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1 BSE prions were found in the sympathetic nervous system
2 BSE was transmitted to the bovine line but did not trans
3 BSE-C causes the fatal prion disease named new variant C
4 Western blotting consistently detected 50% BSE within a mixture, but at higher dilutions it had var
6 6(+/-) mice challenged with red deer-adapted BSE resulted in 90% to 100% attack rates, and BSE from c
8 his sPMCA-based assay specifically amplified BSE PrP(Sc) within brain mixes with 100% specificity and
10 studies revealed the following: (i) CWD and BSE seeded their homologous species' PrP best; (ii) fCWD
12 erence of ~0.3 per mille between bulk EC and BSE has been used to argue against any major contributio
13 encephalopathy (BASE, also named BSE-L) and BSE-H, have been discovered in several countries since 2
14 SE resulted in 90% to 100% attack rates, and BSE from cattle failed to transmit, indicating agent ada
19 into three strains: classic BSE and atypical BSEs (H and L types) that have shorter incubation period
22 within defined CNS regions, compared between BSE and scrapie cases and also between two experimental
24 ) with the RT-QuIC assay and found that both BSE forms can be detected and distinguished using partic
25 human deaths considering exposure to bovine BSE alone, with the upper bound increasing to 150,000 on
26 for the presence of human (vCJD) and bovine (BSE) prions in a human cell therapy product candidate.
28 action products indicated that H-, L-, and C-BSE have distinctive prion seeding activities and can be
31 ested brain tissue from cattle affected by C-BSE and atypical L-type bovine spongiform encephalopathy
32 , experimental transmissions of classical (C-BSE) and atypical (L-BSE) forms of BSE in goats were als
33 lassical bovine spongiform encephalopathy (C-BSE) and the atypical H-type BSE (H-BSE) and L-type BSE
34 lassical bovine spongiform encephalopathy (c-BSE) is the only animal prion disease reputed to be zoon
36 public health perspective, the presence of c-BSE in AS isolates suggest that cattle exposure to small
37 tent with the emergence and replication of c-BSE prions during the in vivo propagation of AS isolates
43 amplified small amounts of ovine and caprine BSE agent which had been mixed into a range of scrapie-p
44 variable with respect to the original cattle BSE prion, suggesting that the naturally low susceptibil
45 have been exposed to BSE early in the cattle BSE epidemic and that serial BSE transmission in sheep m
47 L-BSE agent differs from both ovine classic BSE or CH1641 scrapie maintaining its specific strain pr
49 an be subdivided into three strains: classic BSE and atypical BSEs (H and L types) that have shorter
54 ensitive assays that can specifically detect BSE, even within the presence of scrapie prion protein,
55 t assay (ELISA) method consistently detected BSE only when it was present as 99% of the mixture, with
57 apts to a new species more readily than does BSE and (ii) the barrier preventing transmission of CWD
58 stics of the in vitro-adapted rabbit and dog BSE agent remained invariable with respect to the origin
59 opic resemblance to the bulk silicate Earth (BSE) for many elements, but is considered highly deplete
60 ies suggesting that the bulk silicate Earth (BSE) might have an Sm/Nd ratio 6% higher than chondrites
63 cells, referred to as the bystander effect (BSE), is not well understood in terms of the underlying
65 reduced behavioral (HIC) and electrographic (BSE) signs of seizure activity in a dose-related fashion
66 In conjunction with backscattered electron (BSE) and energy-dispersive spectroscopy (EDS) mapping of
67 ample surface, and a backscattered electron (BSE) detector, used to image the milled surfaces, genera
68 on film has very low backscattered electron (BSE) yield compared to that from the particle, so in the
69 roach that detected backscattered electrons (BSEs) and X-rays (from ionization processes) along a lar
72 f vCJD and bovine spongiform encephalopathy (BSE) and an assessment of the effect of the codon-129 po
74 ackwash of bovine spongiform encephalopathy (BSE) and foot-and-mouth disease (FMD), and the advent of
76 at include bovine spongiform encephalopathy (BSE) and scrapie in animals and Creutzfeldt-Jakob diseas
78 perties of bovine spongiform encephalopathy (BSE) and variant Creutzfeldt-Jakob disease (vCJD) prions
79 ected with bovine spongiform encephalopathy (BSE) appear to be a reservoir for transmission of varian
80 d epidemic bovine spongiform encephalopathy (BSE) are caused by a related group of infectious agents.
81 utbreak of bovine spongiform encephalopathy (BSE) arose in the United Kingdom as a result of prions e
83 ental oral bovine spongiform encephalopathy (BSE) challenge study was performed to elucidate the rout
86 n from the bovine spongiform encephalopathy (BSE) epidemic, led to concerns about the potential risk
87 after the bovine spongiform encephalopathy (BSE) epidemic, when >200 cases of prion disease in human
89 rP(BSE) in bovine spongiform encephalopathy (BSE) in cattle and PrP(CJD) in Creutzfeldt-Jakob disease
90 ervids and bovine spongiform encephalopathy (BSE) in cattle are prion diseases that are caused by the
91 in sheep, bovine spongiform encephalopathy (BSE) in cattle, chronic wasting disease in deer and elk,
92 illance of bovine spongiform encephalopathy (BSE) indicates that cattle are susceptible to both class
98 ith either bovine spongiform encephalopathy (BSE) or variant CJD prions, may develop the neuropatholo
99 (vCJD) and bovine spongiform encephalopathy (BSE) prions are two of the prion strains most relevant t
100 ected with bovine spongiform encephalopathy (BSE) prions causes new variant Creutzfeldt-Jakob disease
101 t to which bovine spongiform encephalopathy (BSE) prions have been transmitted to humans, as a result
102 xposure to bovine spongiform encephalopathy (BSE) prions in the UK, has led to renewed interest in ku
105 ibility to bovine spongiform encephalopathy (BSE) prions, the causal agent of variant Creutzfeldt-Jak
106 6(+/-), to bovine spongiform encephalopathy (BSE) prions, which have the ability to overcome species
109 mission of bovine spongiform encephalopathy (BSE) to humans as variant Creutzfeldt-Jakob disease (CJD
111 in whether bovine spongiform encephalopathy (BSE) was transmitted to sheep in the past via feed suppl
112 ntal ovine bovine spongiform encephalopathy (BSE), and natural sheep scrapie, demonstrating that bloo
114 ected with bovine spongiform encephalopathy (BSE), we examined the extent of a putative epidemic.
116 d the same bovine spongiform encephalopathy (BSE)-contaminated meat and bone meal that was fed to cat
121 patitis C, bovine spongiform encephalopathy (BSE)/variant Creutzfeldt-Jakob disease (vCJD), Nipah vir
122 eases like bovine spongiform encephalopathy (BSE; "mad cow" disease) and Creutzfeldt-Jakob's disease,
124 ch actin filament has a basal strain energy (BSE) when the cell adheres to the substrate without stre
125 01 treatment conditions resulted in enhanced BSE activity during the entire fourth (untreated) withdr
128 its natural source, broccoli sprout extract (BSE) by gavage every other day for 3 months, with four g
129 -25 score at week 52 for better-seeing eyes (BSEs) and worse-seeing eyes (WSEs) also was evaluated.
130 bovine than feline rPrP; (iv) and CWD, fCWD, BSE, and FSE all converted human rPrP, although not as e
131 ies, we studied feline CWD (fCWD) and feline BSE (i.e., feline spongiform encephalopathy [FSE]).
132 w; however, a simple model of flock-to-flock BSE transmission shows that horizontal transmission, if
133 Unlike in rodents and ruminants, foodborne BSE-associated prions entered the simian CNS via afferen
135 osmium tetroxide/potassium ferricyanide, for BSE imaging, for the preparation and platinum deposition
140 as able to discriminate between PrP(Sc) from BSE-infected cattle and Tg(BoPrP) mice as well as from c
142 hs, with four groups: vehicle (0.1 ml/10 g), BSE-low dose (estimated SFN availability at 0.5 mg/kg),
143 esults demonstrate that transmission of goat BSE is genotype dependent, and they highlight the pivota
144 distribution in Europe and suggest that goat BSE could be reliably discriminated from a wide range of
145 genotypes were orally inoculated with a goat-BSE isolate to assess their relative susceptibility to B
146 d on the GW plus Bethe-Salpeter equation (GW-BSE) approach of many-body perturbation theory (MBPT) is
147 sed on a GW plus Bethe-Salpeter equation (GW-BSE) approach, which employed many-body Green's-function
153 Here, we demonstrate an RT-QuIC assay for H-BSE that can detect as little as 10(-9) dilutions of bra
154 as yet been described for the detection of H-BSE or the discrimination of each of the major bovine pr
156 review the likelihood that any UK sheep have BSE, how they might have got it, how a case could be ide
157 samples were tested with the IDEXX HerdChek BSE-Scrapie Ag Kit to detect the abnormal prion protein,
160 hods as listed in the regulation to identify BSE in a blinded series of brain samples, in which ovine
163 the UK has been threatened with slaughter if BSE is found in farmed sheep, largely on the grounds tha
164 However, the results also suggest that if BSE in sheep were to come to resemble scrapie it would l
165 rapolation from our results suggests that if BSE were to infect sheep in the field it may, with time
167 on-ruminant PAPs for avoiding an increase in BSE incidents, these methods are fit for monitoring non-
168 st reliable surrogate marker of infection in BSE-contaminated food, crosses the human intestinal epit
170 signature able to distinguish intracranially BSE-infected macaques from healthy ones, with SERPINA3 s
173 e (estimated SFN availability at 0.5 mg/kg), BSE-high dose (estimated SFN availability at 1.0 mg/kg),
178 SE transmitted similarly to cattle-derived L-BSE, with respect to survival periods, histopathology, a
179 g L-type bovine spongiform encephalopathy (L-BSE), although RQ171 sheep specifically propagated a dis
182 e spongiform encephalopathy (L-type BSE or L-BSE) with the RT-QuIC assay and found that both BSE form
183 ogical properties of QQ171 and RQ171 ovine L-BSE prions were investigated in transgenic mice expressi
188 of ovine PrP transgenic mice infected with L-BSE from RQ171 sheep at first passage, reminiscent, in l
189 hy techniques) were unveiled in detail by LF BSE images and in calcium and phosphorus elemental maps
191 spongiform encephalopathy (BASE, also named BSE-L) and BSE-H, have been discovered in several countr
196 s ill-defined, thus limiting the accuracy of BSE surveillance and spreading fear that BSE might lurk
197 strong evidence that the causative agent of BSE in cattle and vCJD in humans share a common origin.
198 assay based on the specific amplification of BSE PrP(Sc) using the serial protein misfolding cyclic a
199 redicts that fewer than 20 clinical cases of BSE in sheep would be expected in 2001 if maternal trans
200 Despite intensive surveillance for cases of BSE within the small ruminant populations of the United
201 pidemic peak in 1990, the number of cases of BSE-infected sheep would have ranged from fewer than 10
202 e super-chondritic Si isotope composition of BSE does not reflect the sole consequence of high temper
206 , largely on the grounds that an epidemic of BSE in sheep could be harder to contain than was the cas
211 Kingdom and European Union, no instances of BSE have been detected in sheep, and in only two instanc
212 of exposure to infected feed, and number of BSE-susceptible sheep in the United Kingdom showed that
213 To determine if the incubation periods of BSE and vCJD prions could be shortened, we generated tra
215 in Tg mice supports the rapid propagation of BSE and vCJD prions and suggest that Tg(GPPrP) mice may
216 chemical and neuropathological properties of BSE and vCJD prions, including the presence of type 2 pr
218 hat the present-day (143)Nd/(144)Nd ratio of BSE is similar to that of some deep mantle plumes rather
219 ited Kingdom would have been at high risk of BSE infection only if neonatal animals had inadvertently
220 d the implications of different scenarios of BSE spread in sheep for relative human exposure levels a
222 increase the danger of additional spread of BSE or vCJD infection by contaminated blood, surgical in
223 r results decipher the centripetal spread of BSE prions along the autonomic nervous system to the cen
225 inary data demonstrating the transmission of BSE and natural scrapie by blood transfusion in sheep.
228 ever, primary and secondary transmissions of BSE and vCJD in guinea pigs result in long incubation pe
229 esized that low r(be) due to the presence of BSEs would increase the rate of stomatal opening (V) dur
232 then ongoing public health risks from ovine BSE are likely to be greater than those from cattle, but
233 n become infectious at early stages of ovine BSE infection and that the PrP(d) immunohistochemical ph
234 nded series of brain samples, in which ovine BSE and distinct isolates of scrapie are mixed at variou
235 ies of bovine-derived and Tg(BoPrP)-passaged BSE prions were similar, the stability of sheep scrapie
237 indicated that PrP(263K), PrP(CWD), and PrP(BSE) were reduced by at least 2 log10, 1-2 log10, and 1
238 l cellular prion protein PrP(C), such as PrP(BSE) in bovine spongiform encephalopathy (BSE) in cattle
239 ), and bovine spongiform encephalopathy (PrP(BSE)) in lab-scale composters and PrP(263K) in field-sca
240 strain like the one described here; rather, BSE prions may have arisen spontaneously in a cow or by
243 kedly influences infection by sheep scrapie, BSE, mouse-adapted scrapie, deer chronic wasting disease
244 y in the cattle BSE epidemic and that serial BSE transmission in sheep might have resulted in adaptat
248 the thermostability of three prion strains (BSE, RML and 22L) that were heated at 98 degrees C for 2
250 ory, with three related hypotheses: (1) that BSE was acquired from a human TSE (prion disease); (2) t
256 tus and their ecological correlates and that BSEs play several key roles in the functional ecology of
262 ie prions was higher than that found for the BSE prions but lower if the scrapie prions were passaged
263 ompared to that from the particle, so in the BSE mode the particle image is seen with very high contr
264 xchange (SCE) frequencies as a marker of the BSE, we performed cell transfer strategies that enabled
266 that was fed to cattle and precipitated the BSE epidemic in the United Kingdom that peaked more than
267 tle and the continental crust shows that the BSE, reconstructed using the depleted mantle and contine
271 arise after exposure of humans or animals to BSE, this could markedly increase the danger of addition
273 pleted in many volatile elements compared to BSE due to high-temperature volatile loss from Moon-form
274 Kingdom sheep flock may have been exposed to BSE early in the cattle BSE epidemic and that serial BSE
276 al evidence that it is caused by exposure to BSE has highlighted the need to understand the molecular
280 attle, dose responses of cattle and sheep to BSE, levels of exposure to infected feed, and number of
287 ype bovine spongiform encephalopathy (L-type BSE or L-BSE) with the RT-QuIC assay and found that both
289 th 100% specificity and 97% sensitivity when BSE agent was diluted into scrapie-infected brain homoge
291 ivity loss), followed by 22L (5 log10) while BSE was the most thermostable strain with low or null in
292 Similarly, improvements in patients whose BSE and WSE were treated were 7.74 (SD, 13.59) and 5.48
294 United Kingdom could have been infected with BSE by being fed contaminated meat and bone meal supplem
296 ion from donors experimentally infected with BSE; these were either clinically or subclinically affec
298 , primary and secondary human infection with BSE-derived prions may result in sporadic CJD-like or no