ライフサイエンスコーパス: IMT

1 IMT for the common and internal carotid arteries was det

2 IMT was defined as the distance between the luminal-endo

3 IMT was measured through bilateral carotid ultrasound.

4 d NSAIDs in 144 (36.7%), SAIDs in 29 (7.4%), IMT in 149 (38.0%), BRMs in 56 (14.3%), and none (N = 14

5 nd those with NYHA II heart failure (n=689)--IMT was associated with a 26% (0.74; 0.57-0.95; p=0.02)

6 apanese and whites in multivariable-adjusted IMT (mean difference 39 mum, 95% confidence interval [CI

7 ars after the end of DCCT but did not affect IMT progression thereafter (6-12 years).

8 High IMT was defined as an IMT >/=90th percentile according to age-, sex-, race-, a

9 eta +/- SE: -0.043 +/- 0.013, P = 0.005) and IMT progression (beta +/- SE: -0.019 +/- 0.011, P = 0.09

10 association between circulating glucose and IMT by examining the association of a genetic risk score

11 ions between the FFGRS, fasting glucose, and IMT.

12 T and coronary artery disease in the IMT and IMT-Progression as Predictors of Vascular Events (IMPROV

13 VE (Carotid Intima Media Thickness [IMT] and IMT-Progression as Predictors of Vascular Events in a Hi

14 whole carotid tree (IMT(mean), IMT(max), and IMT(mean-max)), were analyzed.

15 there was no correlation between DI-RISK and IMT (r = -0.10, P = .215).

16 o association was observed between sCD93 and IMT, sCD93 levels were significantly lower in subjects w

17 e molecular link between the NMD pathway and IMTs has implications for the diagnosis and treatment of

18 had a lower risk of increased carotid artery IMT (0.66[0.50-0.88]) in compared with those with persis

19 BP had increased risk of high carotid artery IMT (relative risk [95% confidence interval]) 1.82[1.47-

20 these population-based data, carotid artery IMT and carotid plaques had a weak relationship to the i

21 rable to estimation of common carotid artery IMT in imaging cardiovascular risk in PE.

22 en with 6 internal and common carotid artery IMT phenotypes using an additive measured genotype model

23 Carotid artery IMT was evaluated by ultrasound.

24 Carotid artery IMT was measured in the left common carotid artery.

25 stimate the individual common carotid artery IMTs in 55 women at PE diagnosis and in 64 women with no

26 Plaque was defined as IMT >1.5 mm in any segment.

27 sting compromised neuronal viability even at IMT levels below thresholds for clinical end-organ damag

28 Baseline IMT (hazard ratio, 1.18 per 10% increment; 95% confidenc

29 Compared with baseline, IMT regressed in the aggressive group and progressed in

30 ology (i.e., IMT>or=0.9 mm) is needed before IMT consistently relates to poor neuropsychological test

31 The relation between IMT and cerebral metabolite ratios was modeled using a s

32 nstrating a significant relationship between IMT and NAA concentration, suggesting compromised neuron

33 IV-infected participants had CCA-IMT and BIF-IMT values that were similar to or lower than those in H

34 n was associated with higher CCA-IMT and BIF-IMT values.

35 ion assessed associations of CCA-IMT and BIF-IMT with HIV infection and cardiovascular disease risk f

36 CCA-IMT) and carotid artery bifurcation (BIF-IMT) between 2010 and 2013.

37 ith a FRS = 22.6% (cohort average), and both IMT(mean-max) and ICCAD above the median, had a 6.5% ris

38 % risk for those with the same FRS, and both IMT(mean-max) and ICCAD below the median.

39 uch more robust than the 24-hour systolic BP-IMT relationship (r = 0.16, P = 0.04).

40 and 3, respectively; P = 0.004) and common c-IMT >0.8 mm (5% compared with 4% compared with 17% for t

41 essed cardiovascular disease risk factors, c-IMT, and CAC for each micronutrient tertile by using a c

42 nternal c-IMT and CAC scores (P < 0.05 for c-IMT and CAC).

43 associated with higher common and internal c-IMT and CAC scores (P < 0.05 for c-IMT and CAC).

44 duals presented with higher right and left c-IMT (p = 0.005 and p = 0.002, respectively), average 24-

45 We performed multivariate regression of c-IMT and CAC with each micronutrient with adjustment for

46 All measures of C-IMT and the interadventitia common carotid artery diamet

47 A risk stratification strategy based on C-IMT and ICCAD as an adjunct to FRFs is a rational approa

48 easures of carotid intima-media thickness (C-IMT) as predictors of cardiovascular events (CVEs), and

49 position, carotid intimal-media thickness (c-IMT), ambulatory blood pressure monitoring (BP), fasting

50 Carotid IMT as well as MR imaging remodeling index, lipid core,

51 Carotid IMT was assessed by ultrasonography at baseline and 12 a

52 Carotid IMT was measured at 3 locations (common carotid artery,

53 he genetic correlation between the 2 carotid IMT arterial segments was 0.51.

54 ith HeFH who were >/=6 years of age, carotid IMT was significantly greater at baseline compared with

55 fidence interval [CI]: 0.3, 0.7) and carotid IMT (mean difference, 37 mum; 95% CI: 25, 49) were highe

56 th total and regional aortic PWV and carotid IMT while adjusting for several possible confounding fac

57 with aortic pulse wave velocity and carotid IMT.

58 alysis included 14 studies assessing carotid IMT and 7 assessing brachial artery FMD%.

59 calcification in men and with common carotid IMT and ABI in women (all P<0.05) after adjustment for m

60 ive effect of the A allele on common carotid IMT in women only (women: beta=-0.0047, P=1.63 x 10(-4);

61 nt showed stronger effects on common carotid IMT in women, raising questions about the mechanism of t

62 Common carotid IMT progression from EDIC years 1 to 6 was 0.019 mm less

63 orphisms for association with common carotid IMT was undertaken in 5 independent European cohorts (to

64 Internal and common carotid IMT were measured 8 and 14 years later by DCCT/EDIC.

65 was associated favorably with common carotid IMT, ABI, and coronary artery calcification in men and w

66 ions were attenuated and, for common carotid IMT, no longer significant when lipids, hypertension, di

67 For carotid IMT and FMD% values, we computed a pooled estimate of th

68 and Complications Trial (DCCT), had carotid IMT measurements at EDIC years 1, 6, and 12.

69 increase in the odds of having high carotid IMT, respectively, after adjusting for conventional risk

70 any effect on the 40% difference in carotid IMT between Axl genotypes.

71 was used to evaluate differences in carotid IMT between children with HeFH and the unaffected siblin

72 As a result, no difference in carotid IMT could be detected between the 2 groups after 2 years

73 2 years of follow-up, the change in carotid IMT was 0.0054 mm/y (95% confidence interval, 0.0030-0.0

74 owed that SSc patients had increased carotid IMT (summary mean difference 0.11 mm, 95% confidence int

75 ed their relationship with increased carotid IMT and compared the strength of the association with th

76 cantly less progression of increased carotid IMT in children with HeFH than untreated unaffected sibl

77 In addition, the mean internal carotid IMT levels were higher in subjects with plasma PK levels

78 The internal carotid IMT was 0.77 and 0.81 mm in the periodontal disease and

79 lasma PK and progression of internal carotid IMT.

80 The end-of-study difference in mean carotid IMT between children with HeFH and unaffected siblings a

81 so associated with an increased mean carotid IMT of 15 mum (95% CI: 0, 29) but not after additional a

82 with non-BM-derived cells) mediates carotid IMT.

83 er targets resulted in regression of carotid IMT and greater decrease in left ventricular mass in ind

84 esents the first large-scale GWAS of carotid IMT in a non-European population and identified several

85 progression and increased levels of carotid IMT in type 1 diabetes.

86 ifference and explored predictors of carotid IMT using random-effects meta-regression.

87 n in BM cells contributes to <30% of carotid IMT.

88 -year treatment with rosuvastatin on carotid IMT in children with HeFH.

89 differences in the Endo-PAT index or carotid IMT or stiffness.

90 At baseline, mean+/-SD carotid IMT was significantly greater for the 197 children with

91 It is unclear whether the carotid IMT is a risk indicator of processes affecting Bruch's m

92 us on chromosome 16, associated with carotid IMT and coronary artery disease in the IMT and IMT-Progr

93 ctivation is associated with both CAC and CC IMT in otherwise healthy individuals, consistent with th

94 n carotid artery intimal media thickness (CC IMT) in European-Americans [memory: beta = 0.02 (0.006,

95 fied the association between the GRS and CCA IMT (p for interaction=0.001).

96 The associations between the GRS and CCA IMT were stronger in participants with systolic blood pr

97 en genetic predisposition to obesity and CCA IMT.

98 as significantly associated with greater CCA IMT (p<0.001) after adjustment for age and gender.

99 of the GRS relating to 0.028 mm greater CCA IMT, p for trend<0.001) than those with SBP<120 mmHg and

100 The primary outcome was mean CCA IMT, measured at baseline and 12 mo, with B-mode ultraso

101 At 12 mo, CCA IMT regressed (mean +/- SD: -0.01 +/- 0.04 mm; P < 0.001

102 lled type 1 and type 2 diabetes may slow CCA IMT progression.

103 ent of the GRS relating to 0.001 smaller CCA IMT, p for trend=0.930).

104 n carotid artery intima media thickness (CCA IMT) progression, compared with a control group continui

105 ain intake was inversely associated with CCA IMT (beta +/- SE: -0.043 +/- 0.013, P = 0.005) and IMT p

106 y included 428 young Chinese adults with CCA IMT measured using a high-resolution B-mode tomographic

107 t far wall of the common carotid artery (CCA-IMT) and carotid artery bifurcation (BIF-IMT) between 20

108 thickness of the common carotid artery (CCA-IMT), pulse wave velocity (PWV), augmentation index, blo

109 ociations with incident CAD and baseline CCA-IMT were analyzed by using Cox regression and ANCOVA, re

110 in women, 757 to 790 microm in men), but CCA-IMT progression did not differ by HIV serostatus, either

111 ough the 1-y intervention did not change CCA-IMT or BP, clinically relevant improvements in arterial

112 ntervention did not significantly change CCA-IMT, augmentation index, or BP, but pulse pressure varia

113 In the included group, CCA-IMT was significantly correlated with snoring sound ener

114 75 years), HIV-infected participants had CCA-IMT and BIF-IMT values that were similar to or lower tha

115 HIV infection was associated with higher CCA-IMT and BIF-IMT values.

116 were also not associated with increased CCA-IMT.

117 usted rate of progression in the maximal CCA-IMT compared with nonusers (14 mum/year versus 22 mum/ye

118 Among the 158 RA patients, the maximal CCA-IMT increased in 82% (median 16 mum/year; P < 0.001) and

119 ted average yearly change in the maximal CCA-IMT was significantly greater in patients with earlier R

120 Unadjusted mean CCA-IMT increased (725 to 752 microm in women, 757 to 790 mi

121 rospectively enrolled for measuring mean CCA-IMT with B-mode ultrasonography, body mass index, metabo

122 near regression assessed associations of CCA-IMT and BIF-IMT with HIV infection and cardiovascular di

123 n carotid artery intima-media thickness (CCA-IMT) and new focal carotid artery plaque formation (IMT

124 n carotid artery intima-media thickness (CCA-IMT) were available for 846 men.

125 n carotid artery intima-media thickness (CCA-IMT) with snoring sounds in OSA patients.

126 d, controlling for clinical characteristics, IMT reader, and imaging device.

127 th progression of both internal and combined IMT (Wilks Lambda P value of 0.005).

128 and internal carotid arteries, and composite IMT variables considering the whole carotid tree (IMT(me

129 performed significantly worse than composite IMTs that incorporated plaques (p < 0.001).

130 In conclusion, IMT is a rare lung tumor in adults and may simulate mali

131 g charge-spin coupling drives the concurrent IMT and AFM-to-FM transition, which fosters the near roo

132 n, we suggest that the phragmoplast contains IMTs and highly dynamic noninterdigitating MTs, which wo

133 strated that a threshold of pathology (i.e., IMT>or=0.9 mm) is needed before IMT consistently relates

134 In the elderly, clinically elevated IMT is related to diminished attention-executive functio

135 o the neck or chest also had greater femoral IMT.

136 nt regimen had increased carotid and femoral IMTs and higher t-PA and PAI-I levels, indicating vascul

137 years) after treatment, carotid and femoral IMTs in CCSs were not different from those of controls.

138 de significant discovery P=6.75 x 10(-7) for IMT(max); replication P=7.24x10(-6) for common cIMT; adj

139 sed genome-wide association study (GWAS) for IMT to identify polymorphisms influencing IMT and to det

140 d new focal carotid artery plaque formation (IMT >1.5 mm) over median 7 years.

141 Greater IMT was associated with presence of cardiovascular risk

142 Similarly, G1 CHC patients had a greater IMT compared with control patients (1.04 +/- 0.21 versus

143 icrom/y (95% CI 2.6 to 7.4 microm/y) greater IMT progressions among persons in the same metropolitan

144 High IMT was defined as an IMT >/=90th percentile according t

145 ith MetS are at increased risk of adult high IMT and T2DM, these data indicate that the resolution of

146 ce, carotid artery plaque presence, and high IMT for incident CVD events.

147 95% confidence interval: 2.4 to 4.9) of high IMT and 12.2 times the risk (95% confidence interval: 6.

148 and follow-up and examined for risk of high IMT and T2DM.

149 HD more than carotid plaque presence or high IMT.

150 Patients with piHDL also had a higher IMT (P<0.001).

151 evalence of carotid plaque and with a higher IMT.

152 IGT individuals also demonstrated higher IMT in right and left carotid arteries (P = 0.017 and P

153 16 mum/year; P < 0.001) and the maximal ICA-IMT increased in 70% (median 25 mum/year; P < 0.001).

154 For the maximal ICA-IMT, cumulative prednisone exposure was associated with

155 resulting from the combination of FRFs+ICCAD+IMT(mean-max) was +12.1% (p < 0.01).

156 The difference in IMT predicted by a 1 SD increment in the FGGRS (0.0048 m

157 There were no significant differences in IMT between groups.

158 Differences in IMT progression between DCCT intensive and conventional

159 f IMT, explaining most of the differences in IMT progression between DCCT treatment groups.

160 the GRS was related to 0.023 mm increment in IMT.

161 IgE class switching events were observed in IMT samples, consistent with NIK upregulation in these t

162 rgets of the NMD pathway were upregulated in IMT samples, indicating that the UPF1 mutations led to r

163 Increased IMT was associated with significantly lower NAA/Cr ratio

164 3 gene to loss of Id3 function and increased IMT.

165 CCSs treated with localized RT had increased IMT outside the primary irradiation field.

166 concentrations are associated with increased IMT progression and that greater reductions in PM2.5 are

167 although it may be that these loci influence IMT through nonglucose pathways.

168 or IMT to identify polymorphisms influencing IMT and to determine if distinct carotid artery segments

169 festations of three adult patients with lung IMT.

170 The average of 8 maximal IMT measurements (IMT(mean-max)), alone or combined with

171 common carotid arteries and the mean maximal IMT of 12 segments.

172 Similar associations were found for maximum IMT.

173 The presence of at least 1 plaque (maximum IMT >1.5 mm) performed significantly worse than composit

174 Mean IMT was associated with the 10-year incidence of pure ge

175 Mean IMT was regressed on the FGGRS and on the component SNPs

176 Mean IMT>/=75th percentile (for age, sex, and race) alone did

177 n-events better than the common carotid mean IMT (net reclassification improvement [NRI]: +11.6% and

178 r H (CFH) genotypes, and other factors, mean IMT was associated with the 10-year incidence of early A

179 The mean IMT of the LCCA tended to differ across the KD subgroups

180 gnificantly associated (P = 0.009) with mean IMT.

181 nsidering the whole carotid tree (IMT(mean), IMT(max), and IMT(mean-max)), were analyzed.

182 The average of 8 maximal IMT measurements (IMT(mean-max)), alone or combined with ICCAD, classified

183 nce of early AMD (odds ratio [OR] per 0.1 mm IMT, 1.11; 95% confidence interval [CI], 1.00-1.21; P =

184 = 0.02) but not exudative AMD (OR per 0.1 mm IMT, 1.14; CI, 0.97-1.34; P = 0.11).

185 -1.21; P = 0.03) and late AMD (OR per 0.1 mm IMT, 1.27; CI, 1.10-1.47; P = 0.001).

186 ce of pure geographic atrophy (OR per 0.1 mm IMT, 1.31; CI, 1.05-1.64; P = 0.02) but not exudative AM

187 to the incidence of late AMD (OR per 0.1 mm IMT, 2.79 for 4-6 sites vs. none; CI, 1.06-7.37; P = 0.0

188 electively cross-linked interdigitating MTs (IMTs) to allow antiparallel MTs to be closely engaged in

189 nsitive variations in the thermal nanodomain IMT behaviour, this suggests that the IMT is highly susc

190 atients who had a current or past history of IMT or who were in remission.

191 erability by examining subclinical levels of IMT in relation to a sensitive marker of neuronal integr

192 lood pressure were significant predictors of IMT progression.

193 ctors are associated with the progression of IMT and plaque after controlling for traditional CVD ris

194 were strongly associated with progression of IMT, explaining most of the differences in IMT progressi

195 e (ALK) fusion genes in approximately 50% of IMTs and the role of ALK inhibition in the treatment of

196 mmune infiltration that is characteristic of IMTs.

197 Approximately half of IMTs carry rearrangements of the anaplastic lymphoma kin

198 Although the presence of IMTs was not essential for vesicle trafficking, they wer

199 Often IMT is measured as the average of these 2 arteries; yet,

200 PCA 1 was not associated with CAC or IMT.

201 tronic mechanism dominating the photoinduced IMT, but also highlight the difficulty to deduce microsc

202 Predictive values of carotid plaque, IMT, and CAC presence were compared using Cox proportion

203 s with metastatic or inoperable ALK-positive IMT received crizotinib orally twice daily.

204 bout the molecular pathways that precipitate IMT formation.

205 A decay (NMD) pathway, in 13 of 15 pulmonary IMT samples.

206 ated with significantly lower NAA/Cr ratios (IMT beta=-0.62, p=0.001), independent of age and systoli

207 Patients were randomly assigned to receive IMT (n=1213) or placebo (n=1213) by intragluteal injecti

208 The mean left and right IMT were 0.754 (0.210) mm and 0.751 (0.187) mm, respecti

209 was 45.1 +/- 10.3 years, and the mean +/- SD IMT progression rate was 0.011 +/- 0.03 mm per year.

210 Intensive treatment slowed IMT progression for 6 years after the end of DCCT but di

211 eline PM2.5 were also associated with slowed IMT progression (-2.8 microm/y [95% CI -1.6 to -3.9 micr

212 er reductions in PM2.5 are related to slower IMT progression.

213 ctive AA genotype was associated with slower IMT progression in women (P=0.04) but not in men.

214 Segment-specific IMT measurements of common carotid, bifurcation, and int

215 The IMT and presence of plaque were assessed using B-mode ul

216 ue progression rate was higher than, and the IMT progression rate was similar to, those in the contro

217 Fundamentally, the IMT in VO2 can be triggered on femtosecond timescale to

218 rotid IMT and coronary artery disease in the IMT and IMT-Progression as Predictors of Vascular Events

219 months, there were 399 primary events in the IMT group and 429 in the placebo group (hazard ratio 0.9

220 ng techniques, we simultaneously monitor the IMT in VO2 and the change of plasmons on gold infrared n

221 We confirm that the IMT actually occurs concomitantly with the FM transition

222 In this study, we find that the IMT behavior of NbO2 follows the field-induced nucleatio

223 domain IMT behaviour, this suggests that the IMT is highly susceptible to local changes in, for examp

224 based non-specific immunomodulation therapy (IMT) in patients with New York Heart Association (NYHA)

225 ive therapy drugs (immunomodulatory therapy [IMT]), or biologic response modifiers (BRMs) was assesse

226 chanisms of carotid intima-media thickening (IMT) are largely unknown.

227 th increased carotid intima-media thickness (IMT) and cardiovascular events in type 1 diabetes.

228 Intima-media thickness (IMT) and carotid plaques, defined as focal thickening of

229 e changes in carotid intima-media thickness (IMT) and plaque.

230 T was related to the intima-media thickness (IMT) and to atherosclerotic plaque in carotid arteries i

231 od on carotid artery intima-media thickness (IMT) and type 2 diabetes mellitus (T2DM).

232 ommon carotid artery intima-media thickness (IMT) during or after PE has not indicated any increased

233 ls on carotid artery intima-media thickness (IMT) in adulthood.

234 Carotid intima-media thickness (IMT) is a marker of subclinical atherosclerosis that can

235 eased carotid artery intima-media thickness (IMT) is a noninvasive marker of systemic arterial diseas

236 nd increased carotid intima-media thickness (IMT) may indicate elevated cardiovascular disease (CVD)

237 conducted to assess intima-media thickness (IMT) of the carotid artery, coronary artery calcificatio

238 Intima-media thickness (IMT) of the common and internal carotid arteries is an e

239 in the mean maximal intima-media thickness (IMT) of the common carotid artery (CCA) and the internal

240 tude Testing index), intima-media thickness (IMT) of the right common carotid artery (RCCA) and the l

241 Carotid intima-media thickness (IMT) was acquired and measured by trained research nurse

242 hy subjects; carotid intima media thickness (IMT) was assessed as a marker of systemic vascular disea

243 Carotid intima-media thickness (IMT) was assessed by ultrasound.

244 and internal carotid intima-media thickness (IMT) were measured by B-mode ultrasonography in EDIC yea

245 l and common carotid intima-media thickness (IMT) were measured.

246 th increased carotid intima-media thickness (IMT), a measure of subclinical atherosclerosis.

247 carotid artery (CCA) intima-media thickness (IMT), a measure of subclinical atherosclerosis.

248 s plaque and carotid intima-media thickness (IMT), computed tomography, magnetic resonance imaging, f

249 id- and femoral-wall intima-media thickness (IMT), flow-mediated vasodilatation of the brachial arter

250 ommon carotid artery intima-media thickness (IMT).

251 by increased carotid intima-media thickness (IMT).

252 ociated with carotid intima-media thickness (IMT).

253 plaques and measure intima-media thickness (IMT).

254 egulation or carotid intima-media thickness (IMT).

255 Intimal medial thickness (IMT) of both carotid arteries was measured by high-resol

256 progression of the intima-medial thickness (IMT) of the common carotid artery, as an indicator of at

257 mon carotid artery intimal medial thickness (IMT).

258 the IMPROVE (Carotid Intima Media Thickness [IMT] and IMT-Progression as Predictors of Vascular Event

259 of atherosclerosis (intima-media thickness [IMT] by echo-color Doppler) in a large, inclusive survey

260 = 0.23, P = 0.002) were directly related to IMT, and these associations were much more robust than t

261 However, no relationship to IMT was seen.

262 h associated systemic disease may respond to IMT or BRMs.

263 ts with necrotizing scleritis may respond to IMT, mainly alkylating agents.

264 ge daytime BP and clinic B were unrelated to IMT.

265 cally induced insulator-to-metal transition (IMT) characteristic.

266 tching of VO2 insulator-to-metal transition (IMT) locally on the scale of 15 nm or less and control o

267 The insulator-metal transition (IMT) of vanadium dioxide (VO2) has remained a long-stand

268 rs before the insulator-to-metal transition (IMT), which is still controversial.

269 , Pfizer) in a patient with ALK-translocated IMT, as compared with no observed activity in another pa

270 ariables considering the whole carotid tree (IMT(mean), IMT(max), and IMT(mean-max)), were analyzed.

271 with an inflammatory myofibroblastic tumor (IMT) harboring a RANBP2-ALK translocation who progressed

272 Inflammatory myofibroblastic tumor (IMT) is a distinctive mesenchymal neoplasm characterized

273 Inflammatory myofibroblastic tumor (IMT), also known as inflammatory pseudotumor, is a benig

274 Inflammatory myofibroblastic tumors (IMTs) are characterized by myofibroblast proliferation a

275 REVIEW: Inflammatory myofibroblastic tumors (IMTs) are indolent mesenchymal neoplasms associated with

276 CL) and inflammatory myofibroblastic tumors (IMTs).

277 The timescales of the ultrafast IMT vary from 40+/-8 fs, that is, shorter than a suggest

278 relapsed ALCL and metastatic or unresectable IMT highlight the importance of the ALK pathway in these

279 The NRI for US IMT in addition to traditional risk factors was not sign

280 nder the curve, approximately 0.95), whereas IMT was not (area under the curve, 0.49).

281 tions of marine-derived n-3 fatty acids with IMT and CAC prevalence, respectively.

282 h renal and splenic RIs were associated with IMT (renal RI: r = 0.19, P = .022; splenic RI: r = 0.23,

283 Factors associated with IMT measurements in the highest quartile were the presen

284 e physical activity were not associated with IMT or coronary artery calcification in either gender.

285 serum creatinine levels were associated with IMT progression (P = 0.0006).

286 BP metrics are independently associated with IMT.

287 o maintained an independent association with IMT (beta = 0.14, P = 0.04).

288 The significant inverse association with IMT remained after adjusting for traditional cardiovascu

289 sease, renal and splenic RIs correlated with IMT (renal RI: r = 0.33, P < .001; splenic RI: r = 0.30,

290 he significant association of the FGGRS with IMT suggests a possible causal association of elevated f

291 significant associations were not found with IMT progression without adjustment for metropolitan area

292 7,260 nondiabetic Caucasian individuals with IMT measurements and relevant genotyping.

293 ate (eGFR; r = -0.19, P = .001) but not with IMT (r = 0.08, P = .174).

294 long-term partial response in a patient with IMT carrying an ALK translocation but not in a patient w

295 The overall response rate for patients with IMT (treated at 100, 165, and 280 mg/m(2)/dose) was 86%.

296 eatment option for a subset of patients with IMT and pulmonary adenocarcinoma.

297 s, respectively, and in 43% of patients with IMT.

298 CL280, and 36% (five of 14) of patients with IMT.

299 the association of a genetic risk score with IMT.

300 Successful treatment with IMT was associated with diffuse or nodular scleritis wit