NPDPSC).

snip...

Results Clinical History Clinical data on the present patient have been reported in detail [21]. Briefly, the patient lived in Britain until the age of 13 and immigrated to the US in 1992. In early November 2001, at the age of 22 years, the patient was evaluated for depression, emotional instability and memory loss, followed one month later by involuntary movements, gait disturbances and incontinence. During the ensuing three months, the patient’s motor and cognitive deficits worsened, and confusion, hallucination, dysarthria, bradykinesia, and spasticity also occurred. The diagnosis of vCJD was made following brain magnetic resonance imaging and confirmed by immunoblot and immunohistochemistry of tonsil tissue. She received an experimental treatment with quinacrine for 3 months, but showed only minimal and transitory improvement. The patient died in June 2004, 32 months after the clinical onset.

snip...

Discussion Our study confirms the diagnosis of vCJD in the present case, based on the characteristics of the PrPres and the methionine homozygosity at codon 129 of the PrP gene, the last feature being invariably present in vCJD [32]. However, we also observed two unusual features in this case. The first is the long disease duration of 32 months, which is more than twice the 14 month mean duration of the British cases of vCJD [3]. However, cases of up to 40 months duration after the diseases onset have been reported [3,33]. The second unusual feature is the absence of typical spongiform degeneration which likely stemmed from the long duration of the disease. The long disease duration likely led to extensive loss of neurons, in which most of the vacuoles are formed, with ensuing astroglial scar [34].

As previously reported [21], the BSE exposure most likely occurred between the early eighties, when the BSE epidemic emerged in the UK, and 1992, when the patient immigrated to the US. This assumption is consistent with an incubation period of 9 to 21 years, which correlates well with the medium incubation period of 17 years estimated for the UK cases of vCJD [35]. The brain PrPres of the present case displayed the glycoform ratio and electrophoretic mobility characteristic of the PrPres associated with vCJD [5]. One exception is the cerebellum where the monoglycosylated and unglycosylated PrPres isoform migrated slightly faster than the PrPres from other brain regions and resolved in three bands. The variation in PrPres electrophoretic characteristics between the cerebellum and the cerebral cortex is not surprising for it has also been observed in sCJD [36]. Yet to our knowledge it has never been reported in vCJD. Finally, contrary to previous reports [29], PrPres type 1 did not co-occur with type 2. This discrepancy might stem from our rigorous PrP digestion with PK and from the use of different antibodies, an approach that rules out the possibility that partially cleaved fragments derived by the incomplete digestion of PrPSc be misinterpreted as the type 1 fragment [30,37].

The major finding of the present study is the demonstration that PrPres is present in a number of non-CNS tissues and organs which previous studies had reported as free of PrPres (Table 1 and 2) [14– 19, P. Brown, unpublished data]. These tissues include the dura mater, skin, liver, kidney, pancreas, descending colon, uterus and ovary (Table 2 and Fig. 3). The use of NaPTA, along with the long disease duration, may both have contributed to the undisputed detection of PrPres in these organs in this case. The glycoform ratio of the brain PrPres was not retained in every peripheral organ examined (Fig. 4). In the pituitary gland and the skin the diglycosylated and monoglycosylated PrPres isoforms were about equally represented thus the diglycosylated isoform was not dominant. On the other hand, electrophoretic mobility appeared to match that of the brain. Variations in the glycoform ratio could be assessed only on the TH because the glycoform ratio, as well the electrophoretic mobility, is affected by NaPTA enrichment [14].

The presence of prion in the human dura mater is not surprising because sCJD has been transmitted following transplantation of dura obtained from sCJD-affected cases [38]. However, to our knowledge this is the first immunoblot demonstration of PrPres in the dura mater in any prion disease. The detection of relatively large amounts of PrPres in the dura mater raises the possibility of contamination with brain tissue at autopsy. Although this possibility cannot be completely ruled out, extensive rinses in PBS were performed before homogenization in some experiments without observing a reduction in the amount of the PrPres detected.

Prion infectivity of kidney and liver has been demonstrated by bioassay in other human prion diseases [39], and PrPres has been observed in the kidney of scrapie infected sheep [40]. The presence of PrPres has also been reported in kidney, liver and pancreas of scrapie infected mice in association with lymphofollicular proliferation [41]. This last finding is relevant to the present case in which multiple lymphocytic infiltrates with follicular pattern were present in the kidney. However, contrary to this report, we observed no significant inflammatory reaction in any of the other tissues which contained PrPres. A puzzling finding of our study is the presence of PrPres albeit in small amounts in the kidney but not in the urinary bladder. This apparent discrepancy is relevant to the recent demonstrations of prion infectivity in urine

of animals carrying experimental or naturally occurring prion diseases [42–46]. It would indicate that prion infectivity in urine is acquired from the kidney while the urinary bladder acts as a bystander. However the amount of PrPres we observed in the kidney was minimal, and might have not been sufficient to infect the urine and to propagate to the bladder in detectable amounts. Indeed we failed to demonstrate PrPres in the urine in the present case even after hundred-fold urine concentration (data not shown). Obviously more studies are needed to clarify this issue. The present study also demonstrates for the first time the presence of PrPres in the skin in a human prion disease. Previously, PrPres has been detected in the skin from animals with experimental or naturally occurring scrapie [47] as well as in the antler velvet of elk affected by CWD [48].

Furthermore, it is remarkable that we observed PrPres in the uterus and the ovary, a finding which implicates the reproductive system, thereby raising the possibility of maternal transmission of vCJD. Vertical transmissibility of prion infection has been demonstrated in transgenic mice infected with BSE [49]. Related literature on human prion diseases is very scanty. Pregnancy completed to delivery has been reported in sCJD, iatrogenic CJD and vCJD [50,51]; however, transmission to the progeny has not been examined in detail or confirmed in any of these cases. The first detailed determination of PrPC and PrPres in the reproductive and gestational tissues from a sCJD patient has been carried out only recently [51]. Although this study failed to detect PrPres, remarkably it showed that, in uterine tissue obtained at biopsy, most of the PK-sensitive PrP is truncated at the N-terminus and matches the C-terminal PrPC fragment C1 which is generated during normal PrPC metabolism [51]. Similarly, in the present case we observed that the C1-like fragment was largely predominant over the full-length PrPC in the uterus, and it was easily digested by PK but it was present along with a significant amount of characteristic vCJD PrPres (Fig. 4). Since the Nterminus of the PrPres type 2 associated with vCJD is at residues 92–99, the uterine PrPres must have formed from the full length PrPC rather than from C1, the N-terminus of which is at residues 111–112 [31,52]. These findings raise the question of the origin of the PrPres found in the uterus, a question that is currently unanswered. A similar question may be raised for the urine, in

which although the prion infectivity has been demonstrated in animals by bioassay [42–46], the only detected form of PrP under normal condition in animals and humans, is a fragment matching the C1 [53, 54, Notari et al., unpublished data].

All these considerations notwithstanding, the widespread presence of PrPres in visceral organs that we observed in the present case further reinforces the concerns over iatrogenic transmission of vCJD. These concerns are already compelling given the multiple reports of vCJD transmission by blood transfusion.


http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2808239/pdf/pone.0008765.pdf





Wednesday, January 27, 2010


Fast, broad-range disinfection of bacteria, fungi, viruses and prions


http://creutzfeldt-jakob-disease.blogspot.com/2010/01/fast-broad-range-disinfection-of.html




Saturday, January 23, 2010


Experimental Verification of a Traceback Phenomenon in Prion Infection


http://creutzfeldt-jakob-disease.blogspot.com/2010/01/experimental-verification-of-traceback.html




Sunday, January 17, 2010


CJD Following up: Patients never contracted brain disorder UW Hospital patients


http://creutzfeldt-jakob-disease.blogspot.com/2010/01/cjd-following-up-patients-never.html




Sunday, January 17, 2010


Human tissue, recovered from a donor history indicated increased risk factors for Creutzfeldt-Jacob disease Lions Eye Bank


http://creutzfeldt-jakob-disease.blogspot.com/2010/01/human-tissue-recovered-from-donor.html




Saturday, January 16, 2010


Evidence For CJD TSE Transmission Via Endoscopes 1-24-3 re-Singeltary to Bramble et al


http://creutzfeldt-jakob-disease.blogspot.com/2010/01/evidence-for-cjd-tse-transmission-via.html




Sunday, August 09, 2009

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


http://creutzfeldt-jakob-disease.blogspot.com/2009/08/cjdstraight-talk-withjames.html



Tuesday, August 18,

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


http://madcowusda.blogspot.com/2009/08/bse-untold-story-joe-gibbs-and.html



R.I.P. MOM hvCJD confirmed DECEMBER 14, 1997

Monday, December 14, 2009

Similarities between Forms of Sheep Scrapie and Creutzfeldt-Jakob Disease Are Encoded by Distinct Prion Types


http://nor-98.blogspot.com/2009/12/similarities-between-forms-of-sheep.html



Saturday, January 2, 2010

Human Prion Diseases in the United States January 1, 2010 ***FINAL***


http://prionunitusaupdate2008.blogspot.com/2010/01/human-prion-diseases-in-united-states.html


my comments to PLosone here ;


http://www.plosone.org/annotation/listThread.action?inReplyTo=info%3Adoi%2F10.1371%2Fannotation%2F04ce2b24-613d-46e6-9802-4131e2bfa6fd&root=info%3Adoi%2F10.1371%2Fannotation%2F04ce2b24-613d-46e6-9802-4131e2bfa6fd



TSS

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