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1 [Sensitivity 88.6% (95% CI 79.5-94.7%)], 1/2 variant CJD samples, and 9/20 samples from various inher
2 oradic Creutzfeldt-Jakob disease (CJD) and 6 variant CJD brains.
3                                     Although variant CJD can be diagnosed during life by tonsil biops
4 disease, Creutzfeldt-Jakob disease (CJD) and variant CJD in humans.
5 regions in controls, sporadic CJD (sCJD) and variant CJD (vCJD) patients has identified three polymor
6                               Since clinical variant CJD is uniformly associated with tonsillar prion
7  patients with neuropathologically confirmed variant CJD, but not from patients with other prion dise
8 e prion strain and are at risk of developing variant CJD.
9 a rendering plant and the risk of developing variant CJD.
10           Variant Creutzfeldt-Jakob disease (variant CJD) is difficult to distinguish from common psy
11 at causes variant Creutzfeldt-Jakob disease (variant CJD) is indistinguishable from the causative age
12 e appearance of a novel human prion disease, variant CJD, and the clear experimental evidence that it
13 ases between species, suggest that the early variant CJD cases may have been exposed during the precl
14                 In 2002, 17 people died from variant CJD (vCJD) in the UK, compared with 20 in 2001 a
15 licated historically in kuru and recently in variant CJD.
16 ignated type 4t) different from that seen in variant CJD brain (type 4) or in brain from other CJD su
17   These data should inform attempts to model variant CJD epidemiology.
18  dementia, corticobasal degeneration and new variant CJD have been considered in affected individuals
19 iant of Creutzfeldt-Jakob disease (CJD), new variant CJD (nvCJD), was identified in the UK in 1996.
20 and ataxia, including suspected cases of new variant CJD.
21 n that may be especially relevant in the new variant CJD.
22 ve since the emergence, in the mid-1990s, of variant CJD (vCJD), a disease linked to bovine spongifor
23                               The arrival of variant CJD in the UK in the 1990s has intensified the s
24 dt-Jakob disease (CJD); there was no case of variant CJD.
25              One hypothesis is that cases of variant CJD have resulted from exposure to the BSE agent
26 gested that the observation of four cases of variant CJD living in an area with a population of 1.5 m
27                       We identified cases of variant CJD through the National CJD Surveillance Unit,
28              Up to Aug 31, 1998, 26 cases of variant CJD with onset in the UK (Northern Ireland not i
29  We compared the observed number of cases of variant CJD within a particular distance of a rendering
30                      The reported cluster of variant CJD cases in Kent is most probably a chance find
31 or is highly consistent with, a diagnosis of variant CJD and negative in all patients subsequently co
32         It is unclear if a large epidemic of variant CJD will occur in the years ahead.
33         The observed and expected numbers of variant CJD cases living within a specified distance of
34              On second and third passages of variant CJD prions in Tg(MHu2M) mice, multiple strains o
35 cular features of this case overlap those of variant CJD.
36 er bovine spongiform encephalopathy (BSE) or variant CJD prions, may develop the neuropathological an
37 poradic Creutzfeldt-Jakob disease (sCJD), or variant CJD (vCJD) brains.
38 tonsil biopsy sample was positive for PrPSc, variant CJD could be diagnosed, which obviates the need
39    We conducted GWAS of sporadic CJD (sCJD), variant CJD (vCJD), iatrogenic CJD, inherited prion dise
40  of prion disease emerged in the UK, termed "variant CJD", thought to be acquired by consumption of b
41 r results do not support the hypotheses that variant CJD is an emerging illness in Washington or that
42                   Our results also show that variant CJD has a different pathogenesis to sporadic CJD
43   For experimental exposure of astrocytes to variant CJD (vCJD), the kinetics of prion replication oc
44 C and MM2T, and a low sensitivity limited to variant CJD, Gerstmann-Straussler-Scheinker syndrome and
45 re closely similar) but can be infected with variant CJD prions, a human prion strain resulting from
46 es of a macaque experimentally infected with variant CJD.
47  prion protein in the urine of patients with variant CJD (vCJD) using protein misfolding by cyclic am
48        There is no evidence that people with variant CJD tended to live closer than the population as