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1 n otherwise lethal challenge with T3D (100 x 50% lethal dose).
2 ith a lethal dose of ZEBOV (30,000 times the 50% lethal dose).
3 vaccinated mice from a live challenge (>300 50% lethal doses).
4 1 at doses up to 1,000-fold greater than the 50% lethal dose.
5 inst toxin doses of at least 10(4) times the 50% lethal dose.
6 not attenuated for virulence in an assay of 50% lethal dose.
7 intraperitoneal challenge as assessed by the 50% lethal dose.
8 ntracerebral inoculation of HSV-1 KOS at the 50% lethal dose.
9 d NO production that correlated with the LPS 50% lethal dose.
10 dicated by a > or = 400-fold increase in the 50% lethal dose.
11 60% of the animals to die at a dose of three 50% lethal doses.
12 zed mothers showed 100% protection against a 50% lethal dose (1 LD(50)) challenge and 50% protection
17 ate promoter (U(L)38) exhibited an increased 50% lethal dose and a 10-fold decrease in virus yields i
19 iver, kidney and urine and 25-fold-decreased 50% lethal dose and milder histopathological injury in h
20 rease in neurovirulence as determined by the 50% lethal dose and survival distribution in suckling mi
21 al Y. pestis CO92 infection and have similar 50% lethal doses and kinetics of infection with respect
22 ent in the IL-6(-/-) mice (60-fold decreased 50% lethal dose) and colonized systemic tissues more rap
23 on of gK-myc in rabbit skin cells, increased 50% lethal dose, and decreased corneal scarring in ocula
24 challenge with approximately 1,000 times the 50% lethal dose ( approximately 1,000x LD(50)) of B. ant
25 In addition, virulence studies, using the 50% lethal dose assay, showed that the restoration of ca
31 ided protection from lethal challenge (1,000 50% lethal doses) equal to that of the wild-type virus.
33 g Psa) led to a 130,000-fold increase in the 50% lethal dose for mice relative to that of the KIM5 pa
34 etion in rat ileal loops was 200 ng, and the 50% lethal dose for mice was 27.5 ng when injected intra
37 segment, determining lethality with log(10) 50% lethal doses for each PTV genotype as follows (L/M/S
40 nts tested intragastrically, 12 mutants with 50% lethal doses greater than 1, 000 times that of the p
41 le of active immunization (mouse intravenous 50% lethal dose, > 10(7) bacteria), and stable at 4 degr
42 mutants showed a 1-to 3-log increase in the 50% lethal dose; however, the magnitude of its effect wa
44 strain OG1RF showed a considerably increased 50% lethal dose in a mouse peritonitis model, and, at hi
47 /kg body weight intravenously) increased the 50% lethal dose in mice by 100-fold after an intravenous
49 sed pathogenicity as determined by increased 50% lethal doses, indicating that the proteins of the E3
51 ighly neurovirulent in 21 day-old mice, with 50% lethal dose (LD(5)(0)) values of 0.1 and 0.5 log(1)(
53 with the rovA mutant they are attenuated by 50% lethal dose (LD(50)) analysis and have altered kinet
54 s administered i.n. but actually reduced the 50% lethal dose (LD(50)) by 3 orders of magnitude when t
56 vj mouse strains presented no differences in 50% lethal dose (LD(50)) following oral infection with Y
57 ntracerebral inoculation in BALB/c mice, the 50% lethal dose (LD(50)) for Myb34.5 was 2.7 x 10(7) PFU
61 t loss and death in mice challenged with ten 50% lethal dose (LD(50)) inoculums of either H1N1, H3N2,
62 apB is significantly attenuated in mice; the 50% lethal dose (LD(50)) intranasally (i.n.) is >10,000-
65 in a dose-dependent manner with a calculated 50% lethal dose (LD(50)) of 680 PFU, whereas there were
66 or infection by the Ames strain, because the 50% lethal dose (LD(50)) of a PA-deficient (PA(-)) Ames
68 n, following intranasal inoculation with 10x 50% lethal dose (LD(50)) of vaccinia virus strain IHD-J.
70 had an approximately 90-fold increase in the 50% lethal dose (LD(50)) relative to the Yfe(+) Feo(+) p
72 casp-1(-/)- mice) had an oral S. typhimurium 50% lethal dose (LD(50)) that was 1,000-fold higher than
73 ttenuated 100-fold compared to the published 50% lethal dose (LD(50)) values for B. anthracis Ames af
74 rotected against challenge with 10 times the 50% lethal dose (LD(50)), and mice challenged with 1,000
78 tion were completely protected against a 10x 50% lethal dose (LD) challenge of Streptococcus pneumoni
79 solates of S. enteritidis, we determined the 50% lethal doses (LD(50)) in mice of isolates of two maj
80 ed from a dose equivalent to 1,000 to 10,000 50% lethal doses (LD(50)) of BoNT/A when given three or
85 Abs which together neutralized >40,000 mouse 50% lethal doses (LD(50)s) of A1 toxin but less than 500
87 e against intraperitoneal challenge with 200 50% lethal doses (LD(50)s) of virulent Streptococcus pne
88 ulture infections, they exhibited lower oral 50% lethal doses (LD(50)s) than did the wild type in C57
90 CO92 Deltailp had a 55-fold increase in the 50% lethal dose ([LD(50)] 1.64 x 10(4) CFU) compared to
92 taneous challenge with 8 x 10(5) CFU (80,000 50% lethal dose [LD(50)]) and intranasal challenge with
95 ensis LVS is lethal, with an intraperitoneal 50% lethal dose (LD50) approaching a single bacterium.
96 th the latter being unable to kill mice at a 50% lethal dose (LD50) equivalent to 6,800 LD50s of WT C
100 of the ompX mutant survived, compared to the 50% lethal dose (LD50) of 1.2 x 10(3) CFU for the wild-t
101 05) increased mortality, with an approximate 50% lethal dose (LD50) of 10(5) CFU, while an equivalent
103 A) uniformly lethal to these animals, with a 50% lethal dose (LD50) of 5.3 x 10(-2) 50% tissue cultur
105 traperitoneally (i.p.) with 10,000 times the 50% lethal dose (LD50) of gp-adapted EBOV, and naive gps
110 J mutant in the blue gourami fish model: the 50% lethal dose (LD50) of the DeltaeseJ mutant is 2.34 t
112 yphimurium ompD mutants was ascertained by a 50% lethal dose (LD50) study and by determining coloniza
115 398His substitution alone demonstrated log10 50% lethal dose (LD50) values too great to be measured.
116 monstrated no toxicity up to 500-fold of the 50% lethal dose (LD50) when it was injected systemically
117 or plcB resulted in small increases in mouse 50% lethal dose (LD50), deletions in both genes resulted
118 mice were challenged subcutaneously with 60 50% lethal doses (LD50) (1 LD50 = 1.9 CFU) of a virulent
120 Lm/iglC, and subsequently challenged with 10 50% lethal doses (LD50) of aerosolized highly virulent F
121 nst lethal intranasal challenges with 1 or 5 50% lethal doses (LD50) of pathogenic vaccinia virus str
122 nic and protected BALB/c mice against 10,000 50% lethal doses (LD50) of S. Typhimurium or S. Enteriti
125 ations in glnA, ntrA, ntrB, or ntrC had i.p. 50% lethal doses (LD50s) of <10 bacteria, similar to the
126 hen Swiss-Webster mice, challenged with five 50% lethal doses (LD50s) of anthrax spores, were given a
128 thal intraperitoneal spore challenge with 24 50% lethal doses [LD50s] of B. anthracis Sterne and agai
130 eltarpoE mutant was highly attenuated with a 50% lethal dose more than 3 logs higher than that for th
132 brafish developed a lethal infection, with a 50% lethal dose of 10(3) CFU, and died within 2 to 3 day
134 led an approximately twofold decrease in the 50% lethal dose of B. anthracis spores administered in t
136 aspartate, previously shown to increase the 50% lethal dose of beta-toxin for mice nearly 13-fold, s
137 ate the relative degree of attenuation), the 50% lethal dose of CVD 915 (7.7 x 10(7) CFU) was signifi
138 test this, we infected BALB/c mice with 0.1 50% lethal dose of DeltaactA or virulent L. monocytogene
142 tigen-polyhistidine fusion peptide (Vh), the 50% lethal dose of purified lipopolysaccharide (LPS) in
144 ant to protect A/J mice against 10 times the 50% lethal dose of Sterne strain spores introduced subcu
146 significant sensitivity to UV light, and the 50% lethal dose of the mutant strain in a mouse intraper
147 ved an intranasal challenge with 5 times the 50% lethal dose of the pathogenic WR strain of vaccinia
152 accinated mucosally were protected against a 50% lethal dose of wild-type SEB given i.p. or mucosally
153 rum elicited to nine-repeat alpha C protein (50% lethal doses of 1.6 x 10(3) and 1.8 x 10(5), respect
156 st that toxin activation may explain the low 50% lethal doses of B2F1 and H414-36/89 in streptomycin-
157 ee mAbs (oligoclonal Ab) neutralized 450,000 50% lethal doses of BoNT/A, a potency 90 times greater t
161 oNT HCRs and neutralized challenge by 10,000 50% lethal doses of each of the seven BoNT serotypes.
162 flagellin produced by the strains; (ii) the 50% lethal doses of fliA mutant and wild-type strains of
164 n of suckling mice against challenge with 25 50% lethal doses of mouse neurovirulent DENV-4 strain H2
172 absence of YopM significantly increased the 50% lethal dose only in the intradermal model, suggestin
173 n O11 strain (9882-80) at 6 and 12 times the 50% lethal dose showed increased survival in mice that r
174 e levels in plasma and a significantly lower 50% lethal dose than those in LPS-treated control-fed an
175 more resistant to virus than CD1(-/-) mice (50% lethal dose titers: wild-type mice, 10 PFU; CD1(-/-)
177 ed with wild-type F. novicida (100 and 1,000 50% lethal doses) were highly protected (83% and 50% sur
179 peritoneal route at a dose twice that of the 50% lethal dose, which within 2 to 3 days killed 100% of
180 infection (60%) than the WT bacterium at two 50% lethal doses, which resulted in 100% mortality withi
181 CT alone were challenged with 10(6) CFU (one 50% lethal dose) wild-type V. cholerae O1 El Tor strain