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1                      In this issue of Blood, Jakob et al report that hematopoietic progenitor kinase
2 actors in response to the foreign Creutzfeld-Jakob disease agent, it is likely that innate immunity u
3 on of the attenuated SY strain of Creutzfeld-Jakob disease in mice could delay clinical signs and wid
4  studying transmission of variant Creutzfeld-Jakob disease by blood products in humans.
5          The emergence of variant Creutzfeld-Jakob disease, following on from the bovine spongiform e
6 to humans in the form of variant Creutzfeldt Jakob disease, have raised concerns about the zoonotic p
7                                  Creutzfeldt-Jakob disease (CJD) and autoimmune encephalitis with ant
8                                  Creutzfeldt-Jakob disease (CJD) has been accidentally transmitted by
9                                  Creutzfeldt-Jakob disease (CJD) in humans has been shown to be trans
10                                  Creutzfeldt-Jakob disease (CJD) is a neurodegenerative disorder caus
11                                  Creutzfeldt-Jakob disease (CJD) is a rare but invariably fatal neuro
12                                  Creutzfeldt-Jakob disease (CJD) is a rare progressive neurodegenerat
13                                  Creutzfeldt-Jakob disease (CJD), the most common human prion disease
14  were Alzheimer's disease (18%), Creutzfeldt-Jakob disease (12%) and inflammatory disorders (9%).
15 al sclerosis (FTD/ALS, n = 252), Creutzfeldt-Jakob disease (CJD, n = 239), Parkinson's disease (PD, n
16 neity, including patients with a Creutzfeldt-Jakob disease (CJD) phenotype.
17  disease with this feature after Creutzfeldt-Jakob disease, originally reported in 1920.
18 hallenge with the human kuru and Creutzfeldt-Jakob agents as well as with scrapie agent isolated from
19 ms of Alzheimer disease (AD) and Creutzfeldt-Jakob disease (CJD) are clinically distinguishable, atyp
20 (BSE) and scrapie in animals and Creutzfeldt-Jakob disease (CJD) in humans.
21 e spongiform encephalopathy, and Creutzfeldt-Jakob disease in humans.
22 eases, and arguably, scrapie and Creutzfeldt-Jakob disease prions represent the best therapeutic targ
23 as Alzheimer's, Parkinson's, and Creutzfeldt-Jakob disease share a common pathogenetic mechanism invo
24 ne spongiform encephalopathy and Creutzfeldt-Jakob disease, are usually characterized by the accumula
25 hrogenic diabetes insipidus, and Creutzfeldt-Jakob disease.
26 isease, motor neuron disease and Creutzfeldt-Jakob disease.
27 ne spongiform encephalopathy and Creutzfeldt-Jakob disease.
28 tions, including Alzheimer's and Creutzfeldt-Jakob diseases and type II diabetes.
29 itions including Alzheimer's and Creutzfeldt-Jakob diseases represent, on this basis, pathological ca
30 ng Alzheimer's, Parkinson's, and Creutzfeldt-Jakob diseases.
31 s, ataxia, dystonia, chorea, and Creutzfeldt-Jakob with and Jewish.
32 ementias such as Alzheimer's and Creutzfeldt-Jakob's disease and other central nervous system disease
33 thy (BSE; "mad cow" disease) and Creutzfeldt-Jakob's disease, appears to be a beta-sheet-rich amyloid
34 zheimer's (AD), Parkinson's, and Creutzfeldt-Jakob, and in animal diseases such as BSE.
35           Prion diseases such as Creutzfeldt-Jakob disease (CJD) are fatal, neuro-degenerative disord
36           Prion diseases such as Creutzfeldt-Jakob disease (CJD) are incurable and rapidly fatal neur
37 urodegenerative diseases such as Creutzfeldt-Jakob disease (CJD).
38 ions were initially diagnosed as Creutzfeldt-Jakob disease (CJD).
39 o various human diseases such as Creutzfeldt-Jakob disease and Gerstmann-Straussler-Scheinker syndrom
40 enesis of prion diseases such as Creutzfeldt-Jakob disease and scrapie.
41           Prion diseases such as Creutzfeldt-Jakob disease are possibly caused by the conversion of a
42     Human prion diseases such as Creutzfeldt-Jakob disease are transmissible brain proteinopathies, c
43 d both in prion diseases such as Creutzfeldt-Jakob disease, where its monomeric cellular isoform (PrP
44 ction of mice with an attenuated Creutzfeldt-Jakob disease agent (SY-CJD) interferes with superinfect
45 ents, dementia with Lewy bodies, Creutzfeldt-Jakob disease, vascular or unclassified dementia.
46 of the infectious agents causing Creutzfeldt-Jakob disease (CJD), scrapie, and bovine spongiform ence
47 stant to both kuru and classical Creutzfeldt-Jakob disease (CJD) prions (which are closely similar) b
48 o date, 1,147 cases of confirmed Creutzfeldt-Jakob disease deaths in the United Kingdom since 1990 ha
49 wo hundred individuals developed Creutzfeldt-Jakob disease (CJD) worldwide as a result of treatment,
50 cedures were applied to diagnose Creutzfeldt-Jakob disease (CJD).
51 hings was accurate in diagnosing Creutzfeldt-Jakob disease and indicated substantial prion seeding ac
52  invariably lethal prion disease Creutzfeldt-Jakob disease (CJD) and nonprion rapidly progressive dem
53  deer and elk, and Kuru disease, Creutzfeldt-Jakob disease (CJD) and variant CJD in humans.
54 ated with one of these diseases [Creutzfeldt-Jakob disease (CJD)] that was exactly analogous to a pre
55 n causes the rare human disorder Creutzfeldt-Jakob disease (CJD).
56                         Familial Creutzfeldt-Jakob disease and cerebrotendinous xanthomatosis tend to
57 al familial insomnia or familial Creutzfeldt-Jakob disease, depending upon the presence of Met or Val
58  variant, sporadic, and familial Creutzfeldt-Jakob disease, in the presence of blood components.
59 pinal fluid (CSF) biomarkers for Creutzfeldt-Jakob disease (CJD) are established and partly included
60 e shorter incubation periods for Creutzfeldt-Jakob disease (CJD) prions than mice expressing full-len
61  detects the specific marker for Creutzfeldt-Jakob disease, the prion protein (PrP(CJD)), by means of
62 rains of patients suffering from Creutzfeldt-Jakob disease and related conditions, such as Gerstmann-
63 olymorphism protects people from Creutzfeldt-Jakob disease, the Sup35p polymorphisms were selected to
64 poral lobar degeneration (FTLD), Creutzfeldt-Jakob disease (CJD), Alzheimer's disease (AD), Parkinson
65 ic GT cells infected with the FU Creutzfeldt-Jakob disease agent, but not parallel mock controls, dis
66                            Human Creutzfeldt-Jakob disease (CJD) and similar neurodegenerative diseas
67 rently less susceptible to human Creutzfeldt-Jakob disease prions.
68 , including sheep scrapie, human Creutzfeldt-Jakob disease, and cervid chronic wasting disease.
69 dotoxemia, sepsis, or iatrogenic Creutzfeldt-Jakob disease (to date, 1,147 cases of confirmed Creutzf
70 ease and in a case of iatrogenic Creutzfeldt-Jakob disease associated with growth hormone therapy.
71         Patients with iatrogenic Creutzfeldt-Jakob disease due to administration of cadaver-sourced g
72 ts who have developed iatrogenic Creutzfeldt-Jakob disease in the UK since 2003.
73 hort of patients with iatrogenic Creutzfeldt-Jakob disease in the UK suggests that there was a point
74  incubation period of iatrogenic Creutzfeldt-Jakob disease is significantly different between all thr
75 ts who have developed iatrogenic Creutzfeldt-Jakob disease, 56 have been genotyped.
76                      Importance: Creutzfeldt-Jakob disease (CJD) is a fatal neurodegenerative disorde
77 in (PrP) plays a central role in Creutzfeldt-Jakob Disease (CJD) and other transmissible spongiform e
78 xtracts demonstrated that PrP in Creutzfeldt-Jakob disease (CJD) brains is cleaved by a cellular prot
79 rts have claimed anticipation in Creutzfeldt-Jakob disease (CJD) caused by the c.598G > A mutation in
80              Previous studies in Creutzfeldt-Jakob disease (CJD) have shown that myeloid cells in the
81  (BSE) in cattle and PrP(CJD) in Creutzfeldt-Jakob disease (CJD) in humans.
82 athological diversity evident in Creutzfeldt-Jakob disease and whether different prion protein types
83 rions, such as those involved in Creutzfeldt-Jakob disease.
84 enerative diseases which include Creutzfeldt-Jakob disease (CJD) in humans and bovine spongiform ence
85 nerative conditions that include Creutzfeldt-Jakob disease (CJD) in humans and bovine spongiform ence
86 enerative disorders that include Creutzfeldt-Jakob disease in humans, scrapie in sheep and goats, and
87 ommon in the T/BG group included Creutzfeldt-Jakob disease, arbovirus, and Mycobacterium tuberculosis
88 degenerative disorders including Creutzfeldt-Jakob disease (CJD) in humans, is the conversion of the
89  neurological diseases including Creutzfeldt-Jakob disease (CJD), but the aggregation mechanisms rema
90 ion disease in humans, including Creutzfeldt-Jakob disease (CJD).
91 ans and other animals, including Creutzfeldt-Jakob disease and bovine spongiform encephalopathy.
92 egenerative conditions including Creutzfeldt-Jakob disease in humans and scrapie and bovine spongifor
93 degenerative diseases, including Creutzfeldt-Jakob disease in humans, scrapie in sheep and bovine spo
94 odegenerative diseases including Creutzfeldt-Jakob disease, motor neuron disease and Alzheimer's dise
95 sease, and 2 of 2 with inherited Creutzfeldt-Jakob disease) but were negative in 43 of 43 patients wi
96 st common human prion disease is Creutzfeldt-Jakob disease (CJD).
97 ive disorders that include Kuru, Creutzfeldt-Jakob disease, Gerstmann-Straussler-Scheinker syndrome (
98 ort from the Australian National Creutzfeldt-Jakob Disease Registry concerns a 61-year-old British-bo
99 atients referred to the National Creutzfeldt-Jakob Disease Research & Surveillance Unit during the pe
100          Heightened awareness of Creutzfeldt-Jakob disease (CJD) among physicians and the lay public
101 lthough surgical transmission of Creutzfeldt-Jakob disease (CJD) has been demonstrated, these iatroge
102 nd accurate in vivo diagnosis of Creutzfeldt-Jakob disease (CJD) is necessary for quickly distinguish
103             The sporadic form of Creutzfeldt-Jakob disease (sCJD) has been classified on the basis of
104 ince developed a variant form of Creutzfeldt-Jakob disease (vCJD), also mostly in the United Kingdom,
105  prions, the causative agents of Creutzfeldt-Jakob disease and other human prion diseases, requires p
106  candidates for the treatment of Creutzfeldt-Jakob disease and other prion diseases.
107 ective in slowing propagation of Creutzfeldt-Jakob disease prions in transgenic mice.
108 s with the E200K genetic form of Creutzfeldt-Jakob Disease, 20 healthy carriers of this mutation that
109  involved in the pathogenesis of Creutzfeldt-Jakob Disease, and its anatomical connections are suffic
110  detected early in the course of Creutzfeldt-Jakob Disease, and years before symptomatic onset in mut
111  appearance of a variant form of Creutzfeldt-Jakob disease, which has been linked to consumption of p
112 ecognized phenotypic spectrum of Creutzfeldt-Jakob disease.
113  90 to 100) for the detection of Creutzfeldt-Jakob disease.
114 owed early diagnosis of probable Creutzfeldt-Jakob disease before the characteristic clinical picture
115 luding Alzheimer's, Parkinson's, Creutzfeldt-Jakob, and Lou Gehrig's diseases, as well as the tauopat
116 uch as Alzheimer's, Parkinson's, Creutzfeldt-Jakob, and others display remarkable phenotypic heteroge
117 gates extracted from 60 sporadic Creutzfeldt-Jakob disease (CJD) and 6 variant CJD brains.
118 brains of patients with sporadic Creutzfeldt-Jakob disease (CJD) bind to very low-density (VLDL) and
119  from a large number of sporadic Creutzfeldt-Jakob disease (CJD) cases.
120                         Sporadic Creutzfeldt-Jakob disease (CJD) is the most prevalent manifestation
121  those in subjects with sporadic Creutzfeldt-Jakob disease (CJD), as well as CJD-affected subjects wh
122 n human prion disorder, sporadic Creutzfeldt-Jakob disease (CJD), in which prions are formed spontane
123 n a pregnant woman with sporadic Creutzfeldt-Jakob disease (CJD).
124 d as either familial or sporadic Creutzfeldt-Jakob disease (CJD); there was no case of variant CJD.
125 enotypes, identified as sporadic Creutzfeldt-Jakob disease (M/M2 sCJD) and sporadic fatal insomnia (s
126 are these with cases of sporadic Creutzfeldt-Jakob disease (n = 170) in the United Kingdom over the p
127 onfer susceptibility to sporadic Creutzfeldt-Jakob disease (rs1029273), all patients were homozygous
128  were suspected to have sporadic Creutzfeldt-Jakob disease (sCJD) and yet were found to have an alter
129 l fluid (CSF) tests for sporadic Creutzfeldt-Jakob disease (sCJD) are based on the detection of surro
130  (sFI) and a subtype of sporadic Creutzfeldt-Jakob disease (sCJD) identified as sCJDMM2, which share
131               A case of sporadic Creutzfeldt-Jakob disease (sCJD) is described in a young Dutch prote
132 ntiated 94% of cases of sporadic Creutzfeldt-Jakob disease (sCJD) MM1 from the sCJD MM2 phenotype, an
133 firmed the diagnosis of sporadic Creutzfeldt-Jakob disease (sCJD) MM1 subtype.
134  Sc237 prions and human sporadic Creutzfeldt-Jakob disease (sCJD) prions.
135 st common subtype being sporadic Creutzfeldt-Jakob disease (sCJD), a rapidly progressive dementia.
136 st common subtype being sporadic Creutzfeldt-Jakob disease (sCJD), a rapidly progressive dementia.
137 have been identified in sporadic Creutzfeldt-Jakob disease (sCJD), based on the methionine/valine pol
138 o patients, who died of sporadic Creutzfeldt-Jakob disease (sCJD), contained either sCJD(MM1) or sCJD
139                   Human sporadic Creutzfeldt-Jakob disease (sCJD), endemic sheep scrapie, and epidemi
140 ies present in control, sporadic Creutzfeldt-Jakob disease (sCJD), or variant CJD (vCJD) brains.
141 issue of a patient with sporadic Creutzfeldt-Jakob Disease (sCJD), the most common form of human prio
142 ces in individuals with sporadic Creutzfeldt-Jakob disease (sCJD).
143 ions from patients with sporadic Creutzfeldt-Jakob disease (sCJD).
144 ntigens misdiagnosed as sporadic Creutzfeldt-Jakob disease (sCJD).
145 as been also claimed in sporadic Creutzfeldt-Jakob disease (sCJD).
146 levels in some cases of sporadic Creutzfeldt-Jakob disease and conversely, that the form of abnormal
147 alopathies (variant and sporadic Creutzfeldt-Jakob disease and genetic forms of prion disease), patie
148 f the major subtypes of sporadic Creutzfeldt-Jakob disease and in a case of iatrogenic Creutzfeldt-Ja
149 wenty-six patients with sporadic Creutzfeldt-Jakob disease and nine age- and gender-matched healthy c
150 th and patients without sporadic Creutzfeldt-Jakob disease and tested them using RT-QuIC, an ultrasen
151 ived from patients with sporadic Creutzfeldt-Jakob disease are taken up and degraded by immortalized
152 clinically mistaken for sporadic Creutzfeldt-Jakob disease because of a negative family history.
153 tein that characterizes sporadic Creutzfeldt-Jakob disease can be found in certain brain regions of c
154 udy the white matter in sporadic Creutzfeldt-Jakob disease compared to healthy control subjects and t
155   Definite diagnosis of sporadic Creutzfeldt-Jakob disease in living patients remains a challenge.
156 pithelium in diagnosing sporadic Creutzfeldt-Jakob disease in living patients.
157                         Sporadic Creutzfeldt-Jakob disease is considered primarily a disease of grey
158                         Sporadic Creutzfeldt-Jakob disease is the most common of the human prion dise
159 ely, the data show that sporadic Creutzfeldt-Jakob disease PrP(Sc) is not a single conformational ent
160      Cases diagnosed as sporadic Creutzfeldt-Jakob disease with atypical neuropathology were also rev
161 an idiopathic disorder (sporadic Creutzfeldt-Jakob disease) or can be acquired, as is the case for va
162 (15 of 15 with definite sporadic Creutzfeldt-Jakob disease, 13 of 14 with probable sporadic Creutzfel
163  13 of 14 with probable sporadic Creutzfeldt-Jakob disease, and 2 of 2 with inherited Creutzfeldt-Jak
164 amples from humans with sporadic Creutzfeldt-Jakob disease, as well as in rodents with experimental p
165                      In sporadic Creutzfeldt-Jakob disease, disease-associated PrP(Sc) is present not
166 ALS, Alzheimer disease, sporadic Creutzfeldt-Jakob disease, Huntington disease-like syndrome, and oth
167 matter of patients with sporadic Creutzfeldt-Jakob disease, mainly in the left hemisphere, with a str
168 hin the white matter in sporadic Creutzfeldt-Jakob disease, suggesting possible primary involvement o
169 stological diagnosis of sporadic Creutzfeldt-Jakob disease.
170 on human prion disease, sporadic Creutzfeldt-Jakob disease.
171 e encephalopathies from sporadic Creutzfeldt-Jakob disease.
172  diagnostic criteria of sporadic Creutzfeldt-Jakob disease.
173 s that closely resemble sporadic Creutzfeldt-Jakob disease.
174 erited prion disease or sporadic Creutzfeldt-Jakob disease.
175 diagnostic criteria for sporadic Creutzfeldt-Jakob disease.
176 bled those of classical sporadic Creutzfeldt-Jakob disease.
177 een and within cases of sporadic Creutzfeldt-Jakob disease.
178 0% for the diagnosis of sporadic Creutzfeldt-Jakob disease.
179 ttern of involvement in sporadic Creutzfeldt-Jakob disease.
180 e total white matter in sporadic Creutzfeldt-Jakob disease.
181 sed in the diagnosis of sporadic Creutzfeldt-Jakob disease; however, the characteristic waveforms do
182 rimental, acquired, and sporadic Creutzfeldt-Jakob diseases.
183 y for PrP(TSE) after exposure to Creutzfeldt-Jakob disease brain homogenate.
184 e sheep to scrapie and humans to Creutzfeldt-Jakob disease.
185 h a mouse model of transmissible Creutzfeldt-Jakob disease (CJD), the ataxia of Tg(A116V) mice is mor
186 pathy (BSE) to humans as variant Creutzfeldt-Jakob disease (CJD) has affected over 100 individuals, a
187                          Variant Creutzfeldt-Jakob disease (CJD) is thought to be caused by dietary o
188 halopathy to people as a variant Creutzfeldt-Jakob disease (CJD), it becomes critical to identify cel
189 e from a small sample of variant Creutzfeldt-Jakob disease (CJD).
190  prions from humans with variant Creutzfeldt-Jakob disease (CJD); on second passage in Tg(BoPrP) mice
191  autopsy-proved cases of variant Creutzfeldt-Jakob disease (n = 59) and compare these with cases of s
192 rP(Sc) molecular type in variant Creutzfeldt-Jakob disease (termed type 2B), presumably resulting fro
193                          Variant Creutzfeldt-Jakob disease (vCJD) and bovine spongiform encephalopath
194 rodegenerative condition variant Creutzfeldt-Jakob disease (vCJD) and, based on recent human prevalen
195  a prototype blood-based variant Creutzfeldt-Jakob disease (vCJD) assay has sufficient sensitivity an
196 m, a deceased carrier of variant Creutzfeldt-Jakob disease (vCJD) can be followed up to quantify tran
197  of the rising number of variant Creutzfeldt-Jakob disease (vCJD) cases.
198                          Variant Creutzfeldt-Jakob disease (vCJD) differs from other human prion dise
199                          Variant Creutzfeldt-Jakob disease (vCJD) has a pathogenesis distinct from ot
200                          Variant Creutzfeldt-Jakob disease (vCJD) has been recognized to date only in
201 o-person transmission of variant Creutzfeldt-Jakob disease (vCJD) has occurred through blood transfus
202          Infections with variant Creutzfeldt-Jakob disease (vCJD) have almost exclusively occurred in
203  number of patients with variant Creutzfeldt-Jakob disease (vCJD) have been treated with intraventicu
204 rt a case of preclinical variant Creutzfeldt-Jakob disease (vCJD) in a patient who died from a non-ne
205  to be zoonotic, causing variant Creutzfeldt-Jakob disease (vCJD) in humans and having guided protect
206  the current outbreak of variant Creutzfeldt-Jakob disease (vCJD) in the United Kingdom, because all
207       The development of variant Creutzfeldt-Jakob disease (vCJD) in three recipients of non-leukored
208 uman exposure levels and variant Creutzfeldt-Jakob disease (vCJD) incidence.
209                          Variant Creutzfeldt-Jakob disease (vCJD) is a fatal neurodegenerative disord
210                          Variant Creutzfeldt-Jakob disease (vCJD) is a fatal neurodegenerative disord
211                          Variant Creutzfeldt-Jakob disease (vCJD) is a novel human prion disease caus
212                          Variant Creutzfeldt-Jakob disease (vCJD) is a unique and highly distinctive
213  clinical expression of, variant Creutzfeldt-Jakob disease (vCJD) is essential for future management
214 ns have been raised that variant Creutzfeldt-Jakob disease (vCJD) might be transmissible by blood tra
215 n in the distribution of variant Creutzfeldt-Jakob disease (vCJD) might indicate the transmission rou
216 prion-affected patients (variant Creutzfeldt-Jakob disease (vCJD) n = 20, iatrogenic CJD (iCJD) n = 1
217 encephalopathy (BSE) and variant Creutzfeldt-Jakob disease (vCJD) prions are faithfully maintained up
218      The transmission of variant Creutzfeldt-Jakob disease (vCJD) through blood transfusions has crea
219 voir for transmission of variant Creutzfeldt-Jakob disease (vCJD) to humans.
220          Interindividual variant Creutzfeldt-Jakob disease (vCJD) transmission through blood and bloo
221 ern since the reports of variant Creutzfeldt-Jakob disease (vCJD) transmission through blood transfus
222 possible transmission of variant Creutzfeldt-Jakob disease (vCJD) via blood transfusion has caused co
223 the risk of transmitting variant Creutzfeldt-Jakob disease (vCJD) via blood transfusion have relied l
224                          Variant Creutzfeldt-Jakob disease (vCJD) was first described in the United K
225                          Variant Creutzfeldt-Jakob Disease (vCJD) was first reported in 1996; the you
226                          Variant Creutzfeldt-Jakob disease (vCJD), a novel form of human prion diseas
227             The onset of variant Creutzfeldt-Jakob disease (vCJD), and the unknown prevalence of infe
228 nd its human equivalent, variant Creutzfeldt-Jakob disease (vCJD), are caused by the same strain of i
229 cribed in cases of human variant Creutzfeldt-Jakob disease (vCJD), experimental ovine bovine spongifo
230 orm encephalopathy (BSE)/variant Creutzfeldt-Jakob disease (vCJD), Nipah virus, several viral hemorrh
231 tissues of patients with variant Creutzfeldt-Jakob disease (vCJD), sheep with natural scrapie or rode
232 ons, the causal agent of variant Creutzfeldt-Jakob disease (vCJD).
233  profile associated with variant Creutzfeldt-Jakob disease (vCJD).
234 cally silent carriers of variant Creutzfeldt-Jakob disease (vCJD).
235 vidual can propagate the variant Creutzfeldt-Jakob disease agent and that the infectious agent can be
236 ated transmission of the variant Creutzfeldt-Jakob disease agent.
237 umulates in the brain in variant Creutzfeldt-Jakob disease also contains a minority type 1 component.
238 -mortem samples, of both variant Creutzfeldt-Jakob disease and Alzheimer's disease patients, also sug
239 odegenerative conditions variant Creutzfeldt-Jakob disease and Alzheimer's disease.
240 o subsequently developed variant Creutzfeldt-Jakob disease and an asymptomatic red cell transfusion r
241 e urine of patients with variant Creutzfeldt-Jakob disease and had the typical electrophoretic profil
242 ained from patients with variant Creutzfeldt-Jakob disease and in none of the 224 urine samples obtai
243 on of 10% (wt/vol) human variant Creutzfeldt-Jakob disease brain homogenate, with >3,800-fold binding
244 nsfusion-transmission of variant Creutzfeldt-Jakob disease by red cell preparations.
245 iew, the transmission of variant Creutzfeldt-Jakob disease by transfusion has been confirmed.
246  against transmission of variant Creutzfeldt-Jakob disease by transfusion of domestic blood or red bl
247     Recent evidence that variant Creutzfeldt-Jakob disease can be transmitted by transfusion of red c
248  were followed-up in six variant Creutzfeldt-Jakob disease cases with 9.4 T high-resolution magnetiza
249  from a UK cohort of 171 variant Creutzfeldt-Jakob disease cases.
250 ained from patients with variant Creutzfeldt-Jakob disease contained minute quantities of PrP(Sc).
251 culation analysis of the variant Creutzfeldt-Jakob disease epidemic in the United Kingdom is used to
252  The recent emergence of variant Creutzfeldt-Jakob disease has led to major public health concerns, a
253      The outbreak of new variant Creutzfeldt-Jakob disease has raised the specter of a potentially la
254           Three cases of variant Creutzfeldt-Jakob disease have been identified following red cell tr
255 te and probable cases of variant Creutzfeldt-Jakob disease have been methionine homozygotes (MM).
256  scrapie in sheep and of variant Creutzfeldt-Jakob disease in humans.
257 dividuals diagnosed with variant Creutzfeldt-Jakob disease in the USA and Canada.
258 t numbers of subclinical variant Creutzfeldt-Jakob disease individuals in at least the United Kingdom
259 idence of any death from variant Creutzfeldt-Jakob disease or from conditions that could be confused
260 ents for transmission of variant Creutzfeldt-Jakob disease predicted that leukocyte reduction would b
261   Evidence suggests that variant Creutzfeldt-Jakob disease prions circulate in body fluids from peopl
262 found in all 21 cases of variant Creutzfeldt-Jakob disease tested, irrespective of brain region exami
263  results show PrP(Sc) in variant Creutzfeldt-Jakob disease to be remarkably stereotyped.
264  was also present in the variant Creutzfeldt-Jakob disease tonsil.
265          Transmission of variant Creutzfeldt-Jakob disease was observed from the MV blood recipient s
266 ypes was maintained when variant Creutzfeldt-Jakob disease was transmitted to wild-type mice and was
267      We report a case of variant Creutzfeldt-Jakob disease(vCJD) in a 74-year old man in whom diagnos
268 d animals, one of which (variant Creutzfeldt-Jakob disease) is known to be a zoonotic form of the cat
269 ncephalopathies, such as variant Creutzfeldt-Jakob disease, are believed to result from infectious fo
270 is a defining feature of variant Creutzfeldt-Jakob disease, but that the biochemical isoform of PrP(S
271 an effort to prevent new variant Creutzfeldt-Jakob disease, certain "specified offals," including neu
272 ient, who did not die of variant Creutzfeldt-Jakob disease, has been identified with prion protein de
273  transmission studies in variant Creutzfeldt-Jakob disease, including those on the spleen and brain o
274 red human prion disease, variant Creutzfeldt-Jakob disease, is thought to result from oral exposure t
275                       In variant Creutzfeldt-Jakob disease, prion replication is thought to occur fir
276 n humans associated with variant Creutzfeldt-Jakob disease, pulls the N terminus into the sheet.
277 e urine of patients with variant Creutzfeldt-Jakob disease, we used the protein misfolding cyclic amp
278 f mid-2016, 231 cases of variant Creutzfeldt-Jakob disease-the human form of a prion disease of cattl
279 to-human transmission of variant Creutzfeldt-Jakob disease.
280 sporadic, iatrogenic and variant Creutzfeldt-Jakob disease.
281 ote to both sporadic and variant Creutzfeldt-Jakob disease.
282 ired, as is the case for variant Creutzfeldt-Jakob disease.
283  series of nine cases of variant Creutzfeldt-Jakob disease.
284 respiratory syndrome, or variant Creutzfeldt-Jakob disease.
285  (BSE) prions causes new variant Creutzfeldt-Jakob disease.
286 affected by sporadic and variant Creutzfeldt-Jakob disease.
287 rus, enterovirus 70, and variant Creutzfeldt-Jakob disease.
288 humans were diagnosed as variant Creutzfeldt-Jakob disease.
289 ations are applicable to variant Creutzfeldt-Jakob in humans then a method for rendering human red ce
290 probable transmission of variant Creutzfeldt-Jakob infectivity by transfusion of red cell preparation
291 anding of the risks of (variant) Creutzfeldt-Jakob disease transmission via dental practice, and whet
292  successfully propagated various Creutzfeldt-Jakob disease (CJD) isolates (sporadic, variant, and iat
293 sitive in 30 of 31 patients with Creutzfeldt-Jakob disease (15 of 15 with definite sporadic Creutzfel
294 erks develop in individuals with Creutzfeldt-Jakob disease (CJD), an incurable brain disorder caused
295 en exposed to medium spiked with Creutzfeldt-Jakob disease brain homogenate, resulting in a coarse gr
296 mone derived from a patient with Creutzfeldt-Jakob disease expressing prion protein valine 129.
297 NS) in five of six patients with Creutzfeldt-Jakob disease.
298 ive in 43 of 43 patients without Creutzfeldt-Jakob disease, indicating a sensitivity of 97% (95% conf
299 traussler syndrome and hereditary Creuzfeldt-Jakob disease, tau mutations cause autosomal dominant fr
300  was shown to have pathology-proven sporadic Jakob-Creutzfeldt disease.

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