ライフサイエンスコーパス: MMS

1 MMS is an autosomal recessive condition described thus f

2 MMS plus low glucose (2 mm) or pyruvate (5 mm) gave 11-

3 MMS sensitivity of these mutants was contingent on the s

4 MMS-induced DNA damage triggers a metaphase arrest by mo

5 MMS-induced mitochondrial dysfunction, however, is AAG-i

6 r show that PRR pathway preference in 0.001% MMS depends on timing and context; cells preferentially

7 nts in their exquisite sensitivity to 0.001% MMS; thus, low-dose MMS treatment provides a distinctive

8 n cells (7.8 +/- 1.2 DPC per 10(6) nt mM(-1) MMS).

9 ed DNA (6.0 +/- 0.6 DPC per 10(6) nt muM(-1) MMS) and in human cells (7.8 +/- 1.2 DPC per 10(6) nt mM

10 28 (16 MMS, 12 USS) of 58 (48.3%; 95% CI 35.0-61.8) of the inva

11 42 (MMS) and 45 (USS) primary ovarian and tubal cancers were

12 S), and participant changing their mind (483 MMS, 1490 USS).

13 ended on Dec 31, 2011, and included 345,570 MMS and 327,775 USS annual screening episodes.

14 attend three appointments for the screen (72 MMS, 757 USS), and participant changing their mind (483

15 Among 20 821 MMS procedures, 149 adverse events (0.72%), including 4

16 e subunits Rnr1 and Rnr3, thereby abrogating MMS-induced mutagenesis and enhancing cell lethality.

17 A similar result was obtained after MMS treatment of these cells.

18 Mean (SD) time to recurrence after MMS was 3.91 (4.4) years, and after WLE, 4.45 (2.7) year

19 ng and translation influence viability after MMS damage.

20 ncreased sensitivity to the alkylating agent MMS and hyper-recombination in an oligonucleotide-mediat

21 ive to treatment with the DNA damaging agent MMS.

22 t, and its depletion partially suppresses an MMS or HU-induced metaphase block.

23 es, as measured by SE (r=0.642, P<.0001) and MMS (r=0.443, P<.04), and with post-OLT changes (for SE:

24 by NAD(P)H depletion, from both H(2)O(2) and MMS exposures.

25 Spontaneously arising and MMS-induced insertion/deletion mutations and large rearr

26 ue to their role in regulating the basal and MMS-induced expression of DNA glycosylase Mag1.

27 ay between initial physician examination and MMS predicted defect size (p = 0.0004), with greater tha

28 lele exhibited significant filamentation and MMS sensitivity in this background whereas mutations tha

29 are resistant to this combination FK866 and MMS treatment.

30 ing of tRNA modifications caused by H2O2 and MMS.

31 ic increase in sensitivity to chronic HU and MMS treatment; however, these double mutants were not ch

32 ogue, but when added together KIC (2 mm) and MMS stimulated insulin release 7-fold (versus 12-fold fo

33 tag recBCD) were more sensitive to MNNG and MMS than the single mutants suggesting that homologous r

34 h in turn regulates ergosterol synthesis and MMS resistance.

35 cells against cell killing by BCNU, TMZ, and MMS, which is consistent with the possibility that mitoc

36 e RAD6 epistasis group in response to UV and MMS exposure.

37 nner, preventing mutations induced by UV and MMS, respectively.

38 is lower, compared to that caused by UV and MMS, which suggests that ssDNA could be actively protect

39 Both hCG and MMSs will be specifically captured by the fibre sensor,

40 e adhered on the surface of fibre sensor and MMSs respectively.

41 intermediates via a route that is likely At-MMS and UV sensitive81 dependent.

42 can be readily conjugated to magnetic beads, MMS-based SELEX provides a general platform for rapid ge

43 logs of yeast Rad5, can discriminate between MMS-induced versus UV-induced DNA damage.

44 n the mean number for all physicians billing MMS.

45 ly sensitive to replicative stress caused by MMS and not to more direct DNA breaks.

46 scriptional regulation of the RTP801 gene by MMS.

47 or accurate repair of DNA lesions induced by MMS.

48 spatial and temporal resolution provided by MMS observations.

49 metry (LC-ESI-MS) via unmediated sampling by MMS DESI-IMS.

50 to ovarian cancer by Dec 31, 2014, comparing MMS and USS separately with no screening, ascertained by

51 t analysis identified seven highly connected MMS-toxicity modulating proteins associated with transla

52 In contrast, MMS promotes the degradation of HLTF and the interaction

53 Correspondingly, MMS treatment was capable of stimulating a 2.5 kb RTP801

54 A-damaging agents (cisplatin, actinomycin D, MMS, and etoposide), but not the cisplatin isomer, trans

55 te sensitivity to 0.001% MMS; thus, low-dose MMS treatment provides a distinctive opportunity to stud

56 We show that upon exposure to low-dose MMS, a PRR-defective rad18Delta mutant stalls into a len

57 During MMS, unlike WLE, the entire cutaneous surgical margin is

58 cs and antibiotics and sterile gloves during MMS were associated with modest reduction of risk for ad

59 , which is nonetheless managed safely during MMS.

60 cted, including 28 borderline tumours (eight MMS, 20 USS).

61 REV3 cooperates with the endonuclease MMS and UV-sensitive protein81 in response to interstran

62 A further 13 (five MMS, eight USS) women developed primary ovarian cancer d

63 (none MMS, 66 USS), removal of ovaries (five MMS, 29 USS), relocation (none MMS, 39 USS), failure to

64 st-OLT changes (for SE: r=-0.583, P<.01; for MMS: r=-0.536, P<.01).

65 tive values were 89.5%, 99.8%, and 35.1% for MMS, and 75.0%, 98.2%, and 2.8% for USS, respectively.

66 bal cancers were 89.4%, 99.8%, and 43.3% for MMS, and 84.9%, 98.2%, and 5.3% for USS, respectively.

67 exists in the number of stages per case for MMS for head and neck, genitalia, hands, and feet skin c

68 itutional US ambulatory referral centers for MMS.

69 hysicians who received Medicare payments for MMS from any practice performing MMS on the head and nec

70 A screen for MMS-sensitive mutants identified a novel truncation alle

71 ned as those whose mean number of stages for MMS was 2 standard deviations greater than the mean numb

72 Five-year overall survival for MMS was 92% and for WLE was 94% (P = .28).

73 (FLAG)betabeta' isolated from MMS-treated MHY343 cells or cells containing a deletion

74 cordingly, Aag(-/-) cells are protected from MMS-induced NAD(+) depletion and glycolysis inhibition.

75 s resume the cell cycle during recovery from MMS-induced DNA damage in S-phase.

76 utively and in the presence of the genotoxin MMS.

77 determining cellular morphology following HU/MMS treatment.

78 ng a causative role for DONSON disruption in MMS.

79 ete replication fork arrest and lethality in MMS, demonstrating that Rad53 deactivation is a key mech

80 Replication intermediates persisted in MMS-treated cells, suggesting that replication fork move

81 ment contribute to the slowing of S phase in MMS-treated fission yeast cells.

82 in pph3Delta cells slows fork progression in MMS, whereas deactivation of Rad53, through expression o

83 increased and prolonged gamma-H2AX signal in MMS-treated BRCA1/2 cells suggested an aberrant processi

84 In HaCaT human keratinocytes, MMS was able to induce a rapid increase in the mRNA leve

85 riched in response to methyl methanesulfate (MMS) or hydroxyurea (HU) treatment, and its depletion pa

86 ydroxyurea (HU) and methyl methanesulfonate (MMS) activates DNA integrity checkpoints; in checkpoint-

87 ersensitive to both methyl methanesulfonate (MMS) and 5-hydroxymethyl-2'-deoxyuridine, agents that in

88 g reagents, such as methyl methanesulfonate (MMS) and H2O2.

89 DNA-damaging agents methyl methanesulfonate (MMS) and hydroxyurea by a mechanism(s) that requires the

90 of cells exposed to methyl methanesulfonate (MMS) and in the absence of Mag1, Rad30 and Rev3, human p

91 ng reagents such as methyl methanesulfonate (MMS) and N-methyl-N-nitrosourea (MNU), while expression

92 hypersensitivity to methyl methanesulfonate (MMS) and nitrogen mustard (HN2).

93 el of resistance to methyl methanesulfonate (MMS) and temozolomide (TMZ) but simultaneous overexpress

94 ause sensitivity to methyl methanesulfonate (MMS) and/or ionizing radiation, along with follow-up cha

95 he alkylating agent methyl methanesulfonate (MMS) compared to the parent strain.

96 DNA damaging agent methyl methanesulfonate (MMS) in comparison to responses to acute heat shock, loo

97 mined the repair of methyl methanesulfonate (MMS) induced DNA damage in haploid G1 yeast cells, so th

98 he alkylating agent methyl methanesulfonate (MMS) is mediated in part by Dap1p (damage resistance pro

99 A damages caused by methyl methanesulfonate (MMS) or etoposide promote the formation of Ku70-Pol-beta

100 ptothecin (CPT) and methyl methanesulfonate (MMS) sensitivity of nuclease-deficient mre11-3 and sae2D

101 he alkylating agent methyl methanesulfonate (MMS) was also observed for siRNA-mediated ATR silencing.

102 s were sensitive to methyl methanesulfonate (MMS), and rev1 rad30 or rev3 rad30 double mutant cells w

103 spectrum caused by methyl methanesulfonate (MMS), and showed that MMS also induces more base substit

104 ydroxyurea (HU) and methyl methanesulfonate (MMS), and ubiquitination of proliferating cell nuclear a

105 DNA-damaging agent methyl methanesulfonate (MMS), as determined by chemogenomic fitness profiling of

106 mitomycin C (MC) or methyl methanesulfonate (MMS), as well as homologous recombination in Hfr mating

107 the genotoxic agent methyl methanesulfonate (MMS), but the molecular basis of genotoxic stress is unc

108 V)-C radiation, and methyl methanesulfonate (MMS), indicating the broad relevance of HRR to genotoxic

109 DNA damaging agent, methyl methanesulfonate (MMS), induces RTP801 transcription.

110 eroxide (H(2)O(2)), methyl methanesulfonate (MMS), or camptothecin by monitoring NAD(P)H.

111 DNA-damaging agent methyl methanesulfonate (MMS), TOR-dependent cell survival required a functional

112 DNA-damaging agent methyl methanesulfonate (MMS), we carried out two-dimensional gel analyses of rep

113 t in vivo repair of methyl methanesulfonate (MMS)-induced alkylation damage in DNA involves Mag1 but

114 irs the response to methyl methanesulfonate (MMS)-induced DNA lesions and disrupts telomeric silencin

115 3 (E2) and promotes methyl methanesulfonate (MMS)-induced PCNA polyubiquitination.

116 nsitivity to 0.001% methyl methanesulfonate (MMS).

117 A damage induced by methyl methanesulfonate (MMS).

118 thout DNA damage by methyl methanesulfonate (MMS).

119 he alkylating agent methyl methanesulfonate (MMS).

120 he alkylating agent methyl methanesulfonate (MMS).

121 with the genotoxin methyl methanesulfonate (MMS).

122 t (UV) light and to methyl methanesulfonate (MMS).

123 ting agents such as methyl methanesulfonate (MMS).

124 s in sensitivity to methyl methanesulfonate (MMS).

125 he alkylating agent methyl methanesulfonate (MMS).

126 he alkylating agent methyl methanesulfonate (MMS).

127 eplication forks in methyl-methanesulfonate (MMS)-damaged cells, under different conditions of Rad53

128 xposure of yeast to methyl-methanesulfonate (MMS).

129 chemicals such as methyl methanesulphonate (MMS) and N-ethyl-N-nitrosurea.

130 ing agents such as methyl methanesulphonate (MMS), absence of the full-length form of Translation Ini

131 ypersensitivity to methyl methanesulphonate (MMS), camptothecin (CPT) and mitomycin C (MMC), agents t

132 hypersensitive to methyl methanesulphonate (MMS), suggesting that PARP activity and DNA repair respo

133 e alkylating agent methyl methanesulphonate (MMS).

134 to alkylating agent methylmethanesulfonate (MMS).

135 oped microscale molecular mass sensor (micro-MMS) is presented.

136 rates the molecular mass range of the micro-MMS can be, in principle, tuned from less than 10(2) g/m

137 The micro-MMS employs a widely applicable technique of measuring t

138 The ratio data from the micro-MMS is also demonstrated to readily provide a "universal

139 ameters are important to interpret the micro-MMS output: the radius of the interrogating light probe

140 The micro-MMS samples the RIG with probe beams at two positions al

141 nctionalised modified magnetic microspheres (MMSs) to "amplify" the effect of target bio-chemical ana

142 EMS; point mutations required 1.25 microg/mL MMS and 1.40 microg/mL EMS before a mutagenic effect was

143 f chromosomal aberrations was 0.85 microg/mL MMS and 1.40 microg/mL EMS; point mutations required 1.2

144 Also Crt1, the repressor of model MMS-inducible ribonucleotide reductase genes, was found

145 esolution, NASA's Magnetospheric Multiscale (MMS) mission has found direct evidence for electron dema

146 ields with NASA's Magnetospheric Multiscale (MMS) mission, we utilize Earth's magnetosphere as a plas

147 The Magnetospheric Multiscale (MMS) spacecraft encounter an electron diffusion region (

148 y observed by the Magnetospheric Multiscale (MMS) spacecraft.

149 In INS-1 cells, neither MMS nor KIC (10 mm) was an insulin secretagogue, but whe

150 ), non-ovarian cancer or other disease (none MMS, 66 USS), removal of ovaries (five MMS, 29 USS), rel

151 ovaries (five MMS, 29 USS), relocation (none MMS, 39 USS), failure to attend three appointments for t

152 (MRS), whose function is required for normal MMS.

153 of restoring MMS-resistance to the normally MMS-sensitive strain.

154 base excision repair (BER) activity but not MMS sensitivity.

155 were measured in the presence and absence of MMS.

156 mstances in which the additional benefits of MMS outweigh its higher cost are needed, still lacking,

157 Shu complex promotes high-fidelity bypass of MMS-induced alkylation damage, such as N3-methyladenine,

158 ied analysis of death from ovarian cancer of MMS versus no screening with exclusion of prevalent case

159 n does not appear to be the primary cause of MMS sensitivity of the double tailless mutants.

160 nt a determinant of outcome as the choice of MMS or excision.

161 ng fibroblasts treated with a combination of MMS and 4-AN, a complete inhibition of DNA synthesis is

162 Much of the data regarding complications of MMS are anecdotal or report findings from single centers

163 e able to abrogate the stimulatory effect of MMS, indicating that Elk-1 and C/EBP are both involved i

164 are as sensitive to the cytotoxic effects of MMS and MNNG as the most base excision repair (BER)-defi

165 ighly sensitized to the cytotoxic effects of MMS by 4-amino-1,8-naphthalimide (4-AN), an inhibitor of

166 nd 28% (-3 to 49) in years 7-14 in favour of MMS.

167 of RAD51 or RAD54 prevented the formation of MMS-induced HRR intermediates (X-molecules) arising duri

168 Based on the heat-lability of MMS-induced base damage, an assay was developed that mon

169 tant when cells replicate in the presence of MMS, and that double deletions lead to a greater reducti

170 H3 N-tails are important for the removal of MMS-induced DNA lesions due to their role in regulating

171 Rdh54 retains its function in the repair of MMS-induced DNA damage even when recruited to the incorr

172 The sensitivity and specificity of MMS for detection of iEOCs were 85.8% (95% CI, 79.3% to

173 s Snail and vimentin, and a subpopulation of MMS-treated cells displayed an elongated fibroblast-like

174 e that RTP801 is a transcriptional target of MMS in human keratinocytes and that C/EBP is implicated

175 ind, randomized, placebo-controlled trial of MMS in 17- to 45-y-old Gambian women who were menstruati

176 In 20 years, use of MMS has grown approximately 10-fold and its cost now exc

177 utilize magnetic cavity observations by one MMS spacecraft to predict measurements from a second/thi

178 mission, as measured by either SE (P<.01) or MMS (P<.04).

179 roup after OLT, as measured by SE (P<.03) or MMS (P<.02).

180 60 mg of iron and 400 mug of folic acid, or MMS containing a daily allowance of 15 micronutrients, i

181 in response to changing levels of copper or MMS.

182 We have also mapped our MMS-toxicity modulating proteins onto an E. coli protein

183 The mean number of stages per MMS case for all physicians practicing from January 2012

184 305 individual billing physicians performing MMS.

185 ayments for MMS from any practice performing MMS on the head and neck, genitalia, hands, and feet reg

186 nsulin release in fresh islets, and KIC plus MMS gave synergistic insulin release in cultured human i

187 r RNR3 were hypersensitive to rapamycin plus MMS, providing the first demonstration that Rnr3 contrib

188 These agents also potentiated MMS-induced insulin release in fresh islets, and KIC plu

189 efined by ATP-dependent DNA Helicase RECQ4A, MMS and UV-sensitive protein81, REV3, and the ATPase Rad

190 Reduced MMS was largely independent of adult pigmentation patter

191 ound that 4 hypomorphs significantly reduced MMS to varying degrees.

192 d that Mag1 is the major enzyme that removes MMS-damaged bases.

193 d51/Rad54-dependent HRR pathway(s) to repair MMS-induced lesions during S-phase.

194 f these proteins function together to resist MMS-induced DNA damage and promote gene conversion at bl

195 is only recently enabled by high-resolution MMS observations.

196 liminated filamentation and largely restored MMS resistance.

197 eta, iota and kappa are capable of restoring MMS-resistance to the normally MMS-sensitive strain.

198 I-IMS) using microporous membrane scaffolds (MMS) enables enhanced spatiochemical analyses of interac

199 NASA's Magnetospheric Multi-Scale (MMS) mission is designed to explore the proton- and elec

200 we report a Multiparametric Mutation Score (MMS) developed by combining in silico predictions of sta

201 ndom numbers to annual multimodal screening (MMS) with serum CA125 interpreted with use of the risk o

202 as a second-line test (multimodal screening [MMS]; n=50 640); or annual screening with transvaginal u

203 The micromagnetic separation (MMS) chip integrates microfabricated ferromagnetic struc

204 A FACS-based shRNA screen identified several MMS genes as essential for the epithelial-mesenchymal tr

205 We document a mid-millennium shift (MMS) in ocean-atmosphere circulation around 1500-1650 CE

206 nnon entropy (SE) and median mobility shift (MMS) values derived from the heteroduplex mobility assay

207 nated the "mesenchymal metabolic signature" (MMS).

208 or the Shu complex in the repair of specific MMS-induced DNA lesions and elucidate the interplay betw

209 screening by using the multimodal strategy (MMS) in which annual serum cancer antigen 125 (CA-125) w

210 havior, we measured the male mating success (MMS) of 12 hypomorphic y mutants and matched-outbred-bac

211 Monomethyl succinate (MMS) combined with a barely stimulatory concentration of

212 DNA alkylation by methyl methane sulfonate (MMS) induces Cdc6 degradation independently of p53.

213 anidine (MNNG) and methyl methane sulfonate (MMS) produce a wide variety of N- and O-methylated bases

214 cells treated with methyl methane sulfonate (MMS), hydroxyurea (HU) or camptothecin (CPT), we show th

215 droxyurea (HU) and methyl-methane sulfonate (MMS).

216 tion-blocking agent methylmethane sulfonate (MMS) in smc6 mutants, with double deletions conferring s

217 on and DNA targets: methylmethane sulfonate (MMS), methylnitrosourea (MNU), ethylmethane sulfonate (E

218 O2) and alkylation (methylmethane sulfonate, MMS) stresses induced nearly identical patterns of up- a

219 onal multiple-micronutrient supplementation (MMS) affects placental function.

220 cian practices in Mohs micrographic surgery (MMS) and the associated factors.

221 rrence rates with Mohs micrographic surgery (MMS) are modestly better than those for excision surgery

222 s associated with Mohs micrographic surgery (MMS) can guide clinical management.

223 However, Mohs micrographic surgery (MMS) is now used to treat a growing subset of individual

224 likely to receive Mohs micrographic surgery (MMS) over excision.

225 defect size after Mohs micrographic surgery (MMS).

226 involved in the multiple metabolic syndrome (MMS).

227 n disease, microcephaly-micromelia syndrome (MMS).

228 Our data also indicate that MMS-induced mutations at adenine nucleotides are signifi

229 re, a gel mobility shift assay revealed that MMS was able to initiate rapid formation of a protein co

230 thyl methanesulfonate (MMS), and showed that MMS also induces more base substitution mutations in BRC

231 Our data suggest that MMS-induced genes undergo transcription complex assembly

232 The MMS coincided with the deepest LIA cooling and was proba

233 The MMS sensitivity of a Pol4-deficient strain can be rescue

234 ila ortholog of the yeast snm1 gene, and the MMS- and HN2-sensitive mus301 mutant defines the Drosoph

235 We found that both the MMS sensitivity and growth phenotypes of DCDC-deficient

236 proton scale magnetic cavity observed by the MMS spacecraft in the magnetosheath.

237 ar of diagnosis was 2008 (1986-2013) for the MMS group vs 2003 (1978-2013) for the WLE group (P < .00

238 Melanoma-specific mortality for the MMS group was 2 vs 13 patients for the WLE group, with m

239 tage of the multipoint measurements from the MMS constellation, we demonstrate that our kinetic model

240 97 of 50 078 (0.2%) women from the MMS group and 845 of 48 230 (1.8%) from the USS group un

241 d a repeat test, and 167 (0.3%) women in the MMS group and 1894 (3.9%) women in the USS group require

242 verall recurrence rates were 5 (1.8%) in the MMS group and 22 (5.7%) in the WLE group (P = .07).

243 The 5-year recurrence rate was 1.1% in the MMS group and 4.1% in the WLE group (P = .07).

244 Overall, 4355 of 50 078 (8.7%) women in the MMS group and 5779 of 48 230 (12.0%) women in the USS gr

245 Of these women, 148 (0.29%) women in the MMS group, 154 (0.30%) in the USS group, and 347 (0.34%)

246 ncer in 1282 (0.6%) women: 338 (0.7%) in the MMS group, 314 (0.6%) in the USS group, and 630 (0.6%) i

247 e for analysis: 50,624 (>99.9%) women in the MMS group, 50,623 (>99.9%) in the USS group, and 101,299

248 flexible parametric model showed that in the MMS group, this mortality effect was made up of 8% (-20

249 Specificity was higher in the MMS than in the USS group, resulting in lower rates of r

250 4 results in a 6- to 14-fold increase in the MMS-induced mutation frequency and in a significant incr

251 The sensitivity of the MMS and USS screening strategies is encouraging.

252 Operation of the MMS device is facile and robust and demonstrates high re

253 atients on the GUG, 19.0% of patients on the MMS, 44.0% of patients on the GDS15, and 64.9% of patien

254 comes Scores (COS) were used to optimize the MMS for biological and clinical relevance and yield a pa

255 These deletion mutations also rescue the MMS sensitivity of esc2Delta cells.

256 eckpoint-defective mrc1 alleles suppress the MMS sensitivity and the checkpoint recovery defect of di

257 Women randomised to the MMS group had their blood tested for CA125 and those ran

258 y allocated 202,638 women: 50,640 (25.0%) to MMS, 50,639 (25.0%) to USS, and 101,359 (50.0%) to no sc

259 identify chromosomal regions contributing to MMS-related traits represented by composite factors deri

260 tored wild-type resistance of this mutant to MMS, H2O2, and SIN-1.

261 yeast, the response of the Rad53 pathway to MMS is compromised due to a loss of Sod1 activity, consi

262 s modest capacities to provide resistance to MMS and to resolve recombination-dependent X-shaped mole

263 mouse cells were slightly more resistant to MMS than wild-type cells, probably due to the production

264 expression in wild-type cells in response to MMS but was nonresponsive in cells lacking the TF.

265 n even after S phase, and normal response to MMS damage correlates with the maintenance of intact Dfp

266 d Rtt107 with Dpb11 (hTopBP1) in response to MMS-induced DNA alkylation, suggesting that Slx4 and Rtt

267 function separately from REV3 in response to MMS.

268 981 bp of the promoter that is responsive to MMS treatment.

269 -chromosome mutants were solely sensitive to MMS and define 8 new mutagen-sensitive genes (mus212-mus

270 r priA (primosome) genes are as sensitive to MMS and MNNG as alkA tag bacteria.

271 cells were synergistically more sensitive to MMS than the respective single mutant strains.

272 trains without tpa1 are no more sensitive to MMS than WT yeast, whereas mag1-deficient yeast are ~500

273 icient yeast are ~500-fold more sensitive to MMS.

274 fficiency and leads to higher sensitivity to MMS and accumulation of the DNA strand breaks.

275 e short hairpin RNA increases sensitivity to MMS and enhances genomic instability.

276 of PARP activity results in sensitization to MMS through maintenance of an ATR and Chk1-dependent S-p

277 main reasons for withdrawal were death (two MMS, 28 USS), non-ovarian cancer or other disease (none

278 renders tel1-Delta cells (but not wild type) MMS-sensitive, demonstrating that, under certain conditi

279 lence screen, 50 078 (98.9%) women underwent MMS, and 48 230 (95.2%) underwent USS.

280 ifically captured by the fibre sensor, where MMSs act as an "amplifier" to improve the sensor sensiti

281 nd ENU showed linear dose-responses, whereas MMS and EMS had nonlinear curves containing a range of n

282 s 0-14 of 15% (95% CI -3 to 30; p=0.10) with MMS and 11% (-7 to 27; p=0.21) with USS.

283 stone H4; this event is also associated with MMS- or phleomycin-induced DSBs but not with UV-induced

284 e kinetic simulation and its comparison with MMS observations, we show for the first time that ion-sc

285 in in these cells positively correlates with MMS in a subset of mutants.

286 The early invitation with MMS group had an infant mortality rate of 16.8 per 1000

287 Early invitation with MMS group had an under 5-year mortality rate of 18 per 1

288 Usual invitation with MMS group had the highest incidence of spontaneous abort

289 andom sample of patients treated for KC with MMS were selected for telephone interview.

290 nsecutive sample of patients presenting with MMS for 35 weeks at each center, with staggered start ti

291 noted a significant mortality reduction with MMS when prevalent cases were excluded.

292 functional categories over-represented with MMS-toxicity modulating proteins and demonstrate that, i

293 oribosyltransferase (NAMPT), synergizes with MMS to induce cytotoxicity and Aag(-/-) cells are resist

294 There were 277 patients treated with MMS (mean [SD] age, 64.0 [13.1] years; 62.1% male) and 3

295 e outcomes of patients with MIS treated with MMS compared with those treated with WLE.

296 c survival of patients with MIS treated with MMS compared with WLE.

297 The same strains either treated with MMS or containing a crt1Delta gave ratios between 0.49 a

298 sisted of 662 patients with MIS treated with MMS or WLE per standard of care in dermatology and surge

299 UV-irradiated cells or in cells treated with MMS requires Huwe1 and is associated with release of Cdc

300 s an activation of Chk1 after treatment with MMS and 4-AN, which can be suppressed by caffeine.