ライフサイエンスコーパス: Ames

1 Ames dwarf mice survived 987 +/- 24 d (median), longer t

2 Ames mutagenicity and CHO-K1 micronucleus assays were ap

3 Ames waltzer (av) is a recessive mutation found in mice

4 response to intense light was slower by 28% (Ames) and 44% (inhibitory blockers) in the null cells.

5 In a recombinant cytochrome P-450 2E1 Ames bacterial mutagenicity assay, the R597M/W677A prote

6 odent liver TD(50) and lethal dose (LD(50)), Ames tests, and Comet assays for in vitro DNA damage.

7 nd 100x LD(50) (1.2 x 10(6) and 1.2 x 10(7)) Ames strain spores.

8 The inhaled LD50 of aerosolized Ames strain spores in guinea pigs was determined to be 5

9 hly potent and selective but mutagenic in an Ames assay.

10 zole metabolite that would be negative in an Ames test.

11 e sequence of the chromosome of B. anthracis Ames (about 5.23 megabases).

12 ved from wild-type encapsulated B. anthracis Ames (WT) or a control preparation from an isogenic B. a

13 lethal dose (LD(50)) values for B. anthracis Ames after aerosol inoculation.

14 Previous studies suggested that B. anthracis Ames Ancestor, the original Ames fully virulent plasmid-

15 d and compared with that of the B. anthracis Ames ancestor, the progenitor of all B. anthracis Ames s

16 e genomes of pathogenic strains B. anthracis Ames and B. cereus G9241 and nonpathogenic strains B. ce

17 higher than those reported for B. anthracis Ames and more like those of the toxigenic but nonencapsu

18 transformation of plasmid-free B. anthracis Ames and Sterne strains by the original pMR was approxim

19 the fully virulent encapsulated B. anthracis Ames and the non-encapsulated Sterne strain.

20 issues of animals infected with B. anthracis Ames contained high numbers of bacilli, only few vegetat

21 in single-colony environmental B. anthracis Ames isolates associated with the investigation.

22 its given a lethal challenge of B. anthracis Ames spores and doubled the mean time to death in those

23 nst challenge with 100 LD50s of B. anthracis Ames spores, and 100% of the rabbits survived rechalleng

24 s despite lethal challenge with B. anthracis Ames spores.

25 athophysiology in vivo, we used B. anthracis Ames strain and isogenic toxin deletion mutants derived

26 All six SNPs differentiated the B. anthracis Ames strain from the 88 unique B. anthracis strains, whi

27 approximately 1,000x LD(50)) of B. anthracis Ames strain spores (1.38 x 10(3) spores), which killed c

28 n against a lethal challenge of B. anthracis Ames strain spores in rabbits.

29 ol preparation from an isogenic B. anthracis Ames strain that produces only 2% of the capsule of the

30 nment to the recently published B. anthracis Ames strain, while an inquiry for protein sequence simil

31 enge with aerosolized spores of B. anthracis Ames strain.

32 spore challenge by the virulent B. anthracis Ames strain.

33 ed purH mutants of the virulent B. anthracis Ames strain.

34 ancestor, the progenitor of all B. anthracis Ames strains.

35 e highly virulent parent strain B. anthracis Ames, bslA mutants displayed a dramatic increase in the

36 ender the strain as virulent as B. anthracis Ames.

37 s ATCC 10987 was more similar to B.anthracis Ames than B.cereus ATCC 14579, while containing a number

38 larity of B.cereus ATCC 10987 to B.anthracis Ames, as well as the fact that it contains a large pXO1-

39 mids are analogous to the Bacillus anthracis Ames plasmids pXO1 and pXO2 that encode anthrax toxins a

40 l animals challenged with Bacillus anthracis Ames spores by the intranasal route died within 3 to 7 d

41 nst lethal infection with Bacillus anthracis Ames spores, regardless of the inoculation method.

42 lethal dose (LD50) of the Bacillus anthracis Ames strain in guinea pigs and investigating the natural

43 analysis of the genome of Bacillus anthracis Ames strain, we identified two novel putative cell wall-

44 features of the letters' Bacillus anthracis Ames strain.

45 es the 50% lethal dose of Bacillus anthracis Ames).

46 inbred mice and spores of Bacillus anthracis Ames, we investigated host susceptibility to pulmonary a

47 ity using the Salmonella mutagenicity assay (Ames test).

48 In parallel, genotoxicity assays (Ames and micronucleus assays) and transcriptional-report

49 Comparative mutagenicity assays (Ames test) were performed on 1 versus 1NO2, 5 versus 5NO

50 d ERG a- and b-waves were comparable between Ames waltzer mutants and heterozygous littermates as old

51 Bruce Ames that emphasized the documented relationships betwee

52 c extract did not showed mutagenic effect by Ames test against Salmonella typhimurium TA98 and TA100

53 VLDL-TAG using the growth hormone-deficient Ames dwarf mouse model, which has reduced serum TAG.

54 culture supernatant of a non-virulent delta Ames strain (pXO1-, pXO2-).

55 the closely related, long-lived Prop-1(df) (Ames dwarf) mutant, should provide new insights into the

56 challenge with 235,000 (10 50% lethal doses) Ames strain B. anthracis spores.

57 form of murine pituitary-dependent dwarfism (Ames dwarf, df) has been positionally cloned, identifyin

58 location of Prop1, the gene responsible for Ames dwarfism, has been localized within the contig.

59 Fibroblast cells from Ames dwarf mice were more resistant to cadmium than cell

60 terrestrial standards were fractionated from Ames Lu by an average of 1.22 +/- 0.09 per thousand.

61 Cyto-genotoxicity (Ames and micronucleus assays) and potential endocrine di

62 raits in maize and the extensively genotyped Ames Panel.

63 Hypopituitary Ames dwarf mice were injected either with growth hormone

64 ns in Pcdh15 affect hair cell development in Ames waltzer (av) mice.

65 ase in phosphorylation of the kinase JNK2 in Ames dwarf (but not control) mice.

66 stress resistance and extended longevity in Ames dwarf mice.

67 humans and deafness with balance problems in Ames waltzer (av) mice.

68 O2 treatment leads to a positive response in Ames mutagenicity tests, which is then removed after gra

69 ciated methylation changes are suppressed in Ames dwarf and calorie restricted mice and more selectiv

70 B.S. and M.S. from Iowa State University in Ames and his Ph.D. from the Department of Plant Patholog

71 tered in other dwarf mouse models, including Ames, Little, and growth hormone receptor-null mice.

72 - 0.8, respectively), but GH injections into Ames dwarf mice restored the normal level of cadmium res

73 nonmutant control mice.) T4 injections into Ames dwarf mice, in contrast, did not restore normal lif

74 acis were partially protected against lethal Ames spore challenge, which was comparable to vaccinatio

75 opment influences the lifespan of long-lived Ames dwarf and normal littermate control mice in a genot

76 Interestingly, in long-lived Ames dwarf mice, renal FXR and TGR5 expression levels we

77 using a panel of CYP enzymes, mutagenicity (Ames screen), and hepatic stability.

78 wo D-Wave Two quantum annealers, one at NASA Ames Research Center in Moffett Field, California, and a

79 of the stress kinase ERK in control (but not Ames dwarf) mice and to a 50% increase in phosphorylatio

80 cted from NZW rabbits exposed to aerosols of Ames strain Bacillus anthracis.

81 retinal abnormalities in the four alleles of Ames waltzer tested in this study.

82 Studies in a separate cohort of Ames dwarf mice show that this short period of the GH ex

83 e that the remarkable life-span extension of Ames dwarf mice, and the stress resistance of cells from

84 ance pathways were evaluated in the liver of Ames dwarf mice before and after exposure to the oxidati

85 Thus, livers of Ames dwarf mice differ systematically from controls in m

86 cantly suppressed human MPhi phagocytosis of Ames spores.

87 hat B. anthracis Ames Ancestor, the original Ames fully virulent plasmid-containing isolate, was the

88 thal dose (LD(50)) of a PA-deficient (PA(-)) Ames mutant was identical to that of the parent Ames str

89 In a series of papers, Ames and colleagues allege that the scientific and publi

90 s mutant was identical to that of the parent Ames strain.

91 human DCs readily engulfed fully pathogenic Ames and attenuated B. anthracis spores predominately by

92 Mitigation of a potential Ames and hERG liability ultimately led to two promising

93 ve recently positionally cloned the putative Ames dwarf gene Prop1, which encodes a paired-like homeo

94 cis strains, while five of the six separated Ames from its close genetic relatives.

95 Similarly, Ames does not offer any convincing scientific evidence t

96 culture of encapsulated B. anthracis strain Ames in blood.

97 y virulent, ungerminated B. anthracis strain Ames spores.

98 imilar rate as wild-type B. anthracis strain Ames.

99 of the anthrax pathogen B. anthracis strain Ames.

100 +) pXO2(+)) strains of B. anthracis, strains Ames and UT500.

101 tific facts and our perspectives surrounding Ames' nine alleged misconceptions.

102 The Ames dwarf (df) mouse displays a similar phenotype, and

103 The Ames dwarf mouse transmits a recessive mutation (df) res

104 The Ames strain of B. anthracis differed from the Sterne str

105 The Ames test was used to show that propionaldehyde is a mut

106 The Ames waltzer (av) mouse mutant is an autosomal recessive

107 This difference between the Ames strain and the UT500 strain could not be attributed

108 PA- mutant strain, the toxin produced by the Ames strain was not able to promote dissemination of the

109 toxin was not required for infection by the Ames strain, because the 50% lethal dose (LD(50)) of a P

110 he biological activity of flavonoids, by the Ames test, with Salmonella typhimurium strains TA98, TA1

111 phimurium TA102 strain, as determined by the Ames test.

112 antimutagenic activity was evaluated by the Ames test.

113 he lineage of B. anthracis that contains the Ames strain, the strain used in the 2001 bioterrorist at

114 We have extended the Ames test to include both quantitative analysis of rever

115 NPs were found to be highly specific for the Ames strain; four on the chromosome, one on the pX01 pla

116 ulation made up of 384 inbred lines from the Ames Panel was phenotyped by extracting root traits from

117 enic toxin deletion mutants derived from the Ames strain to examine the role of lethal toxin and edem

118 ated and structurally characterized from the Ames, Sterne, and Pasteur strains of B. anthracis.

119 tes that caused the genotoxicity of 1 in the Ames and mouse lymphoma L51784 assays.

120 Only BFDGE was mutagenic in the Ames assay with strain TA100 of Salmonella typhimurium.

121 nes and less mutagenic than cisplatin in the Ames assay.

122 for the absence of retinal phenotype in the Ames mouse should be helpful in understanding USH1F and

123 In the Ames Salmonella typhimurium reversion assay 1,6- and 1,8

124 o found to be a direct-acting mutagen in the Ames test using Salmonella typhimurium tester strains TA

125 pound revealed bacterial mutagenicity in the Ames test using TA97a Salmonella strain, and subsequent

126 enyls that are nonmutagenic (inactive in the Ames test).

127 channel blockage testing, negativity in the Ames test, and 5/5 cure @ <15 mpk x 3 in mice infected w

128 ic or phototoxic effects, is negative in the Ames test, and affects cytochrome P450-dependent enzymes

129 microM and was inactive as a mutagen in the Ames test.

130 parations to activate IQ to a mutagen in the Ames test.

131 4-aminobiphenyls that are not active in the Ames test.

132 associated with cochlear pathogenesis in the Ames waltzer (av) mouse, a model for deafness in Usher s

133 In the Ames/Salmonella assay, using rat colon S9 as the activat

134 y in most genotoxicity assays, including the Ames (Salmonella) assay.

135 cal map, and a partial transcript map of the Ames dwarf critical region on mouse chromosome 11.

136 on of Lu during industrial processing of the Ames Lu standard.

137 at were shown to be genetic relatives of the Ames strain by multiple-locus variable number tandem rep

138 nd (iii) several different lab stocks of the Ames strain, including a clinical isolate from the 2001

139 00 fg of template DNA) identification of the Ames strain.

140 While many institutions use a version of the Ames test in the undergraduate genetics laboratory, stud

141 d mutation in protocadherin 15 (Pcdh15), the Ames waltzer mice have been presented as potential model

142 s anti-mutagenic potential by performing the Ames test against heterocyclic amines (HCAs), in continu

143 ty-promoting interventions, specifically the Ames dwarf Prop1 (df/df) mutation, calorie restriction a

144 To determine whether the Ames waltzer is a model for retinopathy in USH1F, retina

145 When rabbits were coinfected with the Ames strain and the PA- mutant strain, the toxin produce

146 x in rabbits by comparing infection with the Ames strain versus isogenic mutants with deletions of th

147 st (i.e., human lungs) and not only with the Ames test.

148 for mass bias we normalized all unknowns to Ames Lu.

149 n the educational content of the traditional Ames test teaching laboratory, while simultaneously enha

150 Before diquat treatment, Ames dwarf mice, compared with nonmutant littermate cont

151 ed differences in spore binding of wild-type Ames and a bclA mutant of B. anthracis to bronchial epit

152 ores by macrophages for either the wild-type Ames or the bclA mutant strain.

153 The binding of wild-type Ames spores to bronchial epithelial cells appeared to be

154 Under Ames medium, we also observed >30% longer decay time in

155 gs from rod bipolar cells showed, both under Ames medium and after blocking GABA(A/C) and glycine rec

156 ifolia (L.) Huds. subsp. longifolia by using Ames Salmonella test (TA 1535 and TA1537 strains).

157 oth the Sterne strain and the fully virulent Ames strain of B. anthracis, which may have been a resul

158 ith lethal pneumonic doses of fully virulent Ames strain spores.

159 deletion mutant (bclA) of the fully virulent Ames strain.

160 on of mice after infection with the virulent Ames B. anthracis.