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1 herwise lethal challenge with T3D (100 x 50% lethal dose).
2 a lethal dose of ZEBOV (30,000 times the 50% lethal dose).
3 st a lethal BoNT/A dose (1.05 times the 100% lethal dose).
4 tion against challenge infection with a high lethal dose.
5 therapeutic-intervention studies) the median lethal dose.
6 decreased survival time, and decreased mean lethal dose.
7 han WT mice following E. coli infection at a lethal dose.
8 nsient neurological symptoms emerging at sub-lethal doses.
9 of the animals to die at a dose of three 50% lethal doses.
10 sis model, the JPAB02 strain exhibited lower lethal dose 0 (LD0), LD50, and LD100, and dissemination
11 s, LNCaP, ALVA31, Du145, PC3, and PPC1, with lethal dose 50% approximately 1 micromol/L for CDDO-Me a
17 , kidney and urine and 25-fold-decreased 50% lethal dose and milder histopathological injury in hamst
18 . pestis CO92 infection and have similar 50% lethal doses and kinetics of infection with respect to c
19 s, resulting in nanomolar and low micromolar lethal doses and therapeutic indexes of 500 and 75, resp
20 f gK-myc in rabbit skin cells, increased 50% lethal dose, and decreased corneal scarring in ocularly
21 nd rGST-immunized hamsters were subjected to lethal doses, and the hamsters that survived showed seve
22 lenge with approximately 1,000 times the 50% lethal dose ( approximately 1,000x LD(50)) of B. anthrac
26 o possessed enhanced protection against high lethal dose challenges against homologous A/PR/8/34 and
29 of the same population were irradiated with lethal doses compared with their parental mitochondrial-
36 a) led to a 130,000-fold increase in the 50% lethal dose for mice relative to that of the KIM5 parent
38 ment, determining lethality with log(10) 50% lethal doses for each PTV genotype as follows (L/M/S con
39 dney tissue ( approximately 10(9) 50% embryo lethal doses/g) from 1-day-old chickens infected intrave
40 n up by A. cavernicola with no evidence that lethal dose has been reached in our working conditions.
41 a heretofore unknown deleterious role during lethal dose IAV infections by limiting the CD8 T cell re
42 in OG1RF showed a considerably increased 50% lethal dose in a mouse peritonitis model, and, at high i
53 y neurovirulent in 21 day-old mice, with 50% lethal dose (LD(5)(0)) values of 0.1 and 0.5 log(1)(0) P
54 ministered i.n. but actually reduced the 50% lethal dose (LD(50)) by 3 orders of magnitude when the s
58 is significantly attenuated in mice; the 50% lethal dose (LD(50)) intranasally (i.n.) is >10,000-fold
61 dose-dependent manner with a calculated 50% lethal dose (LD(50)) of 680 PFU, whereas there were no d
62 nfection by the Ames strain, because the 50% lethal dose (LD(50)) of a PA-deficient (PA(-)) Ames muta
63 ollowing intranasal inoculation with 10x 50% lethal dose (LD(50)) of vaccinia virus strain IHD-J.
65 an approximately 90-fold increase in the 50% lethal dose (LD(50)) relative to the Yfe(+) Feo(+) paren
67 uated 100-fold compared to the published 50% lethal dose (LD(50)) values for B. anthracis Ames after
68 ard toxicity metrics rodent liver TD(50) and lethal dose (LD(50)), Ames tests, and Comet assays for i
72 were completely protected against a 10x 50% lethal dose (LD) challenge of Streptococcus pneumoniae a
74 vival during the first few days after median lethal dose (LD)100 and LD50 infection, while overall mo
75 rom a dose equivalent to 1,000 to 10,000 50% lethal doses (LD(50)) of BoNT/A when given three or four
80 ainst intraperitoneal challenge with 200 50% lethal doses (LD(50)s) of virulent Streptococcus pneumon
81 2 Deltailp had a 55-fold increase in the 50% lethal dose ([LD(50)] 1.64 x 10(4) CFU) compared to the
84 he latter being unable to kill mice at a 50% lethal dose (LD50) equivalent to 6,800 LD50s of WT CO92.
88 he ompX mutant survived, compared to the 50% lethal dose (LD50) of 1.2 x 10(3) CFU for the wild-type
89 increased mortality, with an approximate 50% lethal dose (LD50) of 10(5) CFU, while an equivalent dos
91 niformly lethal to these animals, with a 50% lethal dose (LD50) of 5.3 x 10(-2) 50% tissue culture in
92 teins exhibit resistance to 10,000 times the lethal dose (LD50) of BoNT/A, and transfusion of these r
93 eritoneally (i.p.) with 10,000 times the 50% lethal dose (LD50) of gp-adapted EBOV, and naive gps wer
95 apoptosis of primary leukemia samples with a lethal dose (LD50) of less than 10 microM in 16 of 27 (6
96 is study was aimed at determining the median lethal dose (LD50) of the Bacillus anthracis Ames strain
97 tant in the blue gourami fish model: the 50% lethal dose (LD50) of the DeltaeseJ mutant is 2.34 times
100 is substitution alone demonstrated log10 50% lethal dose (LD50) values too great to be measured.
102 trated no toxicity up to 500-fold of the 50% lethal dose (LD50) when it was injected systemically.
103 intranasal (i.n.) challenge with ~240 median lethal doses (LD50) (2.4 x 10(4) CFU) of Y. pestis KIM6+
105 glC, and subsequently challenged with 10 50% lethal doses (LD50) of aerosolized highly virulent F. tu
106 and protected BALB/c mice against 10,000 50% lethal doses (LD50) of S. Typhimurium or S. Enteritidis,
109 Swiss-Webster mice, challenged with five 50% lethal doses (LD50s) of anthrax spores, were given a sin
111 intraperitoneal spore challenge with 24 50% lethal doses [LD50s] of B. anthracis Sterne and against
112 ity and are completely protected following a lethal-dose MHV-1 challenge despite mounting only a mode
113 for each serotype is 1 mouse intraperitoneal lethal dose (MIPLD(50)) corresponding to 31 pg of BoNT/A
114 humoral responses upon equivalent 50% mouse lethal dose (MLD(50)) challenges with influenza virus.
120 influenza virus infection, we determined the lethal dose of a highly pathogenic H5N1 virus (A/Hong Ko
121 previously shown that mice challenged with a lethal dose of A/Puerto Rico/8/34-OVA(I) are protected b
122 h before the ferrets were inoculated with a lethal dose of A/Vietnam/1203/04 (H5N1) influenza virus.
123 /Singapore/3/97(H5N3) then inoculated with a lethal dose of A/Vietnam/1203/04(H5N1) (Viet/1203/04).
124 CXCR2 knockout mice exposed to a median lethal dose of acetaminophen had a significantly lower m
126 ression in mice protected the mice against a lethal dose of agonistic anti-Fas antibody (P < .001) an
127 argeting only one population of cells with a lethal dose of alpha-particles, a decreased bystander mu
128 an approximately twofold decrease in the 50% lethal dose of B. anthracis spores administered in the p
131 protects mice from systemic infection with a lethal dose of C. albicans, and deficiency of dectin-1,
132 All SCIDbgMN mice orally infected with a lethal dose of C. parvum survived after they were inocul
133 )CCH(2)CH(2)CH(2)CH(2)CH(3))(2)Cl(2)] (1), a lethal dose of cisplatin was delivered specifically to p
135 rotect mice from a subsequently administered lethal dose of cocaine, suggesting the enzyme may have t
136 t this, we infected BALB/c mice with 0.1 50% lethal dose of DeltaactA or virulent L. monocytogenes an
138 RK5 KO mice following a sublethal dose, at a lethal dose of E. coli, the bacterial burdens remained h
139 macaques infected 24 hours previously with a lethal dose of Ebola virus suppressed viral loads by mor
140 ival time of rhesus macaques infected with a lethal dose of Ebola virus, although it failed to alter
142 on mice against challenge with an otherwise lethal dose of either F. tularensis LVS or a fully virul
143 tious units of VRP-GFP and challenged with a lethal dose of FMDV 24 h later were protected from death
145 ice were able to confer protection against a lethal dose of H1N1 influenza virus A/Puerto Rico 8/34 (
152 ls, healthy mice, and mice challenged with a lethal dose of IFV A/PR/8/34 (H1N1) or A/Victoria/3/75 (
153 ine protected mice against a single high and lethal dose of influenza A virus but was ineffective aga
154 Mice were subsequently challenged with a lethal dose of influenza A/PR/8/34 virus 24 h after the
156 luenza virus, as measured by protection to a lethal dose of influenza virus, which is consistent with
162 hepcidin pretreatment protected mice from a lethal dose of LPS and that hepcidin-knockout mice could
163 hepcidin pretreatment protected mice from a lethal dose of LPS and that hepcidin-knockout mice could
164 for IL-1beta and IL-18 were protected from a lethal dose of LPS by pretreatment with HMGB1-neutralizi
166 resolution of lung inflammation induced by a lethal dose of LPS or by Pseudomonas bacterial pneumonia
168 ment 24 h before intranasal infection with a lethal dose of LVS (10,000 CFU) significantly decreased
169 nd when challenged 4 or 8 weeks later with a lethal dose of LVS i.n., they were 100% protected from i
170 acaca mulatta) infected intravenously with a lethal dose of lymphocytic choriomeningitis virus (LCMV)
173 ed splenocytes rescued allorecipients from a lethal dose of mouse CMV (MCMV) administered on day 0 in
174 E-R(ER) of FVB/N male mice challenged with a lethal dose of paraoxon, with complete elimination of sh
177 Burn wounds were topically inoculated with a lethal dose of Pseudomonas aeruginosa 6 days after injur
184 expression in vitro and protect mice from a lethal dose of S. aureus by sequestering the AIP signal.
187 strain L81905 or intranasal challenge with a lethal dose of S. pneumoniae A66.1 in a pneumonia model.
190 upon request, received a prescription for a lethal dose of secobarbital (35.1% of the 114 patients w
191 lovibrio injection of zebrafish containing a lethal dose of Shigella promotes pathogen killing, leadi
192 1 pathway suppressed cell death induced by a lethal dose of short-wavelength UV light, and high dosag
193 to protect A/J mice against 10 times the 50% lethal dose of Sterne strain spores introduced subcutane
194 imilar amongst the dietary treatments, a sub-lethal dose of Streptococcus iniae was administered to h
198 rvival of mice infected intradermally with a lethal dose of the LVS was slightly improved by deletion
203 ra25 strain are able to survive an otherwise lethal dose of Toxoplasma tachyzoites and that complemen
210 id-ethyl amide provided before exposure to a lethal dose of whole-body irradiation protected WT mice
213 /6 and BALB/c mice survived challenge with a lethal dose of ZEBOV (30,000 times the 50% lethal dose).
215 us macaques were challenged with a uniformly lethal dose of ZEBOV; 11 of these monkeys were treated b
216 stered 6 hours after exposure to a uniformly lethal dose of ~20 LD(50) to prevent death and eliminate
218 ats after nose-only inhalational exposure to lethal doses of aerosolized Francisella tularensis subsp
219 notypic phenomenon of tolerance to otherwise lethal doses of antimicrobials and to other antimicrobia
223 tected mice challenged with 280 mouse median lethal doses of BoNT/H at a mAb dose as low as 5 microg
224 uggests that the adaptation occurring at sub-lethal doses of carvacrol is different from that occurri
225 that can provide protection against multiple lethal doses of chemical warfare nerve agents in vivo.
227 sed survival of recipient mice infected with lethal doses of clinically relevant opportunistic pathog
231 Animals were injected intravenously with lethal doses of Escherichia coli or saline and sacrifice
238 oses of HA22-LR at least 10-fold higher than lethal doses of HA22, and these higher doses exhibited m
239 rotected the mice, that were challenged with lethal doses of highly pathogenic influenza A H5N1 or H1
240 In vivo, CRP rescues mice challenged with lethal doses of histones by inhibiting endothelial damag
241 virus protected mice against challenge with lethal doses of homologous (VN1203; clade 1) and antigen
245 th this virus were completely protected from lethal doses of infection with either influenza virus or
246 gnificantly protect mice from infection with lethal doses of influenza viruses when orally administer
248 in a temporally segregated manner such that lethal doses of ionizing irradiation, if administered ov
250 C57Bl6 mice were exposed to sublethal and lethal doses of irradiation and were subsequently given
252 Here we demonstrate that mice infected with lethal doses of L. monocytogenes produce higher levels o
255 ction of these scFvs to specifically deliver lethal doses of liposome-encapsulated small molecule dru
260 suckling mice against challenge with 25 50% lethal doses of mouse neurovirulent DENV-4 strain H241.
262 articular, a complete protection against the lethal doses of paraoxon was observed with nano-OPH admi
266 tered before or soon after acute exposure to lethal doses of soman, sarin, or paraoxon effectively an
270 tects guinea pigs from the acute toxicity of lethal doses of the nerve agents soman and sarin, and of
272 multidose schedule protected rodents against lethal doses of total body irradiation up to 13 Gy, whet
273 ns for the management of patients exposed to lethal doses of total body radiotherapy, but not doses h
274 ns for the management of patients exposed to lethal doses of total-body radiotherapy, but not doses h
276 fully protected mice against challenge with lethal doses of toxinogenic unencapsulated Sterne 7702 s
279 red with wild-type mice when challenged with lethal doses of virus, correlating with increased expres
280 ence of YopM significantly increased the 50% lethal dose only in the intradermal model, suggesting a
283 valent to 21 to 43 times the estimated human lethal dose; pretreatment serum from the fourth epidemio
287 conditions to estimate the probability of a lethal dose, showing that not all reservoirs with detect
289 e resistant to virus than CD1(-/-) mice (50% lethal dose titers: wild-type mice, 10 PFU; CD1(-/-) mic
293 ed liposomes are most cytotoxic, with median lethal dose values, after 24 h of incubation, equal to 1
296 ith wild-type F. novicida (100 and 1,000 50% lethal doses) were highly protected (83% and 50% surviva
297 ction (60%) than the WT bacterium at two 50% lethal doses, which resulted in 100% mortality within 48
298 lone were challenged with 10(6) CFU (one 50% lethal dose) wild-type V. cholerae O1 El Tor strain N169
300 thology in lung, yet sterilising immunity to lethal dose WT challenge was achieved after low dose (20
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