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1 herwise lethal challenge with T3D (100 x 50% lethal dose).
2 st a lethal BoNT/A dose (1.05 times the 100% lethal dose).
3 tion against challenge infection with a high lethal dose.
4 therapeutic-intervention studies) the median lethal dose.
5 decreased survival time, and decreased mean lethal dose.
6 han WT mice following E. coli infection at a lethal dose.
7 nsient neurological symptoms emerging at sub-lethal doses.
8 sis model, the JPAB02 strain exhibited lower lethal dose 0 (LD0), LD50, and LD100, and dissemination
9 s, LNCaP, ALVA31, Du145, PC3, and PPC1, with lethal dose 50% approximately 1 micromol/L for CDDO-Me a
16 , kidney and urine and 25-fold-decreased 50% lethal dose and milder histopathological injury in hamst
18 s, resulting in nanomolar and low micromolar lethal doses and therapeutic indexes of 500 and 75, resp
19 f gK-myc in rabbit skin cells, increased 50% lethal dose, and decreased corneal scarring in ocularly
20 lenge with approximately 1,000 times the 50% lethal dose ( approximately 1,000x LD(50)) of B. anthrac
24 o possessed enhanced protection against high lethal dose challenges against homologous A/PR/8/34 and
27 of the same population were irradiated with lethal doses compared with their parental mitochondrial-
33 a) led to a 130,000-fold increase in the 50% lethal dose for mice relative to that of the KIM5 parent
35 timates of total 'bee toxic load' (honey bee lethal doses) for insecticides applied in the US between
37 n up by A. cavernicola with no evidence that lethal dose has been reached in our working conditions.
38 a heretofore unknown deleterious role during lethal dose IAV infections by limiting the CD8 T cell re
48 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
50 ministered i.n. but actually reduced the 50% lethal dose (LD(50)) by 3 orders of magnitude when the s
54 ss and death in mice challenged with ten 50% lethal dose (LD(50)) inoculums of either H1N1, H3N2, B/V
55 is significantly attenuated in mice; the 50% lethal dose (LD(50)) intranasally (i.n.) is >10,000-fold
58 dose-dependent manner with a calculated 50% lethal dose (LD(50)) of 680 PFU, whereas there were no d
59 nfection by the Ames strain, because the 50% lethal dose (LD(50)) of a PA-deficient (PA(-)) Ames muta
61 an approximately 90-fold increase in the 50% lethal dose (LD(50)) relative to the Yfe(+) Feo(+) paren
63 uated 100-fold compared to the published 50% lethal dose (LD(50)) values for B. anthracis Ames after
64 ard toxicity metrics rodent liver TD(50) and lethal dose (LD(50)), Ames tests, and Comet assays for i
68 were completely protected against a 10x 50% lethal dose (LD) challenge of Streptococcus pneumoniae a
70 vival during the first few days after median lethal dose (LD)100 and LD50 infection, while overall mo
71 rom a dose equivalent to 1,000 to 10,000 50% lethal doses (LD(50)) of BoNT/A when given three or four
76 ainst intraperitoneal challenge with 200 50% lethal doses (LD(50)s) of virulent Streptococcus pneumon
77 2 Deltailp had a 55-fold increase in the 50% lethal dose ([LD(50)] 1.64 x 10(4) CFU) compared to the
78 ous challenge with 8 x 10(5) CFU (80,000 50% lethal dose [LD(50)]) and intranasal challenge with 5 x
80 he latter being unable to kill mice at a 50% lethal dose (LD50) equivalent to 6,800 LD50s of WT CO92.
84 he ompX mutant survived, compared to the 50% lethal dose (LD50) of 1.2 x 10(3) CFU for the wild-type
85 increased mortality, with an approximate 50% lethal dose (LD50) of 10(5) CFU, while an equivalent dos
87 niformly lethal to these animals, with a 50% lethal dose (LD50) of 5.3 x 10(-2) 50% tissue culture in
88 teins exhibit resistance to 10,000 times the lethal dose (LD50) of BoNT/A, and transfusion of these r
89 eritoneally (i.p.) with 10,000 times the 50% lethal dose (LD50) of gp-adapted EBOV, and naive gps wer
91 Specifically, we determined values of 50% lethal dose (LD50) of MERS-CoV for the 2 strains of mice
92 is study was aimed at determining the median lethal dose (LD50) of the Bacillus anthracis Ames strain
93 tant in the blue gourami fish model: the 50% lethal dose (LD50) of the DeltaeseJ mutant is 2.34 times
97 trated no toxicity up to 500-fold of the 50% lethal dose (LD50) when it was injected systemically.
98 intranasal (i.n.) challenge with ~240 median lethal doses (LD50) (2.4 x 10(4) CFU) of Y. pestis KIM6+
100 glC, and subsequently challenged with 10 50% lethal doses (LD50) of aerosolized highly virulent F. tu
101 and protected BALB/c mice against 10,000 50% lethal doses (LD50) of S. Typhimurium or S. Enteritidis,
104 intraperitoneal spore challenge with 24 50% lethal doses [LD50s] of B. anthracis Sterne and against
105 ity and are completely protected following a lethal-dose MHV-1 challenge despite mounting only a mode
106 for each serotype is 1 mouse intraperitoneal lethal dose (MIPLD(50)) corresponding to 31 pg of BoNT/A
107 humoral responses upon equivalent 50% mouse lethal dose (MLD(50)) challenges with influenza virus.
114 influenza virus infection, we determined the lethal dose of a highly pathogenic H5N1 virus (A/Hong Ko
115 previously shown that mice challenged with a lethal dose of A/Puerto Rico/8/34-OVA(I) are protected b
116 h before the ferrets were inoculated with a lethal dose of A/Vietnam/1203/04 (H5N1) influenza virus.
117 CXCR2 knockout mice exposed to a median lethal dose of acetaminophen had a significantly lower m
120 ression in mice protected the mice against a lethal dose of agonistic anti-Fas antibody (P < .001) an
121 argeting only one population of cells with a lethal dose of alpha-particles, a decreased bystander mu
124 an approximately twofold decrease in the 50% lethal dose of B. anthracis spores administered in the p
127 protects mice from systemic infection with a lethal dose of C. albicans, and deficiency of dectin-1,
128 All SCIDbgMN mice orally infected with a lethal dose of C. parvum survived after they were inocul
129 )CCH(2)CH(2)CH(2)CH(2)CH(3))(2)Cl(2)] (1), a lethal dose of cisplatin was delivered specifically to p
131 rotect mice from a subsequently administered lethal dose of cocaine, suggesting the enzyme may have t
133 RK5 KO mice following a sublethal dose, at a lethal dose of E. coli, the bacterial burdens remained h
134 macaques infected 24 hours previously with a lethal dose of Ebola virus suppressed viral loads by mor
135 ival time of rhesus macaques infected with a lethal dose of Ebola virus, although it failed to alter
136 ate that animals challenged with a uniformly lethal dose of EBOV one day following vaccination, and t
138 on mice against challenge with an otherwise lethal dose of either F. tularensis LVS or a fully virul
139 tious units of VRP-GFP and challenged with a lethal dose of FMDV 24 h later were protected from death
141 ice were able to confer protection against a lethal dose of H1N1 influenza virus A/Puerto Rico 8/34 (
150 ls, healthy mice, and mice challenged with a lethal dose of IFV A/PR/8/34 (H1N1) or A/Victoria/3/75 (
151 ine protected mice against a single high and lethal dose of influenza A virus but was ineffective aga
152 Mice were subsequently challenged with a lethal dose of influenza A/PR/8/34 virus 24 h after the
155 luenza virus, as measured by protection to a lethal dose of influenza virus, which is consistent with
161 hepcidin pretreatment protected mice from a lethal dose of LPS and that hepcidin-knockout mice could
162 for IL-1beta and IL-18 were protected from a lethal dose of LPS by pretreatment with HMGB1-neutralizi
164 resolution of lung inflammation induced by a lethal dose of LPS or by Pseudomonas bacterial pneumonia
168 nd when challenged 4 or 8 weeks later with a lethal dose of LVS i.n., they were 100% protected from i
169 acaca mulatta) infected intravenously with a lethal dose of lymphocytic choriomeningitis virus (LCMV)
172 ed splenocytes rescued allorecipients from a lethal dose of mouse CMV (MCMV) administered on day 0 in
173 E-R(ER) of FVB/N male mice challenged with a lethal dose of paraoxon, with complete elimination of sh
176 Burn wounds were topically inoculated with a lethal dose of Pseudomonas aeruginosa 6 days after injur
183 expression in vitro and protect mice from a lethal dose of S. aureus by sequestering the AIP signal.
186 strain L81905 or intranasal challenge with a lethal dose of S. pneumoniae A66.1 in a pneumonia model.
189 upon request, received a prescription for a lethal dose of secobarbital (35.1% of the 114 patients w
190 lovibrio injection of zebrafish containing a lethal dose of Shigella promotes pathogen killing, leadi
191 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
197 rvival of mice infected intradermally with a lethal dose of the LVS was slightly improved by deletion
198 e survival against systemic infection with a lethal dose of the pathogenic fungus Candida albicans.
203 ra25 strain are able to survive an otherwise lethal dose of Toxoplasma tachyzoites and that complemen
211 id-ethyl amide provided before exposure to a lethal dose of whole-body irradiation protected WT mice
213 green monkeys (AGMs) after challenge with a lethal dose of Y. pestis delivered as an aerosol, in 4 i
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.
228 sed survival of recipient mice infected with lethal doses of clinically relevant opportunistic pathog
236 oses of HA22-LR at least 10-fold higher than lethal doses of HA22, and these higher doses exhibited m
237 rotected the mice, that were challenged with lethal doses of highly pathogenic influenza A H5N1 or H1
238 In vivo, CRP rescues mice challenged with lethal doses of histones by inhibiting endothelial damag
239 virus protected mice against challenge with lethal doses of homologous (VN1203; clade 1) and antigen
244 th this virus were completely protected from lethal doses of infection with either influenza virus or
245 gnificantly protect mice from infection with lethal doses of influenza viruses when orally administer
247 in a temporally segregated manner such that lethal doses of ionizing irradiation, if administered ov
251 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
269 F. hepatica were cultured in lethal and sub-lethal doses of TCBZ and its active metabolites, in orde
271 tects guinea pigs from the acute toxicity of lethal doses of the nerve agents soman and sarin, and of
273 multidose schedule protected rodents against lethal doses of total body irradiation up to 13 Gy, whet
274 ns for the management of patients exposed to lethal doses of total body radiotherapy, but not doses h
276 ns for the management of patients exposed to lethal doses of total-body radiotherapy, but not doses h
277 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
281 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
286 peritoneal sepsis murine model, the minimum lethal dose required by A. baumannii ATCC 17978 Deltapst
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
295 ed liposomes are most cytotoxic, with median lethal dose values, after 24 h of incubation, equal to 1
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