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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
5  of these allegedly resistant species into a BSE-type prion protein.
6 6(+/-) mice challenged with red deer-adapted BSE resulted in 90% to 100% attack rates, and BSE from c
7  propagation of distinct prion strains after BSE prion infection.
8 his sPMCA-based assay specifically amplified BSE PrP(Sc) within brain mixes with 100% specificity and
9                             Sporadic CJD and BSE agents and representative scrapie agents were clearl
10  studies revealed the following: (i) CWD and BSE seeded their homologous species' PrP best; (ii) fCWD
11 nces between the species barriers of CWD and BSE.
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
15 on protein are fully susceptible to vCJD and BSE prions but not to sporadic CJD prions.
16 nd found it to be PMCA-negative for vCJD and BSE prions.
17 zfeldt-Jakob, and in animal diseases such as BSE.
18                                 Two atypical BSE strains, bovine amyloidotic spongiform encephalopath
19 into three strains: classic BSE and atypical BSEs (H and L types) that have shorter incubation period
20                 We demonstrate that atypical BSEs present with increased prion protein accumulation,
21                   This was primarily because BSE prions were found to be transmissible to humans.
22 within defined CNS regions, compared between BSE and scrapie cases and also between two experimental
23                                         Both BSE and SFN significantly prevented diabetes-induced car
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.
27                                            C-BSE prion seeding activity was also detected in brain ti
28 action products indicated that H-, L-, and C-BSE have distinctive prion seeding activities and can be
29 d in the propagation of the classical BSE (c-BSE) agent.
30 tle are susceptible to both classical BSE (C-BSE) and atypical forms of BSE.
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
35 nfected with scrapie or bovine isolates of C-BSE and L-BSE, respectively.
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
38  products could lead to new occurrences of c-BSE.
39              These data also indicate that c-BSE prions, a known zonotic agent in humans, can emerge
40 (PMCA) demonstrated that low levels of the c-BSE agent were present in the original AS isolates.
41 c potential of scrapie might be similar to c-BSE.
42 d using multiple rPrPSen substrates, while C-BSE was much more selective.
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
46 hat allowed us to distinguish prions causing BSE from those causing scrapie.
47  L-BSE agent differs from both ovine classic BSE or CH1641 scrapie maintaining its specific strain pr
48 ropism, clearly differing from ovine classic BSE or from scrapie strain CH1641.
49 an be subdivided into three strains: classic BSE and atypical BSEs (H and L types) that have shorter
50 hat cattle are susceptible to both classical BSE (C-BSE) and atypical forms of BSE.
51 resulted in the propagation of the classical BSE (c-BSE) agent.
52 bit and dog brain homogenates with classical BSE were studied.
53                    The incidence of clinical BSE disease after inoculation was high in unweaned lambs
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
56            It may be possible to distinguish BSE prions from scrapie strains in sheep by combining co
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
61                     The bulk silicate Earth (BSE), and all its sampleable reservoirs, have a subchond
62 ith terrestrial mantle (Bulk Silicate Earth, BSE) for numerous isotope systematics.
63  cells, referred to as the bystander effect (BSE), is not well understood in terms of the underlying
64            For all these preventive effects, BSE at high dose provided a similar effect as did SFN.
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
70  natural bovine spongiform encephalopathies (BSE) have been reported in goats.
71 sed to the bovine spongiform encephalopathy (BSE) agent.
72 f vCJD and bovine spongiform encephalopathy (BSE) and an assessment of the effect of the codon-129 po
73 on between bovine spongiform encephalopathy (BSE) and bovine PRNP exon 3 has not been detected.
74 ackwash of bovine spongiform encephalopathy (BSE) and foot-and-mouth disease (FMD), and the advent of
75            Bovine spongiform encephalopathy (BSE) and its human equivalent, variant Creutzfeldt-Jakob
76 at include bovine spongiform encephalopathy (BSE) and scrapie in animals and Creutzfeldt-Jakob diseas
77 humans and bovine spongiform encephalopathy (BSE) and scrapie in animals.
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
82 exposed to bovine spongiform encephalopathy (BSE) by consumption of BSE-infected beef.
83 ental oral bovine spongiform encephalopathy (BSE) challenge study was performed to elucidate the rout
84  since the bovine spongiform encephalopathy (BSE) crisis, their use has been strictly regulated.
85  since the bovine spongiform encephalopathy (BSE) crisis.
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
88 ntal sheep bovine spongiform encephalopathy (BSE) from classical scrapie.
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
93         In bovine spongiform encephalopathy (BSE) infection, the polymorphism effect is quite differe
94            Bovine spongiform encephalopathy (BSE) is a transmissible spongiform encephalopathy (TSE)
95            Bovine spongiform encephalopathy (BSE) is a TSE that occurs in cattle and can be subdivide
96            Bovine Spongiform Encephalopathy (BSE) is the only animal prion which has been recognized
97 fy them as bovine spongiform encephalopathy (BSE) or non-BSE.
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
103            Bovine spongiform encephalopathy (BSE) prions were responsible for an unforeseen epizootic
104  propagate bovine spongiform encephalopathy (BSE) prions without posing a transmission barrier.
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
107 xposure to bovine spongiform encephalopathy (BSE) prions.
108 r cases of bovine spongiform encephalopathy (BSE) remains an enigma.
109 mission of bovine spongiform encephalopathy (BSE) to humans as variant Creutzfeldt-Jakob disease (CJD
110  effect on bovine spongiform encephalopathy (BSE) transmission to goats is not clear.
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
113            Bovine spongiform encephalopathy (BSE), the prion disease in cattle, was widely believed t
114 ected with bovine spongiform encephalopathy (BSE), we examined the extent of a putative epidemic.
115            Bovine spongiform encephalopathy (BSE)-associated prions were preferentially transported f
116 d the same bovine spongiform encephalopathy (BSE)-contaminated meat and bone meal that was fed to cat
117 umption of bovine spongiform encephalopathy (BSE)-contaminated meat.
118 ction with bovine spongiform encephalopathy (BSE)-like prions.
119 le disease bovine spongiform encephalopathy (BSE).
120 e agent of bovine spongiform encephalopathy (BSE).
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,
123 om cattle (bovine spongiform encephalopathy [BSE]), both PrP variants occur in equal ratios.
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
126  EEG (high-voltage "brief spindle episodes" (BSE)) activity.
127                    Bundle sheath extensions (BSEs) are key features of leaf structure with currently
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
134 transmission rates by transfusion of 36% for BSE and 43% for scrapie.
135 osmium tetroxide/potassium ferricyanide, for BSE imaging, for the preparation and platinum deposition
136 smission rate higher than those reported for BSE-C.
137            In asymptomatic animals, we found BSE in 50% and 12% of gut- and tonsil-derived samples, r
138 sporadic CJD may have a disease arising from BSE exposure.
139 type PrP fractions in PrP(res) material from BSE-infected ARR/VRQ sheep.
140 as able to discriminate between PrP(Sc) from BSE-infected cattle and Tg(BoPrP) mice as well as from c
141               High-definition LF images from BSEs and X-rays were essentially generated by assembling
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
148 mputed by the GW-Bethe-Salpeter equation (GW-BSE) method.
149 red with ab initio calculations using the GW-BSE approach.
150 ly used Tamm-Dancoff approximation to the GW-BSE approach.
151                       In combination with GW-BSE theory, we prove that the excitons are of Wannier ty
152 pathy (C-BSE) and the atypical H-type BSE (H-BSE) and L-type BSE (L-BSE) strains.
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
155 cted in sheep, and in only two instances has BSE been discovered in goats.
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,
158                       Surprisingly, however, BSE transmission to these transgenic mice, in addition t
159 o goats raised the need to reliably identify BSE in small ruminants.
160 hods as listed in the regulation to identify BSE in a blinded series of brain samples, in which ovine
161                         However, identifying BSE in a sheep is not straightforward, because of its si
162                                           If BSE is present within the small ruminant populations, it
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
166                        Here we show that, if BSE entered the sheep population and a degree of transmi
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
169                                  PrP(res) in BSE contained equimolar amounts of VRQ- and ARR-PrP, whi
170 signature able to distinguish intracranially BSE-infected macaques from healthy ones, with SERPINA3 s
171 sion phases identified by CT and by invasive BSE-SEM is demonstrated.
172                                 The new U.K. BSE agent spread to many species, including humans, and
173 e (estimated SFN availability at 0.5 mg/kg), BSE-high dose (estimated SFN availability at 1.0 mg/kg),
174                        Although the C- and L-BSE strains can be detected and discriminated by ultrase
175 th scrapie or bovine isolates of C-BSE and L-BSE, respectively.
176 issions of classical (C-BSE) and atypical (L-BSE) forms of BSE in goats were also reported.
177 typical H-type BSE (H-BSE) and L-type BSE (L-BSE) strains.
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
180 t PrP fragment (HMM PrPres), distinct from L-BSE in QQ171 sheep.
181           Next, CSF samples collected from L-BSE infected goats during pre-symptomatic stage were als
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
184                 In both mouse lines, ovine L-BSE transmitted similarly to cattle-derived L-BSE, with
185                                        PrP(L-BSE) associated seeding activity was detected at early t
186                              Specifically, L-BSE was detected using multiple rPrPSen substrates, whil
187                                        The L-BSE agent differs from both ovine classic BSE or CH1641
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
190                             Mechanistically, BSE, like SFN, significantly up-regulated Nrf2 transcrip
191  spongiform encephalopathy (BASE, also named BSE-L) and BSE-H, have been discovered in several countr
192 ovine spongiform encephalopathy (BSE) or non-BSE.
193 iple human and animal prion diseases but not BSE.
194              Since 2005, naturally occurring BSE has been identified in two goats.
195 lely to determine the presence or absence of BSE.
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
203 iform encephalopathy (BSE) by consumption of BSE-infected beef.
204 exposed to the infectivity by consumption of BSE-infected beef.
205           In the present study, low doses of BSE were fed to lambs of a range of ages (~24 h, 2 to 3
206 , largely on the grounds that an epidemic of BSE in sheep could be harder to contain than was the cas
207                            Atypical forms of BSE appear to be sporadic and thus may never be eradicat
208 ssical (C-BSE) and atypical (L-BSE) forms of BSE in goats were also reported.
209  classical BSE (C-BSE) and atypical forms of BSE.
210                        The identification of BSE in two goats raised the need to reliably identify BS
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
214 A also consistently detected the presence of BSE in mixtures at 0.1%.
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
217                              A proportion of BSE-infected transfusion recipients (3 of 8) survived fo
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
221         Although the elevated delta(30)Si of BSE compared to chondrites is consistent with earlier co
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
224 pie-infected sheep was compared with that of BSE-infected sheep with a similar genotype.
225 inary data demonstrating the transmission of BSE and natural scrapie by blood transfusion in sheep.
226                              Transmission of BSE to human beings is probably restricted by the presen
227  persistence of a barrier to transmission of BSE-derived prions on subpassage.
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
230        These data suggest that more than one BSE-derived prion strain might infect humans; it is ther
231 e include exposure from the worst-case ovine BSE scenario examined.
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
236 ovine or human prion protein for propagating BSE and vCJD prions.
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
241                  Bioassay and sPMCA reported BSE in all samples where it was present, down to 1%.
242 ly practical and sensitive tests for routine BSE detection and strain discrimination.
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
245 g/Si = ~1.01) and closer to BSE (delta(30)Si(BSE) = -0.29 +/- 0.08 per mille).
246 etection and discrimination of at least some BSE forms.
247 ly believed to be caused by only one strain, BSE-C.
248  the thermostability of three prion strains (BSE, RML and 22L) that were heated at 98 degrees C for 2
249 fe expectancy, although fourfold longer than BSE.
250 ory, with three related hypotheses: (1) that BSE was acquired from a human TSE (prion disease); (2) t
251 evant to a deep magma ocean, confirming that BSE's missing Nb is in the core.
252  of BSE surveillance and spreading fear that BSE might lurk unrecognized in goats.
253                 These results indicated that BSE at high dose prevents DCM in a manner congruent with
254                    Our findings suggest that BSE prions did not arise from a sheep scrapie strain lik
255                  Therefore, it suggests that BSE could potentially be used as a natural and safe trea
256 tus and their ecological correlates and that BSEs play several key roles in the functional ecology of
257    These results support the hypothesis that BSEs reduce r(be).
258                  To test the hypothesis that BSEs reduce the hydraulic resistance from the bundle she
259 onnections between DNA damage repair and the BSE.
260                              We detected the BSE prion protein within a large excess of classical, at
261 d ratio 6% higher than chondrites (i.e., the BSE is superchondritic).
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
265 count for the subchondritic signature of the BSE.
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
268 ave been due to past dietary exposure to the BSE agent.
269 bystander signal, helping to explain why the BSE is a low-dose phenomenon.
270 ecreased to zero or increased to twice their BSEs.
271 arise after exposure of humans or animals to BSE, this could markedly increase the danger of addition
272 0.11 per mille, Mg/Si = ~1.01) and closer to BSE (delta(30)Si(BSE) = -0.29 +/- 0.08 per mille).
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
275 ably millions of others have been exposed to BSE-contaminated food substances.
276 al evidence that it is caused by exposure to BSE has highlighted the need to understand the molecular
277 riant in the oral susceptibility of goats to BSE.
278 s and leporids, were apparently resistant to BSE.
279 erable interest in the responses of sheep to BSE inoculation.
280 attle, dose responses of cattle and sheep to BSE, levels of exposure to infected feed, and number of
281 in GPPrP might mediate its susceptibility to BSE and vCJD prions.
282 e to assess their relative susceptibility to BSE infection.
283 ible species) resulting in susceptibility to BSE-derived isolates.
284       Other species were also susceptible to BSE either by natural infection (e.g., felids, caprids)
285 cephalopathy (C-BSE) and the atypical H-type BSE (H-BSE) and L-type BSE (L-BSE) strains.
286 d the atypical H-type BSE (H-BSE) and L-type BSE (L-BSE) strains.
287 ype bovine spongiform encephalopathy (L-type BSE or L-BSE) with the RT-QuIC assay and found that both
288 n humans, the BASE strain is a more virulent BSE strain and likely lymphotropic.
289 th 100% specificity and 97% sensitivity when BSE agent was diluted into scrapie-infected brain homoge
290                         To determine whether BSE is potentially circulating at low levels within the
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
293 as been consistently observed in cattle with BSE.
294 United Kingdom could have been infected with BSE by being fed contaminated meat and bone meal supplem
295 ential if these animals became infected with BSE.
296 ion from donors experimentally infected with BSE; these were either clinically or subclinically affec
297                      In human infection with BSE prions, species-barrier effects, which are character
298 , primary and secondary human infection with BSE-derived prions may result in sporadic CJD-like or no
299                    Mice were inoculated with BSE or vCJD and assessed for clinical and pathological s
300           Inoculation of Tg(GPPrP) mice with BSE and vCJD prions resulted in mean incubation periods

 
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