ライフサイエンスコーパス: Ames

1 Ames DF mice, like Snell dwarf and GHRKO mice, show elev

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

3 Ames mutagenicity and CHO-K1 micronucleus assays were ap

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

36 llenged with the fully virulent B. anthracis Ames wild-type strain or the isogenic toxin-deficient mu

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

38 s tularensis strain SCHU S4 and B. anthracis Ames.

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

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

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

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

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

44 lethal dose 50 (LD50) of Bacillus anthracis Ames spores, animals were treated orally until 30 days p

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

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

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

48 features of the letters' Bacillus anthracis Ames strain.

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

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

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

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

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

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

55 Bruce Ames that emphasized the documented relationships betwee

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

57 in long-living growth hormone (GH)-deficient Ames Dwarf (df/df) mice.

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

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

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

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

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

63 Removal of an embedded Ames-positive heteroaromatic amine by reversing a sulfon

64 well predicted (AUC equals 0.89 and 0.85 for Ames and USNAM, respectively), European populations some

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

66 y in human whole blood, navigation away from Ames mutagenic amine fragments while balancing metabolic

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

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

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

70 raits in maize and the extensively genotyped Ames Panel.

71 Hypopituitary Ames dwarf mice were injected either with growth hormone

72 o-day workshop held September 9-10, 2022, in Ames, Iowa, co-hosted with the United State Department o

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

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

75 stress resistance and extended longevity in Ames dwarf mice.

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

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

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

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

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

81 - 0.8, respectively), but GH injections into Ames dwarf mice restored the normal level of cadmium res

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

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

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

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

86 ions (CYP1A1, IL8, COX-2), and mutagenicity (Ames) show that RNG exhaust has toxicity that is compara

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

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

89 how health and safety professionals at NASA Ames Research Center used CEAT to manage potential risks

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

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

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

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

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

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

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

97 The exceptional longevity of Ames dwarf (DF) mice can be abrogated by a brief course

98 cantly suppressed human MPhi phagocytosis of Ames spores.

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

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

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

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

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

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

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

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

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

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

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

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

111 of the anthrax pathogen B. anthracis strain Ames.

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

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

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

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

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

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

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

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

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

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

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

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

124 antimutagenic activity was evaluated by the Ames test.

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

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

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

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

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

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

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

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

133 demonstrated non-mutagenic properties in the Ames assay, V. cribbiana exhibited mutagenicity at high

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

135 int) and the United States as well as in the Ames inbred diversity panel, using days to flowering as

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

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

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

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

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

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

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

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

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

145 4-aminobiphenyls that are not active in the Ames test.

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

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

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

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

150 The 2021 integration of the Ames Life Sciences Data Archive with GeneLab to establis

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

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

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

154 00 fg of template DNA) identification of the Ames strain.

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

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

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

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

159 then evaluated the four compounds using the Ames test and the potency assays in BV2 cells, selecting

160 ompound 26 was found to be mutagenic via the Ames test.

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

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

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

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

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

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

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

168 tion of 400% following 2 weeks of treatment; Ames and hERG tests excluded potential concerns regardin

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

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

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

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

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

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

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

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

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

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