ライフサイエンスコーパス: MSS

1 MSS also allows for accurate prediction of the number an

2 MSS HNPCC tumors displayed a significantly lower degree

3 MSS HNPCC tumors had KRAS mutations exclusively in codon

4 MSS HTA provides a rapid and sensitive approach for dete

5 MSS promoters are defined by the lack of a TATA box and

6 MSS provides a straightforward approach for modeling hig

7 MSS reduced distress scores during the examination perio

8 MSS was used to define multi-marker panels that were rob

9 MSS-2 provides 9 Mb coverage of the canine genome with n

10 rithmic CRP; 95% CI, 1.30 to 1.59; P < .001; MSS hazard ratio, 1.51 per unit increase of logarithmic

11 and hMSH2 expression, as well as 9 of the 10 MSS cases, lacked methylation of the hMLH1 promoter.

12 integration in a manner consistent with a 12 MSS model.

13 le the results presented here confirm the 12 MSS model, they also indicate that the integration of NK

14 in 8 of 12 MSI cancers whereas only 3 of 16 MSS cancers were methylated.

15 efforts in the dog, Minimal Screening Set 2 (MSS-2) of 327 canine microsatellite markers has been mul

16 2 (50%) of 4 MSI-L tumors, and 8 (35%) of 23 MSS tumors demonstrated HPP1 hypermethylation.

17 ors (5 of 5 MSI-H, 2 of 4 MSI-L, and 1 of 23 MSS) showed evidence of hMLH1 hypermethylation.

18 mean CORE-OM scores of 0.87 (SD 0.50) in 237 MSS participants versus 1.11 (0.57) in 216 support as us

19 MSI-H, 1 (6%) of 16 MSI-L, and 4 (15%) of 27 MSS lesions showed hMLH1 hypermethylation (P = 0.013).

20 tation, negative for KRAS mutation); type 3 (MSS or MSI low, non-CIMP, negative for BRAF mutation, po

21 volved and found elevations in 5 of 15 (33%) MSS CRC cell lines analyzed.

22 tation, positive for KRAS mutation); type 4 (MSS or MSI-low, non-CIMP, negative for mutations in BRAF

23 during the examination period and 182 (59%) MSS participants completed at least half of the course.

24 e-free survival (HR, 6.6; 95% CI, 2.9-14.6), MSS (HR, 6.2; 95% CI, 2.6-14.4), and OS (HR, 2.8; 95% CI

25 These findings may reflect a MSS mutator phenotype contributing to the development of

26 chial epithelial (HBE) cells exposed to air, MSS from 1R5F tobacco reference cigarettes, and e-vapor

27 ACVR2, 62% lacked protein expression but all MSS and MSI-H tumors with wild-type ACVR2 expressed prot

28 KRAS mutation negative; n = 170), alternate (MSS, CIMP low, BRAF mutation negative, and KRAS mutation

29 The predictive value of normal IHC for an MSS/MSI-L phenotype was 96.7%, and the predictive value

30 utator phenotype was reported recently in an MSS CRC cell line.

31 ence-free survival (HR = 1.70, P = .046) and MSS (HR = 1.88, P = .043) in a multivariable analysis.

32 16S rRNA gene sequencing (r(2) = -0.60) and MSS (r(2) = -0.55).

33 To ask whether the cytoplasmic domain and MSS of each protein serve only as a membrane anchor or h

34 differences were noted between the MSI-L and MSS group for any of the parameters tested.

35 15% of colorectal cancers, whereas MSI-L and MSS tumors appear to be phenotypically similar.

36 is distinct from tumor phenotypes MSI-L and MSS, with no apparent differences between MSI-L and MSS.

37 th no apparent differences between MSI-L and MSS.

38 phism has differential influences on MSI and MSS CRC risk.

39 ur findings support a model in which MSI and MSS preferentially target different genes and pathways i

40 expression signature distinguishing MSI and MSS samples.

41 o poorly differentiated histology in MSI and MSS tumors.

42 CRP level was associated with poorer OS and MSS in the initial, confirmatory, and combined data sets

43 ding selectivity, poor pharmacokinetics, and MSS liability.

44 istant metastasis disease-free survival, and MSS after CLND in patients with SLN metastasis.

45 RNA knocking down MRE11 in the wild-type and MSS cell line SW-480 and a second cell line model transf

46 As MSS and HSS mice differ in several immunologic character

47 f this group, 129 (68.6%) were classified as MSS, 17 (9.0%) as MSI-L, and 42 (22.3%) as MSI-H.

48 s subgroups indicated a significantly better MSS for SNB patients with T2 and T3 melanomas (>1.0 to 4

49 patients without mismatch repair deficiency (MSS HNPCC) have certain molecular features, including gl

50 first appear in mice that eventually develop MSS, sera from infected animals were monitored for CRI f

51 In mice that eventually developed MSS, CRI were detected by 5 to 6 wk after infection, pla

52 with AJCC stage IIIB and stage IIIC disease, MSS outcomes were similar to those of patients with stag

53 ining the AQP1 sequence truncated after each MSS.

54 e rat model of musculoskeletal side effects (MSS) was used to assess whether selective MMP-13 inhibit

55 ViroCap substantially enhances MSS for a comprehensive set of viruses and has utility f

56 -Sandri-Sarkar Maximum Likelihood Estimator (MSS-MLE) method, (ii) Lea-Coulson method of the median (

57 ve patients (P < 0.001 for OS, P < 0.001 for MSS).

58 (95% CI, 1.01 to 1.04; P = .0051), 1.02 for MSS (95% CI, 1.00 to 1.04; P = .048), and 1.02 for DFS (

59 paper we propose an efficient algorithm for MSS and evaluate it on both synthetic and real data.

60 A mouse model for MSS was previously produced by disrupting Sil1 using gen

61 5% confidence interval: 2.76, 8.91) than for MSS tumors (odds ratio = 2.33, 95% confidence interval:

62 rs were suggestively stronger than those for MSS tumors; the risk with high (>/=30) body mass index (

63 so that this protein initially adopts a four MSS topology.

64 ility, distinguishing most CRC with MSI from MSS CRC.

65 For FtsQ, MSS swaps supported cell division but cytoplasmic domain

66 However, MSS can lack sensitivity and may yield insufficient data

67 ms some previously identified aberrations in MSS CRC and provides in silico evidence for some novel c

68 ociated with better survival in MSI-H and in MSS/MSI-L patient subgroups.

69 When MTHFR C677T genotype frequencies in MSS CRC cases were compared to controls, individuals wit

70 icular are major targets for inactivation in MSS colon cancers as well as in colon cancers with micro

71 loss of heterozygosity at the ACVR2 locus in MSS tumors.

72 LK4) protein kinase is frequently mutated in MSS CRC with approximately 50% of the mutations occurrin

73 y of the cell toxicity responses observed in MSS-exposed HBE cells, e-vapor exposure is not benign, b

74 embrane was prognostic for poorer outcome in MSS patients.

75 2, 16.1%); and those showing no instability (MSS, n = 317, 62.4%).

76 The risk of MSI-L/MSS tumors was not elevated among long-duration smokers

77 current smoking than there was within MSI-L/MSS tumors.

78 I-H) or MSI-low/microsatellite stable (MSI-L/MSS), was assessed in tumors of 1,202 cases.

79 ght into the mechanisms regulating TATA-less MSS promoters has been hampered by the lack of an in vit

80 Median MSS was not reached for the SLN-only positive group and

81 those reported for primate models and mimic MSS in humans.

82 Although most MSS HNPCC tumors had some degree of CpG island methylati

83 olyadenine tract of exon 10 compared with no MSS tumors.

84 Moreover, another 55% of MSS colon cancers demonstrate a transforming growth fact

85 viral pathogen, we evaluate the accuracy of MSS for real-time parameter estimation and prediction du

86 However, a stratified univariate analysis of MSS for different thickness subgroups indicated a signif

87 all 19 cases of MSI-L and 35 of 82 cases of MSS exhibited EMAST.

88 BAP were identified to be the major cause of MSS.

89 epigenetic alterations to the development of MSS HNPCC tumors.

90 ption system optimized for the expression of MSS promoters, termed the multiple promoter comparison (

91 The majority of MSS CRCs demonstrate chromosomal instability (CIN) with

92 This simple and sensitive model of MSS is an attractive alternative for studying the pathol

93 ve alternative for studying the pathology of MSS.

94 We compare the performance of MSS to three state-of-the-art benchmark 1) a likelihood

95 and KRT16 remained significant predictors of MSS in a joint analysis (HR = 2.3, P = 0.03) although, H

96 mitoses were the most powerful predictors of MSS.

97 sex (P = .01) were independent predictors of MSS.

98 ression and immunohistochemical profiling of MSS and MSI CRC cell lines and tumors revealed significa

99 ion event involving a 180-degree rotation of MSS 3 from an N(lum)/C(cyt) to an N(cyt)/C(lum) orientat

100 The severity of MSS, as judged by clinical criteria (2 blinded observers

101 red and scored for the onset and severity of MSS, using clinical and histologic parameters.

102 harmacological treatment of certain types of MSS by specifically stabilizing the mutant SIL1 protein.

103 To demonstrate the versatility of MSS HTA, we also constructed a probe sensitive to change

104 replacement of the cytoplasmic domain and/or MSS resulted in the loss of the ability to support cell

105 vary in regard to their MSI status (MSI-H or MSS), their hMLH1 protein expression (MLH- or MLH+), and

106 nical course than are stage-matched MSI-L or MSS tumors.

107 ociations of lower vitamin D with poorer OS, MSS, and DFS were independent of this association.

108 Our MSS algorithm outperforms the algorithm of Kuksa and Pav

109 was also an independent predictor of poorer MSS (hazard ratio [HR] = 1.55, P < 0.001).

110 ) microsatellite stable, Amsterdam-positive (MSS HNPCC) (N = 22); (2) Lynch syndrome cancers (identif

111 -negative polyposis and early-onset proximal MSS CRC in whom detection rates will be highest, the exp

112 was not performed had significantly reduced MSS (HR = 2.10; P < 0.001), DFS (P < 0.001), RNRFS (P <

113 o sensory analysis (Mixed Structured Scale - MSS) and seven formulations were selected in respect to

114 call this version as the Motif Stems Search (MSS) problem.

115 domain, a single membrane-spanning segment (MSS), and a large periplasmic domain that probably encod

116 soot measured with an AVL microsoot sensor (MSS) reflected black carbon.

117 uencing, and metagenomic shotgun sequencing (MSS) for Clostridium difficile identification in diarrhe

118 Metagenomic shotgun sequencing (MSS) is an important tool for characterizing viral popul

119 4; 95% CI, 1.48-3.40; P < .001), and shorter MSS (HR, 2.23; 95% CI, 1.46-3.07; P < .001).

120 l, after which males and females had similar MSS.

121 those that initiate at multiple start sites (MSS).

122 4 into the membrane results in the final six MSS topology.

123 less risky alternative to main stream smoke (MSS) of conventional tobacco cigarettes.

124 Marker State Space (MSS) defines "marker states" based on all possible patte

125 his approach, termed multiple-site-specific (MSS) HTA, was directed toward the detection of mutations

126 rate a multichannel smartphone spectrometer (MSS) as an optical biosensor that can simultaneously opt

127 tch repair mutations) (N = 21); (3) sporadic MSS (N = 92); and (4) sporadic MSI (N = 46).

128 e distinction between microsatellite stable (MSS) and low frequency MSI (MSI-L) can only be accomplis

129 ty and those that are microsatellite stable (MSS) but chromosomally unstable.

130 profiles for MSI and microsatellite stable (MSS) cancers, which suggest that cancers with MSI develo

131 d-type cell lines and microsatellite stable (MSS) cell lines.

132 onsistent with EMT in microsatellite stable (MSS) colon cancer cells, whereas cells with MSI and muta

133 Among microsatellite stable (MSS) colon cancers, we now find that non-BAT-RII point m

134 kely to have MSI than microsatellite stable (MSS) CRC [odds ratio (OR) 1.90; 95% confidence interval

135 mutator phenotypes in microsatellite stable (MSS) CRC carcinogenesis.

136 ity (MSI), but not in microsatellite stable (MSS) CRC cell lines and tumors.

137 approaches to detect microsatellite stable (MSS) HNPCC tumors are unclear.

138 ajor driving force of microsatellite stable (MSS) sporadic CRC.

139 cancers and 20 random microsatellite stable (MSS) tumors from a population-based cohort of 503 patien

140 dic CRCs, its role in microsatellite stable (MSS) tumors is debated.

141 ntly mutated genes in microsatellite stable (MSS) tumours and 16 in microsatellite instable (MSI) tum

142 Of these, 680 were microsatellite stable (MSS), 27 were MSI-H, and 111 were MSI-L.

143 es have been defined: microsatellite stable (MSS), low-frequency MSI, and high-frequency MSI (MSI-H).

144 characterized them as microsatellite stable (MSS), MSI high or MSI low, CIMP high or CIMP low, CIMP n

145 (CIN); herein termed microsatellite stable (MSS).

146 infected with EBV and microsatellite stable (MSS).

147 ubgroups of MSI-H and microsatellite stable (MSS)/low-frequency MSI (MSI-L) tumors, diploidy was asso

148 ying MSI-H, MSI-L, or microsatellite-stable (MSS) tumors have never been evaluated.

149 l as in a subgroup of microsatellite-stable (MSS) tumors.

150 icrosatellite status (microsatellite-stable (MSS) vs. microsatellite-instable (MSI)) and histology (t

151 if unstable at only one locus, or MS-stable (MSS) if showing no instability at any loci.

152 AS mutation); type 2 (microsatellite stable [MSS] or MSI-low, CIMP-positive, positive for BRAF mutati

153 romosome instability (microsatellite stable; MSS), are best understood in the context of colon cancer

154 fectiveness of detecting viruses in standard MSS versus MSS following targeted sequence capture.

155 irmed the independent effect of NSLN status (MSS; P = .04).

156 urine specimens from middle-school students (MSS) were tested individually by LCR, and then the proce

157 y students (Mindfulness Skills for Students [MSS]) plus mental health support as usual, or mental hea

158 ncluded the following groupings of subtypes: MSS = 337 and MSI = 130; type I = 458 and type II = 66.

159 In summary, MSS is a promising method that may improve on current ap

160 Conditional melanoma-specific survival (MSS) estimates up to 5 years after diagnosis were adjust

161 The 5-year melanoma-specific survival (MSS) for ulcerated and nonulcerated melanomas was 77.6%

162 nt in predicting melanoma specific survival (MSS) in a univariate analysis, which was also consistent

163 Melanoma-specific survival (MSS) was not significantly different for patients in the

164 urvival (OS) and melanoma-specific survival (MSS) were 82% and 94%, respectively, for histopathology-

165 vival (RFS), and melanoma-specific survival (MSS) were analyzed.

166 e-free survival, melanoma-specific survival (MSS), and overall survival.

167 ficantly reduced melanoma-specific survival (MSS), DFS, regional node recurrence-free survival (RNRFS

168 y reduced OS and melanoma-specific survival (MSS).

169 e recurrence and melanoma-specific survival (MSS).

170 (OS; P < .001), melanoma-specific survival (MSS; P = .0025), and disease-free survival (DFS; P = .04

171 Marinesco-Sjogren syndrome (MSS) is an autosomal recessive, neurodegenerative, multi

172 his gene lead to Marinesco-Sjogren syndrome (MSS), a debilitating autosomal recessive disease charact

173 of mice with moderate splenomegaly syndrome (MSS) at 20 wk after infection.

174 splay either moderate splenomegaly syndrome (MSS) or hypersplenomegaly syndrome (HSS).

175 d, Multiple Shooting for Stochastic systems (MSS), applies a linear noise approximation to describe t

176 We demonstrate that MSS HTA is sensitive and largely specific to all targete

177 We find that MSS significantly outperforms each of these three benchm

178 We show that MSS produces accurate estimates of key epidemic paramete

179 red with 88 (37%) of 235 participants in the MSS group.

180 In the MSS population, the pool-by-4 algorithm was 95.8% sensit

181 None of the MSS and none of the MSI-L tumors had altered expression

182 95% CI four to ten) needed to be offered the MSS course to prevent one from experiencing clinical lev

183 16, we randomly assigned 616 students to the MSS group (n=309) or the support as usual group (n=307).

184 We validated the performance of this MSS via measuring the concentrations of protein and immu

185 t, the results sufficiently showed that this MSS can achieve the comparative analysis detection limit

186 Although most mutations leading to MSS result in deletion of the majority of the protein, t

187 following integrated pathways: traditional (MSS, CIMP negative, BRAF mutation negative, and KRAS mut

188 with a subset of pathway-unassigned tumors (MSS or MSI low, CIMP negative, BRAF mutation negative, a

189 the accurate and robust transcription of two MSS promoters, pgp1 (hamster P-glycoprotein class I homo

190 Furthermore, we used MSS HTA in longitudinal studies of pro gene evolution in

191 86.3% of C. difficile-positive samples using MSS.

192 Hazard ratios (HR) for RFS for MSI-H versus MSS/MSI-L patients were 0.77 (95% CI, 0.40 to 1.48) in t

193 of detecting viruses in standard MSS versus MSS following targeted sequence capture.

194 ree survival (RFS) for MSI-H patients versus MSS/MSI-L patients (P = .10), but showed no difference i

195 The remaining 118 neoplasms (80%) were MSS.

196 nocopies several pathologies associated with MSS, although its ability to assemble and secrete antibo

197 wn-regulated in MSI cancers as compared with MSS cancers.

198 pproximately 15% of cases, and compared with MSS tumors, more often arise in the proximal colon and d

199 phoblastoid cell lines from individuals with MSS, leading us to conclude that the BiP cofactor Sil1 i

200 Males had significantly worse MSS outcomes for up to 2 years of conditional survival,

201 The 5-year MSS and RFS rates were 83% and 76%, respectively (median

202 The 5-year MSS for minimally/moderately ulcerated melanomas (</=70%

203 elanomas (>70% or >5 mm), which had a 5-year MSS of 66.4% and 59.3%.

204 0 months for the NSLN positive group (5-year MSS, 77.8% and 49.5%, respectively).

205 bility to classify both 5-year OS and 5-year MSS.